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9 |
<p>I shipped 10 µL of my vector miniprep to a collaborator in a 1.5 mL eppendorf parafilmed shut and stuffed into a 50 mL conical with some paper-towel padding. However, something happened on the way and there was nothing (no liquid) in the tube when it arrived. They didn't make any comments about the microcentrifuge tube popping open or broken parafilm, so nothing crazy happened but something did.</p>
<p>What's the most reliable way to ship plasmids?</p>
|
[
{
"answer_id": 36,
"pm_score": 5,
"text": "<p><strong>Summary</strong></p>\n\n<ul>\n<li>the 10 uL of plasmid miniprep may have been splattered in the cap of the tube (AnnaF)</li>\n<li>the eppendorf tube may have depressurized during air shipment and allowed the 10 uL to escape and evaporate</li>\n<li><strong>solution:</strong> try air-drying or blotting (Jonas) your minipreps prior to air shipment </li>\n</ul>\n\n<p><strong>Details</strong></p>\n\n<p>As AnnaF wrote, the 10 uL of your plasmid could have been hidden in the cap or dispersed around the tube, making appear empty. You should check with your collaborators to be sure they centrifuged it.</p>\n\n<p>According to a <a href=\"http://www.fedex.com/us/services/pdf/PKG_Pointers_Perishable.pdf\">fedex document on shipping perishables (pdf)</a> and a <a href=\"http://digitalcommons.calpoly.edu/cgi/viewcontent.cgi?article=1038&context=it_fac\">paper measuring the temp and pressure of air shipments (pdf)</a>, fedex and ups air shipments may experience low pressure environments around 0.56 - 0.74 atmospheres (atm). At these relatively low pressures, perhaps an eppendorf tube sealed at 1 atm might breach. The papers also note that ground shipments that pass over the rockies (i.e. in Colorado) may experience ~ 0.64 atm.</p>\n\n<p>So perhaps your 1.5 ml eppendorf tube depressurized during the shipment?</p>\n\n<p>It would be interesting to do some tests on the pressure-worthiness of eppendorf tubes.</p>\n\n<p>Regarding the original question, in 2007 I prepared and shipped (fedex) a library of thousands of minipreps to hundreds of users. 1uL of miniprep was dispensed into wells of 384-well plates and airdried, then sealed with aluminum, then mailed. Users rehydrate a well with 10 uL of water. Generally it works.</p>\n"
}
] |
[
{
"answer_id": 17,
"pm_score": 4,
"text": "<p>Did they try to centrifuge the tube when it got there to push all the liquid to the bottom? I know that especially when working with such little amounts that even shaking it up a little can disperse the contents all over the tube.\nWe have received plasmids from other labs before. Generally speaking the plasmids are sent in Screw-cap microcentrifuge tubes inside of some sort of canister. This is then packaged in a little foam cooler with dry ice to keep everything cold.</p>\n"
},
{
"answer_id": 18,
"pm_score": 4,
"text": "<p>A quite safe way of shipping plasmids is to put them on filter paper (see <a href=\"http://www0.hku.hk/biochem/research/tcf/protocols/Plasmid_shipment.html\">protocol</a> and send a letter. Much cheaper.</p>\n"
},
{
"answer_id": 271,
"pm_score": 3,
"text": "<p>Since tubes can be crushed in the mail, the safest way to ship plasmids is to drip a few uL into a filter paper, and then wrap it up to seal it with parafilm, and fill out a detailed form about its content.</p>\n\n<p>Good luck.</p>\n"
},
{
"answer_id": 318,
"pm_score": 2,
"text": "<p>We have gotten into similar situations when other labs have sent us plasmids (or when we have taken out ancient tubes out from storage boxes at -20), and have since adopted the filter paper method. Another point to note is that you can just add, say, 10 μL of water to the \"empty\" tube (Mac) and use 1 μL for a transformation. It has always worked for us. DNA is seemingly invisible!</p>\n"
},
{
"answer_id": 1306,
"pm_score": 1,
"text": "<p>I will also strongly recommend blotting a microgram of your plasmid DNA on a piece of filter paper (the filter paper is important for extraction on the receiving end). Also, it is very very helpful if you clearly indicate the amount of DNA (approximately) and circle the blotted DNA in pen so there is no ambiguity about cutting out the circle of filter paper containing the DNA.</p>\n\n<p>On the receiving end, you should always freeze the paper right away or elute the DNA off of the paper in TE buffer or water and then freeze. Failure to do so will eventually lead to DNAase degradation of the plasmid DNA and then you'll have to wait for another shipment.</p>\n"
}
] |
38 |
<p>I'm trying to find a good protocol for plasmid minipreps and I'm looking at 3 preps I've found:</p>
<ol>
<li><a href="http://openwetware.org/wiki/One_step_%27miniprep%27_method_for_the_isolation_of_plasmid_DNA" rel="nofollow">Using phenol/chloroform</a>
<ul>
<li>extract with phenol:chloroform:isoamylalcohol,</li>
<li>isopropanol precipitation, 12,000g spin down,</li>
<li>rinse with cold 70% ethanol. </li>
</ul></li>
<li><a href="http://openwetware.org/wiki/Miniprep/Kit-free_high-throughput_protocol" rel="nofollow">Using lysozyme</a>
<ul>
<li>lyse with lysozyme,</li>
<li>remove pellet, </li>
<li>isopropanol precipitation,</li>
<li>wash with cold 80% ethanol.</li>
</ul></li>
<li><a href="http://biotech.biology.arizona.edu/labs/DNA_isolation_plasmid.html" rel="nofollow">Using alkaline lysis</a>
<ul>
<li>open cells with 80% glucose in EDTA buffer,</li>
<li>add SDS and NaOH,</li>
<li>pellet protein/membrane with acetic acid/acetate,</li>
<li>ispropanol precipitation,</li>
<li>wash with cold 70% ethanol.</li>
</ul></li>
</ol>
<p>They all differ in how to break open the cells and separate plasmids from the rest of the cell -- quite a bit. Can anyone help me figure out which protocol is best here? </p>
|
[
{
"answer_id": 55,
"pm_score": 3,
"text": "<p>In my experience, the P:C:I method will get you higher yields, and is a bit more simple (in steps and chems involved), but as @Mad Scientist has said, phenol use might be an issue. It depends on the age of your students.</p>\n"
}
] |
[
{
"answer_id": 47,
"pm_score": 3,
"text": "<p>The protocol I used in my genetics lab course was alkaline lysis followed by ethanol precipitation <a href=\"http://www.protocol-online.org/cgi-bin/prot/view_cache.cgi?ID=1667\">similar to this one</a>. Nothing terribly toxic or requiring a fume hood (at least at the small volumes used).</p>\n\n<p>The more practical, reliable method is to use a miniprep kit (usually spin columns) from one of several suppliers (<a href=\"http://www.qiagen.com/Products/Plasmid/QIAprepMiniprepSystem/QIAprepSpinMiniprepKit.aspx?r=912\">Qiagen</a>, <a href=\"http://www.promega.com/products/dna-and-rna-purification/plasmid-purification/pureyield-plasmid-miniprep-system/\">Promega</a>, <a href=\"http://www.bio-rad.com/prd/en/US/adirect/biorad?cmd=catProductDetail&vertical=LSR&country=US&lang=en&productID=732-6100\">Bio-Rad</a>, etc.) which are fairly affordable at $1-2 per prep.</p>\n"
},
{
"answer_id": 61,
"pm_score": 2,
"text": "<p>Using spin columns, my professor and I extracted ~30 plasmids from ~30 samples in a few hours. It's easy, cheap, and it yields good quality plasmid. My sample was quantified by UV spec and it was at about 200ng/ul.</p>\n"
},
{
"answer_id": 283,
"pm_score": 3,
"text": "<p>I think the spin column kits are the way to go. As mentioned already, the benefits of the kits are that they are easy, safe, and (most importantly) how almost every actual lab does plasmid purification these days. </p>\n\n<p>The biggest criticism of the commercial kits is that you can get by easily without knowing anything about what is actually happening in the tube. However, as noted in the comments to Nick T's answer, there is no secret proprietary technology in the kits--they use the <em>alkaline lysis</em> method. This means that you can still teach the mechanism in the class while getting the benefit of the spin columns.</p>\n\n<p>One option, for teaching purposes, is to make all of your own solutions and just use the spin columns on the supernatant after pelleting the precipitated membrane/protein. That way, you get the benefit of insisting on real names for the solutions (NaOH is a more educational name than P2) and you get to use the spin columns in place of the ethanol precipitation. I believe there are cheap sources that just sell the spin columns, although I have never used them. You want to avoid the ethanol precipitation because it adds a bare minimum of 30 minutes to the protocol (for my protocols, it was more like an 1.5 hours or more). And waiting for ethanol to evaporate so you can resuspend is like watching paint dry unless you have a speed vac.</p>\n\n<p>Yield shouldn't be a big issue in a class situation, but you can boost yield with the column by prolonging the final elution step. I think the given instruction is to let the TE buffer (Tris) \"elute\" for 1 minute before the final spin, but I have routinely let the TE sit for about 15-30 minutes before spinning down. The difference in yield blew out the exposure on the gel camera.</p>\n\n<p>There are certain cases where phenol:chloroform extractions are still desirable, but this is definitely not one of them. I used to do P:Cs routinely when working with RNA and yeast genomic DNA. I have never seen anyone do anything other than a miniprep when preparing plasmids. What's more, the hassle of working in a fume hood and the risk of phenol burns encouraged <em>a lot</em> of people in the lab to prefer the spin kits even when working with genomic DNA.</p>\n"
},
{
"answer_id": 14751,
"pm_score": 0,
"text": "<p>To save cost, you can buy spin columns alone from suppliers such as Syd Labs (<a href=\"http://www.sydlabs.com/spin-column-for-plasmid-miniprep-p110.htm\" rel=\"nofollow\">http://www.sydlabs.com/spin-column-for-plasmid-miniprep-p110.htm</a>) and make home-made buffers. The suppliers normally provide the buffer recipe. </p>\n"
}
] |
58 |
<p>We suspect a bi-directional transcription event is happening at a locus in our organism where two genes are directly adjacent to each other. The annotation data is not well established. The intergenic distance is probably less than 200 base pairs.</p>
<p>The two genes are expressed in opposite directions towards each other. Base on the preliminary transcriptomics data, it seems like one gene is over transcribing (3' UTR perhaps?) into the adjacent gene, possibly resulting in some kind of transcriptional regulation of the adjacent gene. </p>
<p>Here is a rough diagram of what we think might be happening:</p>
<pre><code>------------------------==========gene A================>----------------------
----------------------------------------<====gene B=====-----------------------
</code></pre>
<p>Of course we need to first confirm this by designing primers to see if this over transcription is actually happening. </p>
<p>If this is happening, we intend to do some knock down experiments. We have no transgenesis available in our organism, only RNAi by dsRNA. It is possible to specifically knock down geneA by introducing dsRNA to the 5' region of geneA that does not overlap with geneB. Perhaps this will lead to ectopic/over expression of geneB. </p>
<p>Is there anyway to knock down geneB specifically without knocking down geneA? It looks like designing dsRNA for geneB would knock down both A and B.</p>
|
[
{
"answer_id": 55,
"pm_score": 3,
"text": "<p>In my experience, the P:C:I method will get you higher yields, and is a bit more simple (in steps and chems involved), but as @Mad Scientist has said, phenol use might be an issue. It depends on the age of your students.</p>\n"
}
] |
[
{
"answer_id": 47,
"pm_score": 3,
"text": "<p>The protocol I used in my genetics lab course was alkaline lysis followed by ethanol precipitation <a href=\"http://www.protocol-online.org/cgi-bin/prot/view_cache.cgi?ID=1667\">similar to this one</a>. Nothing terribly toxic or requiring a fume hood (at least at the small volumes used).</p>\n\n<p>The more practical, reliable method is to use a miniprep kit (usually spin columns) from one of several suppliers (<a href=\"http://www.qiagen.com/Products/Plasmid/QIAprepMiniprepSystem/QIAprepSpinMiniprepKit.aspx?r=912\">Qiagen</a>, <a href=\"http://www.promega.com/products/dna-and-rna-purification/plasmid-purification/pureyield-plasmid-miniprep-system/\">Promega</a>, <a href=\"http://www.bio-rad.com/prd/en/US/adirect/biorad?cmd=catProductDetail&vertical=LSR&country=US&lang=en&productID=732-6100\">Bio-Rad</a>, etc.) which are fairly affordable at $1-2 per prep.</p>\n"
},
{
"answer_id": 61,
"pm_score": 2,
"text": "<p>Using spin columns, my professor and I extracted ~30 plasmids from ~30 samples in a few hours. It's easy, cheap, and it yields good quality plasmid. My sample was quantified by UV spec and it was at about 200ng/ul.</p>\n"
},
{
"answer_id": 283,
"pm_score": 3,
"text": "<p>I think the spin column kits are the way to go. As mentioned already, the benefits of the kits are that they are easy, safe, and (most importantly) how almost every actual lab does plasmid purification these days. </p>\n\n<p>The biggest criticism of the commercial kits is that you can get by easily without knowing anything about what is actually happening in the tube. However, as noted in the comments to Nick T's answer, there is no secret proprietary technology in the kits--they use the <em>alkaline lysis</em> method. This means that you can still teach the mechanism in the class while getting the benefit of the spin columns.</p>\n\n<p>One option, for teaching purposes, is to make all of your own solutions and just use the spin columns on the supernatant after pelleting the precipitated membrane/protein. That way, you get the benefit of insisting on real names for the solutions (NaOH is a more educational name than P2) and you get to use the spin columns in place of the ethanol precipitation. I believe there are cheap sources that just sell the spin columns, although I have never used them. You want to avoid the ethanol precipitation because it adds a bare minimum of 30 minutes to the protocol (for my protocols, it was more like an 1.5 hours or more). And waiting for ethanol to evaporate so you can resuspend is like watching paint dry unless you have a speed vac.</p>\n\n<p>Yield shouldn't be a big issue in a class situation, but you can boost yield with the column by prolonging the final elution step. I think the given instruction is to let the TE buffer (Tris) \"elute\" for 1 minute before the final spin, but I have routinely let the TE sit for about 15-30 minutes before spinning down. The difference in yield blew out the exposure on the gel camera.</p>\n\n<p>There are certain cases where phenol:chloroform extractions are still desirable, but this is definitely not one of them. I used to do P:Cs routinely when working with RNA and yeast genomic DNA. I have never seen anyone do anything other than a miniprep when preparing plasmids. What's more, the hassle of working in a fume hood and the risk of phenol burns encouraged <em>a lot</em> of people in the lab to prefer the spin kits even when working with genomic DNA.</p>\n"
},
{
"answer_id": 14751,
"pm_score": 0,
"text": "<p>To save cost, you can buy spin columns alone from suppliers such as Syd Labs (<a href=\"http://www.sydlabs.com/spin-column-for-plasmid-miniprep-p110.htm\" rel=\"nofollow\">http://www.sydlabs.com/spin-column-for-plasmid-miniprep-p110.htm</a>) and make home-made buffers. The suppliers normally provide the buffer recipe. </p>\n"
}
] |
90 |
<p>I'm by no means an expert in the field, merely a curious visitor, but I've been thinking about this and Google isn't of much help. Do we know of any lifeforms that don't have the conventional double-helix DNA as we know it? Have any serious alternatives been theorized?</p>
|
[
{
"answer_id": 106,
"pm_score": 6,
"text": "<p>To follow up what mbq said, there have been a number of \"origin of life\" studies which suggest that RNA was a precursor to DNA, the so-called \"RNA world\" (1). Since RNA can carry out both roles which DNA and proteins perform today. Further speculations suggest things like a Peptide-Nucleic Acids \"<a href=\"https://en.wikipedia.org/wiki/Peptide_nucleic_acid\" rel=\"noreferrer\">PNA</a>\" may have preceded RNA and so on.</p>\n\n<p>Catalytic molecules and genetic molecules are generally required to have different features. For example, catalytic molecules should be able to fold and have many building blocks (for catalytic action), whereas genetic molecules should not fold (for template synthesis) and have few building blocks (for high copy fidelity). This puts a lot of demands on one molecule. Also, catalytic biopolymers can (potentially) catalyse their own destruction.</p>\n\n<p>RNA seems to be able to balance these demands, but then the difficulty is in making RNA prebiotically - so far his has not been achieved. This has lead to interest in \"metabolism first\" models where early life has no genetic biopolymer and somehow gives rise to genetic inheritance. However, so far this seems to have been little explored and largely unsuccessful (2).</p>\n\n<p><em>edit</em></p>\n\n<p>I just saw <a href=\"http://www.newscientist.com/article/dn21335-before-dna-before-rna-life-in-the-hodgepodge-world.html\" rel=\"noreferrer\">this popular article</a> in New Scientist which also discusses TNA (Threose nucleic acid) and gives some background reading for PNA, GNA (Glycol nucleic acid) and ANA (amyloid nucleic acid).</p>\n\n<hr>\n\n<p><a href=\"http://www.nature.com/nature/journal/v319/n6055/abs/319618a0.html\" rel=\"noreferrer\">(1) Gilbert, W., 1986, Nature, 319, 618 \"Origin of life: The RNA world\"</a></p>\n\n<p><a href=\"http://www.ncbi.nlm.nih.gov/pubmed/17897696\" rel=\"noreferrer\">(2) Copley et al., 2007, Bioorg Chem, 35, 430 \"The origin of the RNA world: co-evolution of genes and metabolism.\"</a></p>\n"
}
] |
[
{
"answer_id": 95,
"pm_score": 5,
"text": "<p>There has been a recent report on Science, which had much return in the general press, in which a bacteria was identified that could live in an environment where arsenic was subsituted to phosphorus (one of the components of DNA, forming the backbone of the double helyx).</p>\n\n<p>This is the original paper:<br>\n<a href=\"http://www.sciencemag.org/content/332/6034/1163.full\" rel=\"nofollow noreferrer\">A Bacterium That Can Grow by Using Arsenic Instead of Phosphorus</a><br>\nand the commentary appeared on Nature<br>\n<a href=\"http://www.nature.com/news/2010/101202/full/news.2010.645.html\" rel=\"nofollow noreferrer\">Arsenic-eating microbe may redefine chemistry of life</a></p>\n\n<p>There is, however, much critique on the methodology used in the paper, and on whether arsenic would really be incorporated in DNA instead of phosphorus.</p>\n\n<p>Science published several of these critiques in an <a href=\"http://www.sciencemag.org/content/early/2011/05/26/science.1208877\" rel=\"nofollow noreferrer\">Editor's Note</a>\nAnd here you will find the <a href=\"http://www.sciencemag.org/content/early/2011/05/26/science.1202098.abstract?sid=056401d0-39ae-48b4-a069-76547475c618\" rel=\"nofollow noreferrer\">Response of the Authors</a></p>\n\n<p>Other than that... well if you consider virus as life-forms, there's plenty that do not have double stranded DNA, but have instead single strand DNA or single strand RNA or double strand RNA. </p>\n\n<p><a href=\"http://xkcd.com/829/\" rel=\"nofollow noreferrer\" title=\"According to a new paper published in the journal Science, reporters are unable to thrive in an arsenic-rich environment.\"><img src=\"https://i.stack.imgur.com/b1WBH.png\" alt=\"XKCD on arsenic-based life\"></a></p>\n"
},
{
"answer_id": 96,
"pm_score": 4,
"text": "<p>It depends whether you call prions a life form, but prions do not make (direct) use of DNA to propagate themselves. They force other proteins into a misfolded protein state.</p>\n\n<p>Again, the question remains whether prions should be considered \"alive\".</p>\n"
},
{
"answer_id": 102,
"pm_score": 4,
"text": "<p>There are serious speculations that the origins of life were using RNAs both as enzymes and genetic information carrier.<br>\nLater this informative RNAs evolved into a more stable and less reactive DNAs, enzymatic role was delegated to proteins and RNA only remained into most crucial parts of expression chain (mRNA and rybosome) and some regulation mechanisms. </p>\n"
},
{
"answer_id": 30043,
"pm_score": 2,
"text": "<p>This recent <a href=\"http://www.sciencedirect.com/science/article/pii/S1074552113004262\" rel=\"nofollow\">Cell paper</a> mentions a ribozyme (RNA enzyme) that ligates two oligonucleotides into itself. Given a sufficient source of input oligonucleotides and the correct conditions, it can catalyse its own replication and undergo Darwinian evolution, and can be thought of as a rudimentary form of RNA-based life. </p>\n\n<p>The authors hypothesise that ligase-based RNA replicators could have been the first RNA replicators, which were later replaced by the now-standard polymerisation:</p>\n\n<blockquote>\n <p>A somewhat different approach relies on RNA enzymes with RNA-templated\n RNA ligase activity to join oligonucleotide substrates to form\n complementary RNA products. It has been proposed that the first\n replicating, evolving systems on Earth operated by this mechanism and\n only later came to depend upon residue-by-residue polymerization</p>\n</blockquote>\n\n<p>It should be noted that RNA ribozyme polymerases already exist, but many of them require proteins in addition to the RNA structure. </p>\n"
}
] |
257 |
<p>I am looking for video lectures to go through to guide my reading in intro molecular and cellular biology. I've had intro bio and I study evolutionary theory, but my molecule- and cell-level knowledge is weak. </p>
<p>I'm finding it impossible to know where to look in a big book like Alberts, or to read Lodish without a guide, so I really need lectures to help me out. I've tried the MIT OCW assignments and a few other similar sites, but I can't seem to find a course that includes lectures. Does anyone know of any? Ideally they'd follow Watson et al. for molecular and Lodish for cellular, but I can find other textbooks too.</p>
|
[
{
"answer_id": 266,
"pm_score": 4,
"text": "<p>MIT's OCW is weak when it comes to biology videos. </p>\n\n<p>UC Berkeley has some good video content for molecular and cell biology.</p>\n\n<ul>\n<li><p>See, for example, this playlist:\n<a href=\"http://www.youtube.com/playlist?list=59C08AE05E752758\">http://www.youtube.com/playlist?list=59C08AE05E752758</a></p></li>\n<li><p>And explore the main UC Berkeley video lectures website here: <a href=\"http://webcast.berkeley.edu/\">http://webcast.berkeley.edu/</a></p></li>\n</ul>\n\n<p>UCSD, if I recall correctly, has had some pretty good life science lectures available online to the public, as well. Possibly also UCLA.</p>\n\n<p><a href=\"http://www.apple.com/education/itunes-u/what-is.html\">iTunes U</a> is your friend here. Unfortunately, to really take advantage of it, you <em>need</em> to download iTunes -- but it's worth it. The last time I looked, there was more there than I could possibly watch, and that was 4 years ago. </p>\n"
}
] |
[
{
"answer_id": 258,
"pm_score": 3,
"text": "<p>This one is not precisely molecular and cell biology, but rather systems biology. It might help you as some kind of introduction, though:</p>\n\n<p><a href=\"http://www.youtube.com/watch?v=Z__BHVFP0Lk\">Systems biology lecture 1</a></p>\n\n<p>Also, if you are really really new to the subject, you can probably use \"Molecular and Cell Biology for Dummies\". </p>\n"
},
{
"answer_id": 259,
"pm_score": 3,
"text": "<p><a href=\"http://ocw.mit.edu/index.htm\">MIT OpenCourseWare</a> provides very interesting material, and not only on biology.</p>\n\n<p>You may be interested in seeing the video lectures from some of the Introductory biology courses, such as <a href=\"http://ocw.mit.edu/courses/biology/7-014-introductory-biology-spring-2005/video-lectures/\">this one</a>, <a href=\"http://ocw.mit.edu/courses/biology/7-014-introductory-biology-spring-2005/video-lectures/\">this one</a> or <a href=\"http://ocw.mit.edu/courses/biology/7-013-introductory-biology-spring-2006/video-lectures/\">this other one</a>.</p>\n\n<p>There is, however, much more, check out the index of the <a href=\"http://ocw.mit.edu/courses/biology/\">available material for biology</a>.</p>\n"
},
{
"answer_id": 310,
"pm_score": 3,
"text": "<p>These are some of my favorite biology learning resources:</p>\n\n<p><a href=\"http://www.ibioseminars.org/\">iBioSeminars</a></p>\n\n<p><a href=\"http://academicearth.org/subjects/biology\">Academic Earth - Biology</a> </p>\n\n<p>Others include: <a href=\"http://www.khanacademy.org/#biology\">Khan Academy - Biology</a>, <a href=\"http://www.hhmi.org/biointeractive/video/index.html\">HHMI BioInteractive video collections</a>, W<a href=\"http://www.wellcome.ac.uk/Education-resources/index.htm\">ellcome Trust education resources</a>. </p>\n"
},
{
"answer_id": 1821,
"pm_score": 2,
"text": "<p>While not exclusively cell and molecular biology, I would also like to add the <a href=\"http://www.jove.com/\" rel=\"nofollow\">Journal of Visualized Experiments</a>. It's like Youtube for experiments. :)</p>\n"
},
{
"answer_id": 15799,
"pm_score": 1,
"text": "<p>The Journal of Visualized Experiments (<a href=\"http://www.jove.com/\" rel=\"nofollow\">jove.com</a>) is excellent but based on experimental protocols.</p>\n\n<p><a href=\"https://www.apple.com/apps/itunes-u/\" rel=\"nofollow\">ItunesU</a> also has great resources. Stay away from youtube - a lot of people there don't know what they are talking about.</p>\n"
},
{
"answer_id": 87769,
"pm_score": 0,
"text": "<p>I recommend two YouTube channels.</p>\n\n<ul>\n<li>Shomu's Biology. Probably the channel with the most extensive coverage of biology, but the guy explaining it has a very thick accent that is sometimes hard to follow.</li>\n<li>AK Lectures. Its main focus is on metabolism and physiology. I personally find it easy to understand.</li>\n</ul>\n"
}
] |
328 |
<p>In what ways has DNA been studied to see if there a "programmable" aspect to it? </p>
<p>Has nature produced anything resembling a Turing machine within the cell, perhaps using the "junk DNA" as its code? I expect nature's way would probably be very round-about and not compact.</p>
<p>NOTE: I am not asking about building DNA computers, as this question had recently been contorted to become.</p>
|
[
{
"answer_id": 427,
"pm_score": 5,
"text": "<p>Perhaps this question is whether the regions between genes sometimes known as 'junk DNA' has any function. </p>\n\n<p>In the human genome, out of ~5 billion bases <a href=\"http://www.ornl.gov/sci/techresources/Human_Genome/faq/genenumber.shtml\">there are something like 20-30,000 genes</a> which take up perhaps 10s of millions of base pairs, depending on how you count it. 1% of all human DNA is the common figure. </p>\n\n<p>It is sometimes asked as if biologists commonly think of it as having no use, but in fact this is a researched topic, and few feel that it has no evolutionary or biological function at all. </p>\n\n<p>Some of the most common uses for intergenic DNA in eukaryotes (bacteria are an entirely different topic with very different responses.</p>\n\n<ul>\n<li>Transcriptional Regulation</li>\n</ul>\n\n<p>Outside the coding sequences of the gene, there can be an extensive set of binding sities for proteins which regulate the gene. In this paper in Figure 1 the celebrated regulatory sequence of ENDO16 is <a href=\"http://www.pnas.org/content/102/24/8591.full\">can be seen in Figure 1</a>. As you can see for almoat 2000 bp there are numerous binding sites for many sorts of promotors and inhibitory factors, as well as factors which may splice the gene in various ways. </p>\n\n<p>As I recall, ENDO16 only turns on for a brief period in the development of the sea urchin and so its very tightly controlled, which means that its got a lot of regulatory elements upstream of it, controlling transcription. Its one of the most exhaustively studied genes ever and the believe they have most of it. Other human genes ive seen perusing medical literature have seen 20kb are necessary to reproduce the regulation of a gene. Still all this might at best only triple the amount of DNA actively involved.</p>\n\n<ul>\n<li><p>Centromeres and Telomeres\nThe physiology of the chromosomes have large regions as Deniz mentions are necessary for cell reproduction and for development. In animals (like humans) the regions are devoid of transcribed genes and might be 10-15% of the genome length (I'm eyeballing this from the UCSC genome browser on chr21 - in some organisms like yeast the centromere can be just a few hundred base pairs. So anyway we are getting somewhere now!</p></li>\n<li><p>Non translated genes.\nThere are lots of pieces of DNA that might be copied into RNA and then do not function as templates for proteins. some folks say there is a lot of this stuff. The typical view is that there are a few thousand of these sorts of beasts known, and <a href=\"http://mirbase.org/cgi-bin/browse.pl?org=hsa\">humans are currently thought to have about 1500 of them</a>. A small tweak in the number of genes, but they are there nonetheless.</p></li>\n<li><p>Chromatin binding and organization sites\nAlthough Centromeres are places where chromatin binds, the several families of proteins which bind DNA and wrap them <a href=\"http://en.wikipedia.org/wiki/Nucleosome#Higher_order_structure\">into organized coiled coils thought to be like spools of telephone wire to form the Nucleosome</a> which makes the chromosomes look like the little stick men you see in text books. Chromatin can spool up just about any sort of DNA but seems to have a preference for regions which are at the ends of genes. They can be modified by enzymes (acylated, methylated) to modulate their affinity for some classes of DNA sequence. This is a hot topic of research. The ability for RNA polymerase to find transcribe a gene is not good if its wound onto chromatin and though its not a precise binding like a transcription factor, chromatin binding and regulation must be affected greatly by changes in the distance between genes and the DNA sequences which surround a gene for thousands of base pairs, which is one of the main differences between species. </p></li>\n</ul>\n\n<p>Of all biological systems (at least that I know of) this one accounts for the most bulk DNA sequence and is probably as related to the difference between different species as transcription factors and almost certainly is an older system of gene regulation, if you think about it. </p>\n\n<ul>\n<li>Copy Number Variations and repetitive regions\njust a side note, but small and very long repeat sequences can show up in the intergenic regions as well as inside a gene boundary to account for some of the differences between individuals. they can be quite short or quite long. </li>\n</ul>\n\n<p>Well hope this helps?</p>\n"
}
] |
[
{
"answer_id": 418,
"pm_score": 3,
"text": "<p>By programmable, I suppose you mean that it contains information or can be altered in response to some input or stimulus. The answer is \"no\" for both. Well, sort of.</p>\n\n<p>Does noncoding DNA contain information? By definition, no. There are probably many regions of the genome that appear to have no information, only later to be found to contain introns, regulatory elements such as enhancers, boundary element, MAR/SARs, targeting sites, etc. Even functional tests (such as removing the region) may not reveal anything because the effects could be minor, or only evident under special conditions. But arguably, if you remove a region and it has an effect on the organism, then it's not really a noncoding DNA, it's just you didn't see the coding before hand.</p>\n\n<p>As for the latter, can it altered, the answer is again \"no,\" or at least \"apparently not.\" Intergenic regions (those stretches of DNA that do not contain obvious or characterized transcribed regions or their control elements) are very stable between organisms and even between species. They seem to have a mutation rate expected for having no information, and thus free to mutate slowly without being swept away. There is no evidence (as far as I know) of any region of the genome being purposefully altered, with the exception of a handful of specific genes whose regulation is controlled by DNA nicking or some such.</p>\n\n<p>Perhaps I am missing your question, being a biologist and not really knowing what a \"Turing Machine\" is. If I misunderstood, please clarify.</p>\n"
},
{
"answer_id": 420,
"pm_score": 3,
"text": "<p>Depends on what you mean by \"non-coding\".</p>\n\n<p>There are structural elements in telomeres & centromeres -- although the DNA there does not code for proteins, it contributes to the three dimensional structure of the chromosome.</p>\n\n<p>\"Non-Coding\" DNA can also act as a binding substrate for many proteins: transcription factors, enhancers, histone proteins; and thus control regulation indirectly through these intermediaries. </p>\n\n<p>Promoter regions upstream of transcribed/translated regions are the combinatorial control switches/dials of our genome, and have tremendous regulatory importance.</p>\n\n<p>Non-Coding DNA also acts as repertoires of mobile DNA elements, which enable fast evolution / \"plasticity\" by copying&pasting exons around (L1 transductions) or by copying into coding regions & interrupting them. </p>\n\n<p>Lastly, they can act as the sandbox of evolution: Non-coding regions not genetically linked to functional regions are very likely to not suffer from purifying selection, so they can act as templates of random evolution - where the vast majority of mutations won't have any impact positive or negative. This enables exploring brand new combinations, which may then become new exons / miRNA / regulatory regions or get shuffled into other regions to enable new functionality. </p>\n"
},
{
"answer_id": 446,
"pm_score": 2,
"text": "<p>Nature has done pretty well in the subject of formal computation. So much that we are still trying to keep its pace. </p>\n\n<p>As about your question, it depends on your definition of \"non-coding DNA\". </p>\n\n<p>In general, DNA together with the machinery in charge of its maintenance <em>is</em> Turing-complete in several senses. Take a look, for example, to the existence of mobile genetic elements: some of them are \"subprograms\" coding for reverse transcriptases which in turn are able to reproduce the original program. I must note that for doing this with a Turing-complete formalism like the lambda-calculus, well, you need to do a fairly long and complicated program: <a href=\"http://crpit.com/confpapers/CRPITV26Larkin.pdf\" rel=\"nofollow\">http://crpit.com/confpapers/CRPITV26Larkin.pdf</a> . And the lambda calculus is \"easier\" than bare Turing-machines, meaning that you can write shorter programs than with Turing machines for doing the same thing. So, my (somehow specious) argument is that any real-world information machine capable of self-replication is with high likelihood Turing-machine equivalent. </p>\n\n<p>It just happens that the essential feature of mobile genetic elements is to ensure its survival, so, that's probably the reason we haven't found a fragment of DNA able to do something as interesting as calculating square root. </p>\n\n<p>If you refer to the part of DNA that can not do anything at all, well, for talking about Turing-machines and computation you need a way in which some \"data\" can be \"interpreted\" as a program. A totally inert piece of DNA does not fill that role, by definition. </p>\n"
},
{
"answer_id": 461,
"pm_score": 3,
"text": "<p>I am very suprised nobody mentioned the field of DNA-computing. It is proofen by Leonard Adleman and Richard Lipton that you can compute with DNA molecules.</p>\n\n<p>In the article of Adleman they present an experiment to solve an instance of the Traveling-Salesman-Problem. Because this problem is in NP one can say that the DNA is turing-complete. </p>\n\n<p><a href=\"http://dx.doi.org/10.1126/science.7973651\">Article of Adleman</a></p>\n\n<p><a href=\"http://rads.stackoverflow.com/amzn/click/3540641963\">For a deeper understanding see</a></p>\n"
},
{
"answer_id": 486,
"pm_score": 1,
"text": "<p>Let me answer your question by splitting it into two parts:</p>\n\n<p><strong>Can DNA be used as an programmable medium (=band) for Turing machine?</strong></p>\n\n<p>The answer is <strong>YES.</strong></p>\n\n<p>Starting from the breaking <a href=\"http://www.cs.duke.edu/bioComp/references/shapiroJohn/ShapiroNature2001explained.pdf\" rel=\"nofollow\">paper by Shapiro et al. in Nature</a>, followed by another great article by <a href=\"http://www.nature.com/embor/journal/v4/n1/full/embor719.html\" rel=\"nofollow\">Parker</a>, there are many scientific publications about how to use DNA for computing. Unfortunately, these findings are still not applicable for classic computations and DNA computers will hardly substitute the normal ones in the nearest future.</p>\n\n<p><strong>Can a junk DNA work as Turing machine?</strong></p>\n\n<p>There is a known principle in Computer Science called \"Junk In, Junk Out\". Same in the case of DNA -- there is a way to use junk DNA for computing, but the result of the computation will mostly be junk too: as long as we don't know what this DNA is for, and this doesn't seem to operate as Turing machine on its own, there is hardly possible to get something reasonable by running this DNA on a turin machine...</p>\n"
}
] |
344 |
<p>There seem to be a number of ideas about why we age. Hypotheses include the gradual accumulation of cell metabolic products affecting organism function and the reduction of <a href="https://biology.stackexchange.com/questions/186/is-telomere-length-a-reliable-measure-of-health-lifespan">telomere length</a> during cell division.
My hand-wavey idea would be "wear and tear".</p>
<p>Are we anywhere near a consensus theory of senescence?</p>
|
[
{
"answer_id": 362,
"pm_score": 6,
"text": "<p>The 'wear and tear' argument is most likely true but it is also interesting to reason about ageing as inevitable from the evolutionary point of view.</p>\n\n<p>To set up the argument, we need two things:\nFirst, each individual has got a 'reproductive potential' which is realised throughout life. This means a deleterious mutation which has an effect in early life, will affect reproductive value more than a mutation which manifests itself in later life, after the individual has already had offspring. Thus selection will act strongly on genes which are expressed in early life than on those which are expressed later. For that reason, there's no strong selection against diseases such as diabetes or cancer. This argument can be applied not only to occurrence of disease but also to decay of ordinary functions of the body.</p>\n\n<p>Secondly, cells in the body are constantly renewed and defects such as telomeric breaks are repaired. Mutations in the soma are taken care of by the immune system and can be in principle avoided. The fact that they tend to accumulate in later life can be explained by the first point: <a href=\"http://onlinelibrary.wiley.com/doi/10.1111/j.1749-6632.2000.tb06651.x/full\">selection is weaker to oppose telomeric breaks and mutations in later life</a>.</p>\n\n<p>I was trying to be brief here, but there are more sides to the argument (e.g. Williams' antagonistic pleiotropy). <a href=\"http://www.amazon.co.uk/Modular-Evolution-Selection-Biological-Complexity/dp/0521728770\">Modular Evolution</a> (Vinicius, CUP 2010) provides a good overview of the evolutionary aspect of theory of senescence (and many other interesting evolutionary arguments).</p>\n"
}
] |
[
{
"answer_id": 404,
"pm_score": 3,
"text": "<p>Once could argue that we die because it is advantageous to get rid of mature individuals once they have reproduced. Because mature individuals have no more offspring to convey beneficial genes, those offspring which will benefit from knocking off their ancestors will have an evolutionary advantage.</p>\n"
},
{
"answer_id": 1549,
"pm_score": 2,
"text": "<p>There is a pretty good discussion on this topic in <a href=\"http://books.google.com/books?id=OWD3V9bFWV8C&pg=PA17&lpg=PA17&dq=loose%20cannon%20and%20weak%20link%20theories&source=bl&ots=UPPbTZrB_t&sig=a_W4f5Ob1wuOQ5wT1r4DotJFy-E&hl=en&sa=X&ei=uY5tT4W4I4nXrQejlMygDg&redir_esc=y#v=onepage&q&f=false\" rel=\"nofollow\">chapter 2</a> of <em>Geriactric Medicine - An Evidence Based Approach (4th ed)</em> by Cassel. This is the main reference for the info below which can hopefully add something to the answers already given.</p>\n\n<p>In terms of views on ageing, there's evidence to support both:</p>\n\n<ul>\n<li>general principles that may apply to it; and </li>\n<li>it being a consequence of a collection of degenerative processes (this is apparently the more supported view).</li>\n</ul>\n\n<p>Since almost all biological systems in the body degenerates with age and this happens seemingly at random, it's been difficult to identify particular catalysts that cause this. Consequently, biologists apparently steer away from a general theory or mechanism.</p>\n\n<p>However, there are two classes of theories that have been floating around. That is 'loose cannon' and 'weak link'.</p>\n\n<p><em>Loose Cannon</em> encompasses theories that support the 'wear and tear' proposition. Two popular theories under this banner are <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/1383768\" rel=\"nofollow\">free radicals</a> and <a href=\"http://www.springerlink.com/content/qq764j6548k56266/\" rel=\"nofollow\">glucose</a>.</p>\n\n<p><em>Weak Link</em> suggests that particular physiological systems are vulnerable during senescence and if a system fails, the whole body begins to decline. It's suggested that the neuroendocrine and immune systems are particularly vulnerable. </p>\n\n<p>There is also a limit on the ability of cells to replicate - this is called the Hayflick Phenomenon (or limit). The reduction of the enzyme <a href=\"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1933587/\" rel=\"nofollow\">Telomerase</a>, which lengthens telomeres during mitosis, is implicated in limiting a cell's ability to replicate indefinitely.</p>\n"
},
{
"answer_id": 2764,
"pm_score": 2,
"text": "<p>\"WHY\" we age is a different question from \"HOW\" we age. The \"WHY\" refers to ageing from an evolutionally standpoint, whereas the \"HOW\" refers to biology of ageing. As for the \"WHY\" I would read a few papers on the antagonistic pleiotropy hypothesis (<a href=\"http://www.ncbi.nlm.nih.gov/pubmed/22329645\" rel=\"nofollow\">click here</a>). As for the \"HOW\", there is no definitive understanding of mechanisms of ageing. However, the role of cellular senescence in ageing and age-related disease is a major player in the biology of ageing (<a href=\"http://www.ncbi.nlm.nih.gov/pubmed/19234764\" rel=\"nofollow\">click here</a> for example). When cells become senescent (due to either telomere shortening/DNA-damage) they can no longer divide to regenerate damaged tissue. Additionally, senescent cells are highly pro-inflammatory and so have the potential to damage the surrounding tissue if the are not removed. In younger organisms, senescent cells are most likely removed my the immune system, but as organisms age, the immune system also ages and can no longer effectively remove senescent cells.</p>\n"
},
{
"answer_id": 2789,
"pm_score": 2,
"text": "<p>I know this question has closed out, but I wanted add this recent reference. The reactivation of telomerase (which inhibits telomere shortening) <a href=\"http://www.guardian.co.uk/science/2010/nov/28/scientists-reverse-ageing-mice-humans\" rel=\"nofollow\">seems to have rejuvinated mice, including neuronal growth in the brain</a>. This is crazy awesome for a couple of reasons. </p>\n\n<p>One being that we may all get to see our 140th birthday.</p>\n\n<p>But since there were a reversal of aging from telomere extension, that implies that aging is adaptive and not a 'wear and tear' phenomenon, at least in animals like mice (and hopefully humans). hard to believe. </p>\n\n<p>i.e. If there was a mutant that turned on telomerase, why is it not a ubiquitous trait? </p>\n"
}
] |
378 |
<p>I am very interested in the evolution of the evolution process itself. There are of course a lot of things that influence how evolution will work, but for this question, I am interested in things that are only related to the evolution process. Examples could be increase chance of mutations in newborns, change in reproduction age, and similar. I am specifically interested in observation where the evolution process itself has adapted to a change in the environment.</p>
|
[
{
"answer_id": 382,
"pm_score": 6,
"text": "<p>Bacteria such as E. coli are known to increase their mutation rate (by switching to a more error prone polymerase among other things) when under stress. This can mean being placed in a medium where it's not adapted to grow (<a href=\"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1088971/?tool=pmcentrez\">http://www.micab.umn.edu/courses/8002/Rosenberg.pdf</a>) or when treated with antibiotics (<a href=\"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1088971/?tool=pmcentrez\">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1088971/?tool=pmcentrez</a>).</p>\n"
}
] |
[
{
"answer_id": 379,
"pm_score": 4,
"text": "<p>I think this falls into your criteria but correct me if i'm wrong :).</p>\n\n<p>The <a href=\"http://en.wikipedia.org/wiki/HIV\">HIV</a> reverse transcriptase protein has evolved to have relatively low fidelity (leading to a high mutation rate in replicated virus particles). Reverse transcriptase is also recombinogenic, ie. it can switch templates during replication leading to even more variability. Combined, these two properties lead to each individual having a large number of variant viral genomes, which leads to increased resistance to antiretroviral drugs etc.</p>\n\n<p>EDIT:</p>\n\n<p>I thought of <a href=\"http://en.wikipedia.org/wiki/Influenza\">influenza</a> as a second example. The viral genome has evolved to be fragmented into 7-8 pieces of RNA, which can be swapped with other strains during co-infection of a single cell. This can lead to more virulent or transmissible strains of influenza; these can also be helpful to create new strains that influenza vaccines are no longer useful against.</p>\n"
},
{
"answer_id": 380,
"pm_score": 2,
"text": "<p>How about species actively changing the factors that play a role in the selection process?</p>\n\n<p>Humans are a species that have heavily modified this process. In the western world, we have gone away from selection by survival skills and genetic fitness to move to a social selection, where genome is secondary to social skills and adaptation to fashion, which are acquired skills.</p>\n"
},
{
"answer_id": 384,
"pm_score": 4,
"text": "<p>The \"change in reproduction age\" you mention is one major aspect of life history evolution.</p>\n\n<p>A massive literature exists on this topic, including several books: e.g., <em>The evolution of life histories: Theory and analysis</em> (Roff, 1992) and <em>The evolution of life histories</em> (Stearns, 1992).</p>\n\n<p>Reznick and various colleagues have carried out extensive studies of experimental life history evolution in Trinidadian guppies going back ~30 years. For example:</p>\n\n<ul>\n<li><a href=\"http://www.jstor.org/stable/10.2307/2407978\">Reznick, D.N. and Endler, J.A. 1982. The impact of predation on life history evolution in Trindadian guppies (<em>Poecilia reticulata</em>). <em>Evolution</em> 36:160-177</a>. </li>\n<li>Reznick, D.N. and Bryga, H. 1987. Life-history evolution in guppies. 1. Phenotypic and genotypic changes in an introduction experiment. <em>Evolution</em> 41:1370-1385.</li>\n<li><a href=\"http://www.jstor.org/stable/10.2307/2409363\">Reznick, D.N. 1989. Life history evolution in guppies. 2. Repeatability of field observations and the effects of season on life histories. <em>Evolution</em> 43:1285-1297</a>.</li>\n<li><a href=\"http://www.sciencemag.org/content/275/5308/1934.short\">Reznick, D.N., Shaw, F.H., Rodd, F.H. and Shaw, R.G. 1997. Evaluation of the rate of evolution in natural populations of guppies (<em>Poecilia reticulata</em>). <em>Science</em> 275: 1934-1937</a>. </li>\n<li><a href=\"http://www.ncbi.nlm.nih.gov/pubmed/9193894\">Reznick, D.N. 1997. Life history evolution in guppies (<em>Poecilia reticulata</em>): guppies as a model for studying the evolutionary biology of aging. <em>Experimental Gerontology</em> 32:245-258.</a></li>\n</ul>\n\n<p>Life history evolution has also been documented in response to human pressures. Fisheries stocks are evolving in response to overfishing. For example:</p>\n\n<ul>\n<li><a href=\"http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=2&ved=0CCgQFjAB&url=http://onlinelibrary.wiley.com/doi/10.1111/j.1461-0248.2005.00858.x/abstract&ei=tpv8TtzDEI6-gAfb69CbAg&usg=AFQjCNFioK4lBCfYb81DnmlPW2g_QDShKg&sig2=HCg_ywYhaZ04tFYMhg156Q\">Walsh, M.R., Munch, S.B., Chiba, S. and Conover, D.O. 2006. Maladaptive changes in multiple traits caused by fishing: impediments to population recovery. <em>Ecology Letters</em> 9:142-148</a>.</li>\n<li><a href=\"http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=1&ved=0CB8QFjAA&url=http://www.somas.stonybrook.edu/people/munchpdf/conover_etal_05_cjfas.pdf&ei=9Jv8To20F8jBgAe26uGdAg&usg=AFQjCNGCeA8otCOCiD89gsmDB3fV_ah3_Q&sig2=ypfDhTxkVQ2Oq6lPfkb70g\">Conover, D.O., Arnott, S.A., Walsh, M.R. and Munch, S.B.. 2005. Darwinian Fishery Science: lessons from the Atlantic silverside. <em>Canadian Journal of Fisheries and Aquatic Science</em> 62:730-737</a>.</li>\n</ul>\n"
},
{
"answer_id": 390,
"pm_score": 3,
"text": "<p>Species have been observed in controlled experiments to use different sources of energy, for instance axenic <em>E. coli</em> cultures picking up citrate metabolism in <a href=\"http://myxo.css.msu.edu/ecoli/\">Lenski's Lab at MSU</a>. They have also shown that mutations to the mutator gene mutT can accelerate the process of evolution, though it's evolution directed by fitness in a very specific setting.</p>\n"
},
{
"answer_id": 3307,
"pm_score": 2,
"text": "<p>If you look at <a href=\"http://en.wikipedia.org/wiki/Adaptive_immune_system\" rel=\"nofollow\">the adaptive immune system</a>, the process of <a href=\"http://en.wikipedia.org/wiki/V%28D%29J_recombination\" rel=\"nofollow\">B-cell recombination</a>, clonal expansion and <a href=\"http://en.wikipedia.org/wiki/Somatic_hypermutation\" rel=\"nofollow\">somatic hypermuation</a> is, in essence, induced evolution.</p>\n"
},
{
"answer_id": 9698,
"pm_score": 2,
"text": "<p>Pigliucci gives a good review of some aspects of this topic in <a href=\"http://evolution.binghamton.edu/evos/wp-content/uploads/2009/08/Pigliucci-evolvability.pdf\" rel=\"nofollow\">\"Is evolvability evolvable?\" (2008)</a>. He sees what you're asking about, which he calls \"evolvability\", as one of the key topics for the future of the study of evolution.</p>\n\n<p>It's very conceptually dense evo-devo-theory, so I'll probably do a poor job trying to explain it, but he tries to set up a framework that deals not just with things like life-history (per kmm's answer) and mutation/recombination rate (low fidelity in HIV per GWW's answer, and, I suppose, the evolution of sex itself), but also with constraints that evolve at various levels to \"positively channel\" mutation (that is, the understanding that while mutations are effectively random, the phenotypes that emerge, and are acted upon by natural selection, are not random, but are channelled by the developmental system of the organism).</p>\n\n<p>He also includes the role of development in opening up \"phenotypic space\" into which a lineage may evolve. For instance, single-celled organisms have a limit on size and complexity, the evolution of multicellularity opens up this huge zone of evolvability. In a sense, this is also the \"evolution of evolution\".</p>\n\n<hr>\n\n<ul>\n<li><a href=\"http://dx.doi.org/10.1038/nrg2278\" rel=\"nofollow\"> <strong>Pigliucci M</strong>. 2008. Is evolvability evolvable? Nat Rev Genet 9: 75–82.</a> Behind paywall, but <a href=\"http://evolution.binghamton.edu/evos/wp-content/uploads/2009/08/Pigliucci-evolvability.pdf\" rel=\"nofollow\">free pdf here</a></li>\n</ul>\n"
},
{
"answer_id": 41285,
"pm_score": 1,
"text": "<p>The following paper published on August 25, 2015 claims that there are indeed directed mutations.\n<em>Evidence for Retromutagenesis as a Mechanism for Adaptive Mutation in Escherichia coli</em>\n<a href=\"http://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1005477\" rel=\"nofollow\">http://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1005477</a></p>\n"
}
] |
450 |
<p>I know plants are green due to chlorophyll.</p>
<p>Surely it would be more beneficial for plants to be red than green as by being green they reflect green light and do not absorb it even though green light has more energy than red light.</p>
<p>Is there no alternative to chlorophyll? Or is it something else?</p>
|
[
{
"answer_id": 462,
"pm_score": 8,
"text": "<p>Surely it would be even more beneficial for plants to be black instead of red or green, from an energy absorption point of view. And <a href=\"http://en.wikipedia.org/wiki/Solar_cell\" rel=\"noreferrer\">Solar cells</a> are indeed pretty dark.</p>\n\n<p>But, as Rory <a href=\"https://biology.stackexchange.com/a/451/303\">indicated</a>, higher energy photons will only produce heat. This is because the chemical reactions powered by photosynthesis require only a certain amount of energy, and any excessive amount delivered by higher-energy photons cannot be simply used for another reaction<sup>1</sup> but will yield heat. I don't know how much trouble that actually causes, but there is another point:</p>\n\n<p>As explained, what determines the efficiency of solar energy conversion is not the energy per photon, but the amount of photons available. So you should take a look at the <a href=\"http://en.wikipedia.org/wiki/Sunlight#Composition\" rel=\"noreferrer\">sunlight spectrum</a>:</p>\n\n<p><a href=\"http://en.wikipedia.org/wiki/File:Solar_Spectrum.png\" rel=\"noreferrer\" title=\"Solar Radiation Spectrum\"><img src=\"https://upload.wikimedia.org/wikipedia/commons/4/4c/Solar_Spectrum.png\" alt=\"Solar Radiation Spectrum\"></a></p>\n\n<p>The Irradiance is an energy density, however we are interested in photon density, so you have to divide this curve by the energy per photon, which means multiply it by λ/(hc) (that is higher wavelengths need more photons to achieve the same Irradiance). If you compare that curve integrated over the high energy photons (say, λ < 580 nm) to the integration over the the low energy ones, you'll notice that despite the atmospheric losses (the red curve is what is left of the sunlight at sea level) there are a lot more \"red\" photons than \"green\" ones, so making leaves red would waste a lot of potentially converted energy<sup>2</sup>.</p>\n\n<p>Of course, this is still no explanation why leaves are not simply black — absorbing all light is surely even more effective, no? I don't know enough about organic chemistry, but my guess would be that there are no organic substances with such a broad absorption spectrum and adding another kind of pigment might not pay off.<sup>3</sup></p>\n\n<p><sup>1)</sup> Theoretically that <em>is</em> possible, but it's a highly non-linear process and thus too unlikely to be of real use (in plant medium at least)<br>\n<sup>2)</sup> Since <a href=\"http://en.wikipedia.org/wiki/Electromagnetic_absorption_by_water\" rel=\"noreferrer\">water absorbs red light stronger than green and blue light</a> deep sea plants are indeed better off being red, as Marta Cz-C <a href=\"https://biology.stackexchange.com/questions/450/why-do-plants-have-green-leaves-and-not-red#comment-469\">mentioned</a>.<br>\n<sup>3</sup> And other alternatives, like the semiconductors used in Solar cells, are rather unlikely to be encountered in plants...</p>\n\n<p>Additional reading, <a href=\"https://biology.stackexchange.com/review/suggested-edits/20188\">proposed</a> by <a href=\"https://biology.stackexchange.com/users/11677/dave-jarvis\">Dave Jarvis</a>:</p>\n\n<ul>\n<li><a href=\"http://pcp.oxfordjournals.org/content/50/4/684.full\" rel=\"noreferrer\">http://pcp.oxfordjournals.org/content/50/4/684.full</a></li>\n<li><a href=\"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3691134/\" rel=\"noreferrer\">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3691134/</a></li>\n<li><a href=\"http://www.life.illinois.edu/govindjee/photosynBook/Chapter11.pdf\" rel=\"noreferrer\">http://www.life.illinois.edu/govindjee/photosynBook/Chapter11.pdf</a></li>\n<li><a href=\"https://www.heliospectra.com/sites/default/files/general/What%20light%20do%20plants%20need_5.pdf\" rel=\"noreferrer\">https://www.heliospectra.com/sites/default/files/general/What%20light%20do%20plants%20need_5.pdf</a></li>\n</ul>\n"
}
] |
[
{
"answer_id": 451,
"pm_score": 5,
"text": "<p>I believe it is because of a trade off between absorbing a wide range of photons and not absorbing too much heat. Certainly this is a reason why leaves are not black - the enzymes in photosynthesis as it stands would be denatured by the excess heat that would be gained. </p>\n\n<p>This may go some of the way towards explaining why green is reflected rather than red as you suggested - reflecting away a higher energy colour reduces the amount of thermal energy gained by the leaves.</p>\n"
},
{
"answer_id": 560,
"pm_score": 5,
"text": "<p>There is quite a fun article <a href=\"http://www.ebscohost.com/uploads/imported/thisTopic-dbTopic-1033.pdf\">here</a> which discusses the colours of hypothetical plants on planets around other stars. </p>\n\n<p>Stars are classified by their spectral type which is dictated by their surface temperatures. The Sun's is relatively hot, and it's spectral energy distribution peaks in the green region of the spectrum. However the majority of stars in the Galaxy are K and M type stars which emit mainly in the red and infrared. </p>\n\n<p>This is relevant to this discussion since any photosynthesis on these worlds would have to adapt to these wavelengths of light in order to proceed. On planets around cool stars plant life (or its equivalent) might well be black!</p>\n\n<p>OK, this is not entirely pie in the sky astrobiologist rubbish. It is actually quite relevant to the search for biosignatures and life on other planets. In order to model the reflectance spectrum of planets we observe (i.e. the light reflected from the primary star) we need to try and take into account any potential vegetation.</p>\n\n<p>For example, if we take a reflectance spectrum of the Earth, we see a characteristic peak in the red \"the red edge\" which is due to surface plant life.</p>\n\n<p>NASA also has a short page on this <a href=\"http://www.nasa.gov/centers/goddard/news/topstory/2007/spectrum_plants.html\">here</a>.</p>\n"
},
{
"answer_id": 3891,
"pm_score": 4,
"text": "<p>There are two factors at play here. First is the balance between how much energy a plant can collect and how much it can use. It is not a problem of too much heat, but too many electrons. If it were a question of heat, a number of flowers selected for their black pigmentation would have their petals cooked off. ;)</p>\n\n<p>If a plant does not have enough water, is too cold, is too hot, collects too much light, or has some other condition that prevents the electron transport chain from functioning properly, the electrons pile up in a process called <a href=\"http://en.wikipedia.org/wiki/Photoinhibition\">photoinhibition</a>. </p>\n\n<p>These electrons are then transferred to molecules that they should not be transferred to, creating <a href=\"http://en.wikipedia.org/wiki/Free_radicals\">free radicals</a>, wreaking havok within the plant's cells. Fortunately, plants produce other compounds that prevent some of the damage by absorbing and passing around the electrons like hot potatos. These antioxidants are also beneficial to us when we eat them.</p>\n\n<p>This explains why plants collect the amount of light energy they do, but does not explain why they are green, and not grey or dark red. Surely there are other pigments that would be able to generate electrons for the electron transport chain.</p>\n\n<p>The answer to that is the same as why <a href=\"http://en.wikipedia.org/wiki/Adenosine_triphosphate\">ATP</a> is used as the main energy transport molecule in organisms rather than GTP or something else.</p>\n\n<p><a href=\"http://en.wikipedia.org/wiki/Chlorophyll\">Chlorophyll a and b</a> were just the first things that came about that fulfilled the requirement. Certainly some other pigment could have collected the energy, but that region of parameter space never needed to be explored.</p>\n"
},
{
"answer_id": 17836,
"pm_score": 4,
"text": "<p>The biologist John Berman has offered the opinion that evolution is not an engineering process, and so it is often subject to various limitations that an engineer or other designer is not. Even if black leaves were better, evolution's limitations can prevent species from climbing to the absolute highest peak on the fitness landscape. Berman wrote that achieving pigments that work better than chlorophyll could be very difficult. In fact, all higher plants (embryophytes) are thought to have evolved from a common ancestor that is a sort of green alga – with the idea being that chlorophyll has evolved only once. (<a href=\"http://en.wikipedia.org/wiki/Chlorophyll#Why_green_and_not_black.3F\" rel=\"nofollow noreferrer\">reference</a>)</p>\n\n<p>Plants and other photosynthetic organisms are largely filled with pigment-protein complexes that they produce to absorb sunlight. The part of the photosynthesis yield that they invest in this, therefore, has to be in proportion. The pigment in the lowest layer has to receive enough light to recoup its energy costs, which cannot happen if a black upper layer absorbs all the light. A black system can therefore only be optimal if it does not cost anything (<a href=\"http://www.news.leiden.edu/news/why-are-plants-not-black.html\" rel=\"nofollow noreferrer\">reference</a>). </p>\n\n<p>Red and yellow light is longer wavelength, lower energy light, while the blue light is higher energy. It seems strange that plants would harvest the lower energy red light instead of the higher energy green light, unless you consider that, like all life, plants first evolved in the ocean. Seawater quickly absorbs the high-energy blue and green light, so that only the lower energy, longer wavelength red light can penetrate into the ocean. Since early plants and still most plant-life today, lived in the ocean, optimizing their pigments to absorb the reds and yellows that were present in ocean water was most effective. While the ability to capture the highest energy blue light was retained, the inability to harvest green light appears to be a consequence of the need to be able to absorb the lower energy of red light (<a href=\"http://scienceline.ucsb.edu/getkey.php?key=1668\" rel=\"nofollow noreferrer\">reference</a>).</p>\n\n<p>Some more speculations on the subject: (<a href=\"http://thesymbiont.blogspot.in/2010/09/why-arent-plants-black-true-evo.html\" rel=\"nofollow noreferrer\">reference</a>)</p>\n"
},
{
"answer_id": 34847,
"pm_score": 3,
"text": "<p>There are several parts to my answer.</p>\n\n<p>First, evolution has selected the current system(s) over countless generations through natural selection. Natural selection depends on differences (major or minor) in the efficiency of various solutions (fitness) in the light (ho ho!) of the current environment. Here's where the solar energy spectrum is important as well as local environmental variables such as light absorption by water etc. as pointed out by another responder. After all that, what you have is what you have and that turns out to be (in the case of typical green plants), chlorophylls A and B and the \"light\" and \"dark\" reactions. </p>\n\n<p>Second, how does this lead to green plants that appear green? Absorption of light is something that occurs at the atomic and molecular level and usually involves the energy state of particular electrons. The electrons in certain molecules are capable of moving from one energy level to another without leaving the atom or molecule. When energy of a certain level strikes the molecule, that energy is absorbed and one or more electrons move to a higher energy level in the molecule (conservation of energy). Those electrons with higher energy usually return to the \"ground state\" by emitting or transferring that energy. One way the energy can be emitted is as light in a process called fluorescence. The second law of thermodynamics (which makes it impossible to have perpetual motion machines) leads to the emission of light of lower energy and longer wavelength. (n.b. wavelength (lambda) is inversely proportional to energy; long wavelength red light has less energy per photon than does short wavelength violet (ROYGBIV as seen in your ordinary rainbow)).</p>\n\n<p>Anyway, chlorophylls A and B are complex organic molecules (C, H, O, N with a splash of Mg++) with a ring structure. You will find that a lot of organic molecules that absorb light (and fluoresce as well) have a ring structure in which electrons \"resonate\" by moving around the ring with ease. It is the resonance of the electrons that determine the absorption spectrum of a given molecule (among other things). Consult Wikipedia article on chlorophyll for the absorption spectrum of the two chlorophylls. You will note that they absorb best at short wavelengths (blue, indigo, violet) as well as at the long wavelengths (red, orange, yellow) but not in the green. Since they don't absorb the green wavelengths, this is what is left over and this is what your eye perceives as the color of the leaf.</p>\n\n<p>Finally, what happens to the energy from the solar spectrum that has been temporarily absorbed by the electrons of chlorophyll? Since its not part of the original question, I'll keep this short (apologies to plant physiologists out there). In the \"light dependent reaction\", the energetic electrons get transferred through a number of intermediate molecules to eventually \"split\" water into Oxygen and Hydrogen and generate energy-rich molecules of ATP and NADPH. The ATP and NADPH then are used to power the \"light independent reaction\" which takes CO2 and combines it with other molecules to create glucose. Note that this is how you get glucose (at least eventually in some form, vegan or not) to eat and oxygen to breath.</p>\n\n<p>Take a look at what happens when you artificially uncouple the chlorophylls from the transfer system that leads to glucose synthesis. <a href=\"http://en.wikipedia.org/wiki/Chlorophyll_fluorescence\" rel=\"nofollow noreferrer\">http://en.wikipedia.org/wiki/Chlorophyll_fluorescence</a> Notice the color of the fluorescence under UV light!</p>\n\n<p>Alternatives? Look at photosynthetic bacteria.</p>\n"
},
{
"answer_id": 55200,
"pm_score": 1,
"text": "<p>Tobias Keinzler does a good job of explaining why black plants would not work, this is an explanation of why plants are <strong>green</strong> and not some other color. </p>\n\n<p>Color of foliage is based on whatever the color is of bacteria (or archaea) that get incorporated to become chloroplasts. Or more specifically the color of their light absorbing pigments. there is a huge range in nature for color in photosynthetic organisms, plants are green becasue chlorophyll is green, it could have just as easily been red or purple. <a href=\"http://www.ucmp.berkeley.edu/glossary/gloss3/pigments.html\" rel=\"nofollow noreferrer\">http://www.ucmp.berkeley.edu/glossary/gloss3/pigments.html</a></p>\n\n<p>There is decent <a href=\"https://books.google.com/books?id=vtI9MPk3oVkC&pg=PA48&lpg=PA48&dq=green%20chlorophyll%20halobacteria%20competition&source=bl&ots=s5Fb4lZOTG&sig=7ErYFJGacjt49WCu9TBD6VU_7MU&hl=en&sa=X&ved=0ahUKEwiRtv7Rw7_RAhXC1IMKHeceD38Q6AEIIjAB#v=onepage&q=green%20chlorophyll%20halobacteria%20competition&f=false\" rel=\"nofollow noreferrer\">evidence</a> that chloroplast ancestors absorb the margins of the visible spectrum becasue <a href=\"https://en.wikipedia.org/wiki/Halobacterium\" rel=\"nofollow noreferrer\">halobacterium</a> absorb the major constituents, becasue the chlorophyll users did not compete with them directly instead absorbing the leftover light. It was only later when they got incorporated into larger cells that they came to dominate and eventually giving rise to plants. \nPlants are not green becasue green is better, plants are green becasue that is the first efficient photosynthetic pigment to evolve that did not compete with the dominate photosynthesizer. </p>\n\n<p><a href=\"https://i.stack.imgur.com/Z3DZY.gif\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/Z3DZY.gif\" alt=\"enter image description here\"></a></p>\n"
},
{
"answer_id": 56739,
"pm_score": 4,
"text": "<p>I know this question was asked and answered a number of years ago (with many <em>great</em> answers), but I couldn't help but notice that no one had approached this from an <em>evolutionary</em> perspective (like the <a href=\"https://biology.stackexchange.com/a/56498/16866\">answer</a> to this question)...</p>\n<h2> Short Answer </h2>\n<p>Pigments appear as whatever color is not absorbed (i.e., they appear as whichever wavelength(s) of light they reflect).</p>\n<p>Blue light was the most available wavelength of light for early plants growing underwater, which likely led to the initial development/evolution of chlorophyll-mediated photosytems still seen in modern plants. Blue light is the most available, most high-energy light that continues to reach plants, and therefore plants have no reason not to continue taking advantage of this abundant high energy light for photosynthesis.</p>\n<p>Different pigments absorb different wavelengths of light, so plants would ideally incorporate pigments that can absorb the most available light. This is the case as both chlorophyll <em>a</em> and <em>b</em> absorb primarily blue light. Absorption of red light likely evolved once plants moved on land due to its increased abundance (as compared to under water) and its higher efficiency in photosynthesis.</p>\n<hr />\n<h2> Long Answer </h2>\n<h3> Early Plants Develop Modern Photo-system </h3>\n<p>It turns out, just like the variability in transmittance of different wavelengths of light through the atmosphere, certain wavelengths of light are more capable of penetrating deeper depths of water. Blue light typically travels to deeper depths than all other visible wavelengths of light. Therefore, the earliest plants would have evolved to concentrate on absorbing this part of the EM spectrum.</p>\n<p><a href=\"https://i.stack.imgur.com/oTrO5.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/oTrO5.png\" alt=\"https://disc.sci.gsfc.nasa.gov/education-and-outreach/additional/science-focus/ocean-color/images/spectral_light_absorption.gif\" /></a></p>\n<p>However, you'll notice that green light penetrates relatively deeply as well. The <a href=\"http://hyperphysics.phy-astr.gsu.edu/hbase/Biology/ligabs.html\" rel=\"nofollow noreferrer\">current understanding</a> is that the earliest photosynthetic organisms were aquatic archaea, and (based on modern examples of these ancient organisms) these archaea used <a href=\"https://en.wikipedia.org/wiki/Bacteriorhodopsin\" rel=\"nofollow noreferrer\">bacteriorhopsin</a> to absorb most of the green light.</p>\n<p><a href=\"https://i.stack.imgur.com/xJ2AO.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/xJ2AO.png\" alt=\"http://hyperphysics.phy-astr.gsu.edu/hbase/Biology/imgbio/plantblack.gif\" /></a></p>\n<p>Early plants grew below these purple bacteriorhopsin-producing bacteria and had to use whatever light they could get. As a result, the chlorophyll system developed in plants to use the light available to them. In other words, based on the deeper penetrative ability of blue/green light and the loss of the availability of green light to pelagic bacteria above, <strong>plants evolved a photosystem to absorb primarily in the blue spectrum because that was the light most available to them</strong>.</p>\n<ul>\n<li><p>Different pigments absorb different wavelengths of light, so plants would ideally incorporate pigments that can absorb the most available light. This is the case as both chlorophyll <em>a</em> and <em>b</em> absorb primarily blue light.</p>\n</li>\n<li><p>Here's two example graphs (from <a href=\"http://smartgrowtechnologies.com/wp-content/uploads/2014/06/chlorohyll_a_b_carotenoids.jpg\" rel=\"nofollow noreferrer\">here</a> and <a href=\"http://hyperphysics.phy-astr.gsu.edu/hbase/Biology/imgbio/stagrn.gif\" rel=\"nofollow noreferrer\">here</a>) showing the absorption spectrum of typical plant pigments:</p>\n</li>\n</ul>\n<p><a href=\"https://i.stack.imgur.com/J8XBf.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/J8XBf.png\" alt=\"Photosynthesis\" /></a></p>\n<h3> So Why Are Plants Green? </h3>\n<p>As you can guess from the above paragraphs, since early under water plants received so little green light, they evolved with a chlorophyll-mediated photo-system that did not have the physical properties to absorb green light. <strong>As a result, plants reflect light at these wavelengths and appear green</strong>.</p>\n<h3> But Why Are Plants Not Red?... </h3>\n<p><strong>Reason to ask this question:</strong></p>\n<p>This would seem to be equally plausible given the above information. Since red light penetrates water incredibly poorly and is largely unavailable at lower depths, it would seem that early plants would not develop a means for absorbing it and therefore would also reflect red light.</p>\n<ul>\n<li><p>In fact, [relatively] closely related <a href=\"https://en.m.wikipedia.org/wiki/Red_algae\" rel=\"nofollow noreferrer\">red algae</a> <em>did</em> evolve a red-reflecting pigment. These algae evolved a photo-system that also includes the pigment <a href=\"https://en.wikipedia.org/wiki/Phycoerythrin\" rel=\"nofollow noreferrer\">phycoerythrin</a> to help absorb available blue light. This pigment did not evolve to absorb the low levels of available red light, and so therefore this pigment reflects it and makes these organisms <a href=\"https://biology.stackexchange.com/a/56546/16866\">appear red</a>.</p>\n</li>\n<li><p>Interestingly, according to <a href=\"http://phototroph.blogspot.com/2006/11/phycobilins.html\" rel=\"nofollow noreferrer\">here</a>, cyanobacteria that also contain this pigment can readily change it's influence on the organism's observed color:</p>\n<blockquote>\n<p>The ratio of phycocyanin and phycoerythrin can be environmentally altered. Cyanobacteria which are raised in green light typically develop more phycoerythrin and become red. The same Cyanobacteria grown in red light become bluish-green. This reciprocal color change has been named 'chromatic adaptation’.</p>\n</blockquote>\n</li>\n<li><p>Further, (although it's still under debate) according to work by <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/10811219\" rel=\"nofollow noreferrer\">Moreira et al (2000)</a> (and corroborated by numerous <a href=\"https://en.m.wikipedia.org/wiki/Archaeplastida#Taxonomy\" rel=\"nofollow noreferrer\">other</a> researchers) plants and red algae likely have a shared photosynthetic phylogeny:</p>\n</li>\n</ul>\n<blockquote>\n<p>three groups of organisms originated from the primary photosynthetic endosymbiosis between a cyanobacterium and a eukaryotic host: green plants (green algae + land plants), red algae and glaucophytes (for example, Cyanophora).</p>\n</blockquote>\n<p>So what gives?</p>\n<p><strong>Answer:</strong></p>\n<p>The simple answer of why plants aren't red is <strong>because chlorophyll absorbs red light</strong>.</p>\n<p>This leads us to ask: <strong>Did chlorophyll in plants <em>always</em> absorb red light</strong> (preventing plants from appearing red) <strong>or did this characteristic appear later</strong>?</p>\n<ul>\n<li><p>If the former was true, then plants don't appear red simply because of the physical characteristics that the chlorophyll pigments evolved to have.</p>\n</li>\n<li><p>As far as I know, we don't have a clear answer to that question.</p>\n<ul>\n<li>(others please comment if you know of any resources discussing this).</li>\n</ul>\n</li>\n<li><p>However, regardless of <em>when</em> red light absorption evolved, <strong>plants nevertheless evolved to absorb red light very efficiently</strong>.</p>\n<ul>\n<li><p>A number of sources (e.g., Mae et al. 2000, Brins et al. 2000, and <a href=\"https://web.archive.org/web/20170523174126/https://spot.colorado.edu/%7Ebasey/bluer.htm\" rel=\"nofollow noreferrer\">here</a>) as well as numerous other answers to this question, suggest that the most efficient photosynthesis occurs under red light. In other words, red light results in the highest "photosynthetic efficiency."</p>\n<ul>\n<li>This <a href=\"https://www.ncbi.nlm.nih.gov/books/NBK21598/#_A4448_\" rel=\"nofollow noreferrer\">NIH page</a> suggests the reason behind this:</li>\n</ul>\n<blockquote>\n<p>Chlorophyll <em>a</em> also absorbs light at discrete wavelengths shorter than 680 nm (see Figure 16-37b). Such absorption raises the molecule into one of several higher excited states, which decay within 10<sup>−12</sup> seconds (1 picosecond, ps) to the first excited state P*, with loss of the extra energy as heat. Photochemical charge separation occurs only from the first excited state of the reaction-center chlorophyll a, P*. This means that the quantum yield — the amount of photosynthesis per absorbed photon — is the same for all wavelengths of visible light shorter than 680 nm.</p>\n</blockquote>\n<ul>\n<li><p>Note, however, that other sources suggest blue light is better than red. For example, see Muneer et al, (2014).</p>\n<blockquote>\n<p>Biomass and photosynthetic parameters increased with an increasing light intensity under blue LED illumination and decreased when illuminated with red and green LEDs with decreased light intensity</p>\n</blockquote>\n</li>\n</ul>\n</li>\n</ul>\n</li>\n</ul>\n<h3> Why Did Plants Remain Green? </h3>\n<p>So why have plants not evolved to use green light after moving/evolving on land? As discussed <a href=\"https://biology.stackexchange.com/a/56498/16866\">here</a>, plants are terribly inefficient and can't use all of the light available to them. As a result, there is likely no competitive advantage to evolve a drastically different photosystem (i.e., involving green-absorbing pigments).</p>\n<p>So earth's plants continue to absorb blue and red light and reflect the green. Because green light <a href=\"http://gsp.humboldt.edu/olm_2015/Courses/GSP_216_Online/lesson2-1/atmosphere.html\" rel=\"nofollow noreferrer\">so abundantly reaches the Earth</a>, green light remains the most strongly reflected pigment on plants, and plants continue to appear green.</p>\n<ul>\n<li>(However, note that other organisms such as birds and insects likely see plants very differently because their eyes can distinguish colors differently and they see more of the strongly reflected UV light that ours cannot).</li>\n</ul>\n<hr />\n<p><em>Citations</em></p>\n<p><sup> Moreira, D., Le Guyader, H. and Philippe, H., 2000. The origin of red algae and the evolution of chloroplasts. Nature, 405(6782), pp.69-72. </sup></p>\n<p><sup> Muneer, S., Kim, E.J., Park, J.S. and Lee, J.H., 2014. Influence of green, red and blue light emitting diodes on multiprotein complex proteins and photosynthetic activity under different light intensities in lettuce leaves (Lactuca sativa L.). International journal of molecular sciences, 15(3), pp.4657-4670. </sup></p>\n"
},
{
"answer_id": 106688,
"pm_score": 2,
"text": "<p>Small addition to the conversation: <strong>plants reflect green</strong> yes, but <strong>chlorophyll (a and b) does not (it is mostly transparent to it</strong>).</p>\n<p>The organic material (walls of cells, etc.) around the chlorophyll behave as reflectors and scatterers of the non-absorbed green light, and that's what we see.</p>\n<p><a href=\"https://www.tandfonline.com/doi/full/10.1080/00219266.2020.1858930\" rel=\"nofollow noreferrer\">https://www.tandfonline.com/doi/full/10.1080/00219266.2020.1858930</a></p>\n<p>In general there are 3 types of interactions of a photon with matter:</p>\n<ul>\n<li><strong>reflection</strong> (and scattering elastic or not)</li>\n<li><strong>absorption</strong> (inelastic process)</li>\n<li><strong>transmission</strong> (no energetically-lossy-interaction)</li>\n</ul>\n<p>(My reply targets better the OP formulation of <a href=\"https://biology.stackexchange.com/questions/45333/why-is-chlorophyll-green-isnt-there-a-more-energetically-favorable-color\">this duplicate question</a>)</p>\n"
}
] |
452 |
<p>My biology teachers never explained why animals need to breathe oxygen, just that we organisms die if we don't get oxygen for too long. Maybe one of them happened to mention that its used to make ATP. Now in my AP Biology class we finally learned the specifics of how oxygen is used in the <a href="http://www.science.smith.edu/departments/Biology/Bio231/etc.html">electron transport chain</a> due to its high electronegativity. But I assume this probably isn't the only reason we need oxygen. </p>
<p>What other purposes does the oxygen we take in through respiration serve? Does oxygen deprivation result in death just due to the halting of ATP production, or is there some other reason as well? What percentage of the oxygen we take in through respiration is expelled later through the breath as carbon dioxide?</p>
|
[
{
"answer_id": 456,
"pm_score": 6,
"text": "<p>Oxygen is actually highly toxic to cells and organisms – <a href=\"http://en.wikipedia.org/wiki/Reactive_oxygen_species\" rel=\"noreferrer\">reactive oxygen species</a> cause <a href=\"http://en.wikipedia.org/wiki/Oxidative_stress\" rel=\"noreferrer\">oxidative stress</a>, essentially cell damage and contributing to cell ageing. A lot of anaerobic organisms have never learned to cope with this and die almost immediately when exposed to oxygen. One classical example of this is <em><a href=\"http://en.wikipedia.org/wiki/C._botulinum\" rel=\"noreferrer\">C. botulinum</a></em>.</p>\n<p>Oxygen <em>is</em> incorporated in several molecules in the cell (for instance riboses and certain amino acids) but as far as I know, all of this comes into the cell as metabolic products, not in the form of pure oxygen.</p>\n<p>The oxygen (<span class=\"math-container\">$\\ce{O2}$</span>) we breathe is completely used up during aerobic respiration. The stoichiometry of this is given by the following <a href=\"https://en.wikipedia.org/wiki/Cellular_respiration#Aerobic_respiration\" rel=\"noreferrer\">simplified equation</a>:</p>\n<p><span class=\"math-container\">$$\\ce{C_6H12O6 + 6 O2 -> 6 CO2 + 6 H2O + heat}$$</span></p>\n<p><a href=\"/a/35166/166\">WYSIWYG’s answer</a> goes into more detail.</p>\n"
}
] |
[
{
"answer_id": 455,
"pm_score": 5,
"text": "<p><a href=\"http://en.wikipedia.org/wiki/Superoxide\" rel=\"noreferrer\">Superoxide</a>, O<sub>2</sub><sup>−</sup> is created by the immune system in <a href=\"http://en.wikipedia.org/wiki/Phagocyte\" rel=\"noreferrer\">phagocytes</a> (including neutrophils, monocytes, macrophages, dendritic cells, and mast cells) which use NADPH oxidase to produce it from O<sub>2</sub> for use against invading microorganisms. However, under normal conditions, the mitochondrial electron transport chain is a major source of O<sub>2</sub><sup>−</sup>, converting up to perhaps 5% of O<sub>2</sub> to superoxide. [1]</p>\n<p>As a side note, there are two sides to this coin. While this is a useful tool against microorganisms, the formation of the reactive oxygen species has been incriminated in autoimmune reactions and diabetes (type 1). [2]</p>\n<blockquote>\n<p>[1] Packer L, Ed. <em>Methods in Enzymology</em>, Volume 349. San Diego, Calif: Academic Press; 2002</p>\n<p>[2] Thayer TC, Delano M, et al. (2011) <em>Superoxide production by macrophages and T cells is critical for the induction of autoreactivity and type 1 diabetes,60</em>(8), 2144-51.</p>\n</blockquote>\n"
},
{
"answer_id": 459,
"pm_score": 4,
"text": "<p>The overwhelming use of oxygen is to provide us (in combination with food) with energy. We have a great need for energy in our cells, which is why we have these lungs, diaphragms, red blood cells, etc.; they assure we get the oxygen to obtain the energy (via the electron transport chain).</p>\n\n<p>The overall metabolism of glucose (C<sub>6</sub>H<sub>12</sub>O<sub>6</sub>) is a representative reaction:</p>\n\n<pre> C<sub>6</sub>H<sub>12</sub>O<sub>6</sub> + 6 O<sub>2</sub> --> 6 CO<sub>2</sub> + 6 H<sub>2</sub>O + energy</pre> \n\n<p>You can see that just as much oxygen goes out as gaseous CO<sub>2</sub> as came in as gaseous oxygen (O<sub>2</sub>). </p>\n\n<p>The energy is temporarily kept in the form of the phosphate bond in ATP molecules so that it can be shuttled around the cell to the multitude of cellular processes that need energy.</p>\n\n<p>Energy is so essential to the cellular processes that maintain animal cells that lack of that energy, which results quickly when there is oxygen deprivation, soon causes irreversible damage and death.</p>\n"
},
{
"answer_id": 473,
"pm_score": 4,
"text": "<p>You probably know by now that cytochrome <em>c</em> oxidase, the last complex of the electron transport chain, belongs to a class of enzymes called oxidoreductases, that use oxygen atoms as electron acceptors. One type of oxidoreductases are oxidases, enzymes that (at least in theory [1]) use molecular oxygen--O<sub>2</sub>, like in air--as their electron acceptor. From what I know, however, sometimes that isn't the case: xanthine oxidase, that converts xanthine to uric acid, gets its oxygen atoms from water [2]. Examples of the \"true\" oxidases include L-amino-acid oxidase and cytochrome P450 (aka. CYP family).</p>\n\n<p>Despite cytochrome P450 being a numerous and important enzyme family, responsible for most of known drugs metabolism and some essential lipids transformations, it probably consumes only a fraction of oxygen that animals breathe in. I wasn't able to find any estimations, but would be surprised if it was more than perhaps 0,1%.</p>\n\n<hr>\n\n<p>[1] <a href=\"http://www.chem.qmul.ac.uk/iubmb/enzyme/EC1/intro.html\">Introduction to EC1 class</a></p>\n\n<p>[2] Metz, S. & Thiel, W. <a href=\"http://pubs.acs.org/doi/abs/10.1021/jp909999s\">A Combined QM/MM Study on the Reductive Half-Reaction of\nXanthine Oxidase: Substrate Orientation and Mechanism</a>. J. Am. Chem. Soc. 2009, 131, 14885–14902, PMID: 20050623.</p>\n"
},
{
"answer_id": 35166,
"pm_score": 3,
"text": "<p><strong>Another small addition</strong></p>\n\n<hr>\n\n<p>There is class of oxidoreductases called <strong>oxygenases</strong> which incorporate molecular oxygen into the substrates and not just use it as an electron acceptor like in oxidases (note that the terminal enzyme in ETC is an oxidase and there are other such oxidases). In other words, oxygen is not a cofactor but a co-substrate. Oxygenases are further classified into dioxygenases and monooxygenases which incorporate two oxygen atoms and one oxygen atom respectively. Examples:</p>\n\n<ul>\n<li>Cytochrome P450 family (monooxygenease): involved in detoxification of xenobiotics</li>\n<li>Cyclooxygenase (dioxygenase): involved in production of prostaglandins which are involved in pain and inflammation. Many NSAID painkillers like aspirin, paracetamol and ibuprofen target cyclooxygenase-2 (COX2)</li>\n<li>Lipoxygenase (dioxygenase): Involved in production of leukotrienes which are involved in inflammation.</li>\n<li>Monoamine oxidase (monooxygenase): Involved in catabolism of neurotransmitters such as epinephrine, norepinephrine and dopamine. </li>\n</ul>\n\n<blockquote>\n <p>Does oxygen deprivation result in death just due to the halting of ATP\n production, or is there some other reason as well?</p>\n</blockquote>\n\n<p>Death predominantly occurs because of halt in ATP production. Some cells such as neurons (and also perhaps cardiac muscles) are highly sensitive to loss of oxygen (for energy requirements) and clinical death because of hypoxia usually occurs because of loss basic brain function. </p>\n\n<blockquote>\n <p>What percentage of the oxygen we take in through respiration is\n expelled later through the breath as carbon dioxide?</p>\n</blockquote>\n\n<p>As already mentioned, it is said that there is a rough 1:1 ratio of CO<sub>2</sub> production and O<sub>2</sub> consumption. However, as indicated in a comment by CurtF, O<sub>2</sub> does not form CO<sub>2</sub>; it forms water in the last reaction of ETC. CO<sub>2</sub> is produced in other reactions of Krebs cycle. </p>\n\n<p>Glycolysis produces 32 molecules of ATP for 1 molecule of glucose via ETC (see <a href=\"http://www.uic.edu/classes/bios/bios100/lecturesf04am/lect12.htm\" rel=\"nofollow noreferrer\">here</a>). There are three complexes in ETC and the third is dependent on oxygen; so you can assume that 1/2 a molecule of O<sub>2</sub> consumed for production of 3 ATP molecules. Therefore 32 molecules of ATP would consume 4 molecules of O<sub>2</sub>. Seems like there is a 1:1 ratio of CO<sub>2</sub> production and O<sub>2</sub> consumption.</p>\n\n<p>We can see it like this:</p>\n\n<p>FADH<sub>2</sub> enters ETC at the second complex whereas NADH enters at the first. We can say that as long as NADH is present FADH<sub>2</sub> would not require an extra oxygen.</p>\n\n<p>An NADH or a FADH<sub>2</sub> molecule would require 1/2 molecule of O<sub>2</sub>. There are 8 molecules of NADH and 2 molecules of FADH<sub>2</sub> produced during glycolysis+krebs cycle which would require 10/2 = <strong>5</strong> molecules of O<sub>2</sub>. Glycolysis produces 4 molecules of CO<sub>2</sub> during krebs cycle. </p>\n\n<p>However, 2 cytosolic NADH molecules require 2 ATPs (in other words another NADH molecule) to be transported to mitochondria. So the net effect may be actually close to 1:1 O<sub>2</sub>:CO<sub>2</sub>.</p>\n\n<p>Another factor to keep in consideration is that the three complexes do not actually produce ATP; they just pump proton to create a chemical potential. The F<sub>0</sub>F<sub>1</sub>-ATP synthase would probably work only after a threshold of H<sup>+</sup> potential is established. The 1 ATP molecule per complex is most likely the mean value and not exactly what really happens per reaction.</p>\n"
}
] |
551 |
<p>I have many friends who are interested in Biology and want to know more about the subject in general (like a history of biology, from Darwin's theory, to DNA structure discovery, to the human genome project). Of course, I cannot suggest to them to read Alberts or Lenninger. Do you know whether such a book exist? I guess that a book that covers most fields of biology cannot be compiled, but even more focused book would do. </p>
<p>Let me try to narrow it down: something like the greatest discoveries in the field of biology (like <a href="http://science.discovery.com/convergence/100discoveries/big100/biology.html">this article</a>) would be an interesting book to read.</p>
<p>I am not sure how appropriate this question is for SE, but I am sure that I will get the best answer here. Besides, it would be great if lay people can be more excited about biology and contribute to the site growth.</p>
|
[
{
"answer_id": 556,
"pm_score": 4,
"text": "<p>It doesn't have very many reviews, but <a href=\"http://rads.stackoverflow.com/amzn/click/073820577X\">The Epic History of Biology</a> sounds like it's perfect.</p>\n\n<p>Flipping through the first chapter in the preview, it doesn't seem overly technical in any way, so secondary school-level knowledge is probably enough. If your associates have absolutely no biology experience, perhaps a run through a popular press book would provide all of the background necessary. </p>\n"
}
] |
[
{
"answer_id": 552,
"pm_score": 2,
"text": "<p>I don't know very many books that might be referred to as the Grand History of Biology or anything like that. That's...a big topic. Really big. How about some suggestions for good Biology/Medical History books accessible to lay people:</p>\n\n<ul>\n<li>And the Band Played On, by Randy Shilts, an account of the beginning of the AIDS epidemic in the U.S.</li>\n<li>The Great Influenza, by John Berry, which is about the 1918 influenza pandemic.</li>\n<li>The Demon Under the Microscope, by Thomas Hager, which is about sulfa and the development of early antibiotics.</li>\n</ul>\n\n<p>Finally, I believe James Watson wrote a somewhat popular science-oriented account of the discovery of DNA, which would no doubt be interesting, though likely somewhat skewed in favor of his own awesomeness.</p>\n"
},
{
"answer_id": 557,
"pm_score": 4,
"text": "<p>Some that just come to mind, in random order:</p>\n\n<p>One cannot skip reading: </p>\n\n<ul>\n<li>Richard Dawkins - <a href=\"http://rads.stackoverflow.com/amzn/click/0199291152\" rel=\"nofollow\">The selfish gene</a></li>\n</ul>\n\n<p>And, obviously: </p>\n\n<ul>\n<li>Charles Darwin - <a href=\"http://rads.stackoverflow.com/amzn/click/0451529065\" rel=\"nofollow\">The Origin of Species</a></li>\n</ul>\n\n<p>And, for those interested in the evolution of the brain (and its quirks): </p>\n\n<ul>\n<li>David J Linden - <a href=\"http://rads.stackoverflow.com/amzn/click/0674030583\" rel=\"nofollow\">The Accidental Mind</a></li>\n<li>Oliver Sacks - <a href=\"http://rads.stackoverflow.com/amzn/click/0684853949\" rel=\"nofollow\">The Man Who Mistook His Wife for a Hat</a></li>\n</ul>\n\n<hr>\n\n<p>Not very DNA/evolution-oriented, but wonderful science books nonetheless:</p>\n\n<ul>\n<li>Primo Levi - <a href=\"http://rads.stackoverflow.com/amzn/click/0679444637\" rel=\"nofollow\">The Periodic table</a></li>\n<li>And the neveraging must-read:<br>\nIsaac Asimov - <a href=\"http://books.google.co.uk/books/about/A_short_history_of_chemistry.html?id=QszZAAAAMAAJ&redir_esc=y\" rel=\"nofollow\">A Short History of Chemistry</a></li>\n</ul>\n"
},
{
"answer_id": 564,
"pm_score": 2,
"text": "<p>I just came across <a href=\"http://my.safaribooksonline.com/book/biotechnology/0131010115\" rel=\"nofollow\">Understanding Biotechnology</a>. There is one very positive and one very negative review. I haven't read the book myself, but it looks that it is exactly what I was looking for: the table of content includes topics like small history overview, genetic engineering, gene therapy, pharmacogenomics, etc. It might be even useful for people with biology background. </p>\n\n<p>Has anyone heard about this book?</p>\n"
},
{
"answer_id": 565,
"pm_score": 2,
"text": "<p>A fantastic book that covers the evolution of modern science since the Renaissance (including a great deal of biology) is <a href=\"http://www.worldcat.org/title/scientists/oclc/690763545\" rel=\"nofollow\">The Scientists</a> by John Gribbin. I found that by focusing on the people doing the science in the context of the society in which they lived, I got a much better understanding for why early scientists thought the way they did and researched the questions that they did.</p>\n\n<p>Here's the blurb from the publisher:</p>\n\n<blockquote>\n <p>In this ambitious new book, John Gribbin tells the stories of the\n people who have made science, and of the times in which they lived and\n worked. He begins with Copernicus, during the Renaissance, when\n science replaced mysticism as a means of explaining the workings of\n the world, and he continues through the centuries, creating an\n unbroken genealogy of not only the greatest but also the more obscure\n names of Western science, a dot-to-dot line linking amateur to genius,\n and accidental discovery to brilliant deduction.</p>\n</blockquote>\n"
},
{
"answer_id": 573,
"pm_score": 3,
"text": "<p>A good recollection of the early days of micro and molecular biology is <a href=\"http://www.cshlpress.com/default.tpl?cart=132622550197204983&fromlink=T&linkaction=full&linksortby=oop_title&--eqSKUdatarq=294\">\"The Eighth day of Creation\"</a></p>\n\n<p>It covers the early use of <em>e. coli</em>, the discovery of phage, transcriptional elements and the impact that DNA structure had. It's very comprehensive and really useful if you are doing molecular biology today. </p>\n"
},
{
"answer_id": 864,
"pm_score": 2,
"text": "<p>By far the best book I've read on the history of biology is <a href=\"http://rads.stackoverflow.com/amzn/click/0674032276\" rel=\"nofollow\">A Guinea Pig's History of Biology</a>, by Jim Endersby. It tells the history of the field by focusing on experimental organisms and the contributions which were made by studying them. It has an engaging narrative style and the idea of focussing on organisms' stories is an excellent and original one.</p>\n\n<p>However, the best resource there is on the history of science is the TTC History of Science lecture series. It comes in two parts:</p>\n\n<ol>\n<li><a href=\"http://www.thegreatcourses.com/tgc/courses/course_detail.aspx?cid=1200\" rel=\"nofollow\">Antiquity to 1700 by Lawrence M Principe of Johns Hopkins University</a></li>\n<li><a href=\"http://www.thegreatcourses.com/tgc/courses/course_detail.aspx?cid=1210\" rel=\"nofollow\">1700-1900 by Professor Frederick Gregory of Harvard</a></li>\n</ol>\n\n<p>The lecture series are VERY expensive - around $200 each. However, most good libraries will have them, and I strongly recommend getting hold of them if you can.</p>\n"
},
{
"answer_id": 872,
"pm_score": 1,
"text": "<p>There is a free video course <a href=\"https://oli.web.cmu.edu/openlearning/forstudents/freecourses/biology\" rel=\"nofollow\">\"Modern Biology\"</a> at Carnegie-Mellon University's Open learning initiative. This is very technical and does not cover history of biology.</p>\n\n<p>I quite liked D.A. Sadava's non-free video course <a href=\"http://www.thegreatcourses.com/tgc/courses/course_detail.aspx?cid=1533#\" rel=\"nofollow\">Understanding Genetics: DNA, Genes, and Their Real-World Applications</a>. This is Genetics and Molecular Biology oriented, but also not a book. It is suitable for a reader with high-school knowledge of chemistry. Maybe it contains too few basics, so it is also not for the absolute layperson. He starts with Mendel and mentions many other 20th-century researchers. </p>\n\n<p>The author has co-authored one of those <a href=\"http://www.whfreeman.com/Catalog/static/whf/thelifewirebridge2/\" rel=\"nofollow\">thick, expensive college-level biology textbooks</a> as well. </p>\n"
},
{
"answer_id": 2640,
"pm_score": 2,
"text": "<p>This book, although a little dated, has given me an incredible appreciation of biology that I never gained in school:</p>\n\n<blockquote>\n <p><a href=\"http://en.wikipedia.org/wiki/What_Is_Life%3F\" rel=\"nofollow\"><em>What is Life?</em></a> by Erwin Shrodinger</p>\n</blockquote>\n\n<p>I am not a biologist, but I occasionally work on mathematical-biology and have training in physics and theoretical computer science. This book was much more accessible to me that other books on biology. Before reading the book I perceived biology as a collection of fun facts (what Rutherford would call \"stamp collecting\"). Shrodinger's presentation was well tailored to the typical reductionist and \"everything must have a reason\" thinking of a theoretical physicists.</p>\n\n<p>I think the book does a good job of explaining the basics and providing intuition and grounding. The excited reader can then move on to more orthodox treatments.</p>\n"
},
{
"answer_id": 2834,
"pm_score": 2,
"text": "<p>My two favorite books are <a href=\"http://rads.stackoverflow.com/amzn/click/1889899097\" rel=\"nofollow\">Molecular Biology made simple and fun</a> and <a href=\"http://rads.stackoverflow.com/amzn/click/0123735815\" rel=\"nofollow\">Biotechnology for Beginners</a>. Both are well written and fun to read. As their names suggest, the former covers the basics of biology and the latter covers the basics of biotechnology.</p>\n"
}
] |
594 |
<p>Why are nearly all amino acids in organisms left-handed (exception is glycine which has no isomer) when abiotic samples typical have an even mix of left- and right-handed molecules?</p>
|
[
{
"answer_id": 615,
"pm_score": 6,
"text": "<p>I know that you are referring to the commonly ribosome-translated L-proteins, but I can't help but add that there are some peptides, called nonribosomal peptides, which are not dependent on the mRNA and can incorporate D-amino acids. They have very important pharmaceutical properties. I recommend <a href=\"https://www.annualreviews.org/doi/full/10.1146/annurev.micro.58.030603.123615\" rel=\"nofollow noreferrer\">this</a> (1) review article if you are interested in the subject. It is also worth mentioning that D-alanine and D-glutamine are incorporated into the peptidoglycane of bacteria.</p>\n<p>I read several papers (2, 3, 4) that discuss the problem of chirality but all of them conclude that there is no apparent reason why we live in the L-world. The L-amino acids should not have chemical advantages over the D-amino acids, as biocs already pointed out.</p>\n<p><a href=\"https://doi.org/10.1007/BF01795749\" rel=\"nofollow noreferrer\">Reasons for the occurrence of the twenty coded protein amino acids</a> (2) has an informative and interesting outline. This is the paragraph on the topic of chirality:</p>\n<blockquote>\n<p>This is related to the question of the origin of optical\nactivity in living organisms on which there is a very\nlarge literature (<a href=\"https://pubmed.ncbi.nlm.nih.gov/4669121/\" rel=\"nofollow noreferrer\">Bonner 1972</a>; <a href=\"https://pubmed.ncbi.nlm.nih.gov/722806/\" rel=\"nofollow noreferrer\">Norden 1978</a>; <a href=\"https://pubmed.ncbi.nlm.nih.gov/7401179/\" rel=\"nofollow noreferrer\">Brack and\nSpack 1980</a>). We do not propose to deal with this\nquestion here, except to note that arguments presented\nin this paper would apply to organisms constructed from\neither D or L amino acids.</p>\n</blockquote>\n<p>It might be possible that both L and D lives were present (L/D-amino acids, L/D-enzymes recognizing L/D-substrates), but, by random chance the L-world outcompeted the D-world.</p>\n<p>I also found the same question in a <a href=\"https://web.archive.org/web/20121104115217/http://forums.studentdoctor.net:80/archive/index.php/t-854644.html\" rel=\"nofollow noreferrer\">forum</a> where one of the answers seems intriguing. I cannot comment on the reliability of the answer, but hopefully someone will have the expertise to do so:</p>\n<blockquote>\n<p>One, our galaxy has a chiral spin and a magnetic orientation, which causes cosmic dust particles to polarize starlight as circularly polarized in one direction only. This circularly polarized light degrades D enantiomers of amino acids more than L enantiomers, and this effect is clear when analyzing the amino acids found on comets and meteors. This explains why, at least in the milky way, L enantiomers are preferred.</p>\n<p>Two, although gravity, electromagnetism, and the strong nuclear force are achiral, the weak nuclear force (radioactive decay) is chiral. During beta decay, the emitted electrons preferentially favor one kind of spin. That's right, the parity of the universe is not conserved in nuclear decay. These chiral electrons once again preferrentially degrade D amino acids vs. L amino acids.</p>\n<p>Thus due to the chirality of sunlight and the chirality of nuclear radiation, L amino acids are the more stable enantiomers and therefore are favored for abiogenesis.</p>\n</blockquote>\n<ol>\n<li><p><a href=\"https://www.annualreviews.org/doi/full/10.1146/annurev.micro.58.030603.123615\" rel=\"nofollow noreferrer\">BIOSYNTHESIS OF NONRIBOSOMAL PEPTIDES</a></p>\n</li>\n<li><p><a href=\"https://doi.org/10.1007/BF01795749\" rel=\"nofollow noreferrer\">Reasons for the occurrence of the twenty coded protein amino acids</a></p>\n</li>\n<li><p><a href=\"https://www.mdpi.com/1422-0067/12/7/4745\" rel=\"nofollow noreferrer\">Molecular Basis for Chiral Selection in RNA Aminoacylation</a></p>\n</li>\n<li><p><a href=\"https://pubmed.ncbi.nlm.nih.gov/8749373/\" rel=\"nofollow noreferrer\">How nature deals with stereoisomers</a></p>\n</li>\n<li><p><a href=\"https://pubmed.ncbi.nlm.nih.gov/4669121/\" rel=\"nofollow noreferrer\">The adaptation of diastereomeric S-prolyl dipeptide derivatives to the quantitative estimation of R- and S-leucine enantiomers. Bonner WA, 1972</a></p>\n</li>\n<li><p><a href=\"https://pubmed.ncbi.nlm.nih.gov/722806/\" rel=\"nofollow noreferrer\">The asymmetry of life. Nordén B, 1978</a></p>\n</li>\n<li><p><a href=\"https://pubmed.ncbi.nlm.nih.gov/7401179/\" rel=\"nofollow noreferrer\">Beta-Structures of polypeptides with L- and D-residues. Part III. Experimental evidences for enrichment in enantiomer. Brack A, Spach G, 1980</a></p>\n</li>\n</ol>\n"
}
] |
[
{
"answer_id": 597,
"pm_score": 4,
"text": "<p>As far as I know, it is unknown why we only see left-handed and not right–handed amino acids. A <a href=\"http://www.nature.com/news/frontier-experiments-tough-science-1.9723\">recent article</a> speculates that the <a href=\"http://en.wikipedia.org/wiki/Weak_force\">weak force</a> could be responsible for a tiny asymmetry in energy levels between the stereo-isomers. However, if the effect is tiny, its hard to see why it should have biological implications. In 2004, <a href=\"http://www.sciencemag.org/content/305/5688/1253.full\">Tamura and Schimmel</a> showed that RNA has a preference for L-amino acids, whereas mirrored RNA has a preference for D-amino acids. They conclude:</p>\n\n<blockquote>\n <p>These results suggest the possibility that the selection of L-amino acids for proteins was determined by the stereochemistry of RNA. </p>\n</blockquote>\n\n<p>So the next question is: Why do we observe only one kind of RNA? It could just be by chance, that a polymer of one RNA configuration became self-replicating. </p>\n"
},
{
"answer_id": 599,
"pm_score": 4,
"text": "<p>The ribosome holds the peptide-bound tRNA and aminoacyl-tRNA in the right orientation to catalyze the peptidyltransferase reaction.</p>\n\n<p><a href=\"http://www.pnas.org/content/103/36/13327/F1.expansion.html\">http://www.pnas.org/content/103/36/13327/F1.expansion.html</a></p>\n\n<p>If the incoming aminoacyl-tRNA was the other enantiomer, the amino acid moiety would not fit properly into the ribosome active site. In other words, the shape of the ribosome selects for specific amino acid enantiomers. In abiotic mixes, the creation of amino acids and their polymerization is non-catalytic, and so there is no specificity or selection for certain enantiomers.</p>\n\n<p>If you're asking the \"biogenesis\" question, then I think the answer is that we don't know the original selection, and it may just be chance. But once biochemistry began making and using them, of course they were all the same. But frankly \"why not D-amino acids\" makes about as much sense as \"why not 22 amino acids, or 23, or 24, or 25?\" Because that's what happened.</p>\n"
},
{
"answer_id": 634,
"pm_score": 3,
"text": "<p>The normal results of an attempt to assemble proteins with mixed chiral amino acids is a protein that fails to fold.</p>\n\n<p>The general assumption due to this result is a choice has to be made very early on to use all right-handed or all left-handed amino acids. There doesn't seem to be any particular reason to choose one way over the other except for prevalence.</p>\n"
},
{
"answer_id": 64614,
"pm_score": 0,
"text": "<p>Using only 1 chirality for the ecosystem simplifies protein formation and folding frameworks. In theory, you could have a codon system with 40 distinct values (and 24 redundant values): glycine, stop codon, and left/right variations of each other amino acid. However, the proteins and nano-\"machinery\" required to support this would be crazy complex. It's much more efficient to build around 1 chirality and stick with it.</p>\n\n<p>Alternately, you could have enzymes specifically designed to flip proteins of the \"wrong\" chirality depending on species.</p>\n\n<p>With that in mind, an ecosystem with different species having different amino acid chirality would be digestive chaos. If you eat a dextro-protein steak, your digestion will break the proteins into... dextro amino acids. Best outcome: they fail to absorb and get flushed down the toilet. Worst outcome: they get absorbed and your cells use them to make proteins - causing severe folding errors, nonfunctional proteins, and a host of untraceable health problems that would likely get misdiagnosed as a spirochaete infection (wide-ranging health problems that aren't limited to a specific region and have no discernible pattern).</p>\n"
},
{
"answer_id": 107769,
"pm_score": 0,
"text": "<p>Most answers to the question of homochirality have considered the reason (if any) for amino acids in proteins being L rather than D. i.e. Why L? I have nothing further to add to that discussion.</p>\n<p>A couple of answers have addressed the question of <em>why there is not a mixture of L- and D- amino acids in proteins</em>, i.e. Why all L? Two distinct arguments have emerged. I shall consider them in turn, and attempt to develop them a little further.</p>\n<p>@Joshua stated that “the results of an attempt to assemble proteins with mixed chiral amino acids is a protein that fails to fold”. I think one can cast this more precisely in evolutionary terms. The α-helical secondary structure component of proteins probably arose early as it involves only the protein backbone, rather than the particular amino acid side-chain. Nevertheless, it is not possible to substitute a D-amino acid in an α-helix of L-amino acids, <a href=\"https://pubs.acs.org/doi/pdf/10.1021/ja00039a086\" rel=\"nofollow noreferrer\">without disrupting the structure</a>. Hence one can suppose that homochirality was necessary for the creation of standard ‘building blocks’ for early protein development.</p>\n<p>@KAM has considered the question of the stereochemistry of the active site, specifically that of the peptidyl transferase. The stereochemistry of the active site of the interaction of enzymes with their substrates is a strong argument for homochirality, but it struck me that this needs to be addressed <em>before</em> peptide-bond formation — in the synthesis of the amino acids themselves.</p>\n<p>It turns out that I was late to the party. In the 2002 edition (I haven’t checked earlier ones) of the text book, “Biochemistry”, by Berg <em>et al.</em>, section 24.2.2 of the chapter on amino acid synthesis is entitled:</p>\n<p><em><strong>A common step determines the chirality of all amino acids</strong></em></p>\n<p>Amino acids are synthesized, directly or indirectly, via reactions catalysed by transaminases (aminotransferases) which convert keto-acids to amino acids:</p>\n<p>Oxaloacetate → Asp → (Asn, Met, (Thr→Ile), Lys)<br>\nPyruvate → (Ala, Val, Leu)<br>\nPhosphoenol pyruvate → (Phe, Tyr, Trp)<br>\nα-Ketoglutarate → Glu → (Gln, Pro, Arg)<br>\n3-Phosphoglycerate → Ser → (Cys, Gly)<br>\nRibose 5-phosphate → His<br></p>\n<p>These transaminases have a similar active site involving a lysine and arginine residue and use the cofactor, pyridoxal phosphate. The reaction mechanism (below) may appear a little complex, but the step at which the chirality of the amino acid is determined is the conversion of quinoid intermediate to external aldimine:</p>\n<p><a href=\"https://i.stack.imgur.com/XTCMf.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/XTCMf.png\" alt=\"Mechanism of Action of Aminotransferases\" /></a></p>\n<p>To quote from Berg <em>et al.</em> (from which the diagrams are taken):</p>\n<blockquote>\n<p><em>The chirality of the amino acid formed is determined by the direction\nfrom which this proton is added to the quinonoid form.</em> This\nprotonation step determines the l configuration of the amino acids\nproduced. The interaction between the conserved arginine residue and\nthe α-carboxylate group helps orient the substrate so that, when the\nlysine residue transfers a proton to the face of the quinonoid\nintermediate, it generates an aldimine with an L configuration at the\nC<sub>α</sub> center.</p>\n</blockquote>\n<p><a href=\"https://i.stack.imgur.com/SCij1.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/SCij1.png\" alt=\"Proton transfer in aminotransferases\" /></a></p>\n<p>So it would seem more likely that the stereochemistry of the active site of peptidyl transferase was an evolutionary response to the existing homochirality of amino acids, rather than <em>vice versa</em>.</p>\n"
}
] |
623 |
<p>From what I can tell and what thus far all people with whom I discussed this subject confirmed is that time appears to "accelerate" as we age.</p>
<p>Digging a little, most explanations I found basically reduced this to two reasons:</p>
<ul>
<li>As we age physically, a time frame of constant length becomes ever smaller in contrast to the time we spent living</li>
<li>As we age socially, we are burdened with an increasing amount of responsibility and thus an increasing influx of information which impairs our perception of the present</li>
</ul>
<p>To be honest, neither sounds entirely convincing to me because:</p>
<ul>
<li>In my perception "local time" (short time frames that I don't even bother to measure on the scale of my lifetime) is also accelerating. Just as an example: When I wait for the bus, time goes by reasonably fast as opposed to my childhood tortures of having to wait an eternity for those five minutes to pass.</li>
<li>Even after making a great effort to cut myself off from society and consciously trying to focus on the moment, the perceived speed of time didn't really change. (Although I did have a great time :))</li>
</ul>
<p>Which leads me to a simple question (and a few corollaries):</p>
<ul>
<li>Am I just in denial of two perfectly plausible and sufficient explanations, or are there actual biological effects (e.g. changes in brain chemistry) in place, that cause (or at least significantly influence) this?</li>
<li>Is there a mechanism, that "stretches out" time for the young brain so that weight of an immense boredom forces it to benefit from its learning ability, while it "shrinks" time as the brain "matures" and must now act based on what it has learned, which often involves a lot of patience?</li>
<li>If there is such a mechanism, are there any available means to counter it? (not sure I'd really want to, but I'd like to know whether I could)</li>
</ul>
|
[
{
"answer_id": 1240,
"pm_score": 6,
"text": "<p>This is not really a biological answer, but a psychological one:</p>\n\n<p>One important fact to consider is that the perception of time is essentially a recollection of past experience, rather than perception of the present.</p>\n\n<p>Researchers who study autobiographical memory have suggested that part of this effect may be explained by the number of recallable memories during a particular time period. During one's adolescence, one typically has a large number of salient memories, due to the distinctness of events. People often make new friends, move frequently, attend different schools, and have several jobs. As each of these memories is unique, recollection of these (many) memories gives the impression that the time span was large.</p>\n\n<p>In contrast, older adults have fewer unique experiences. They tend to work a single job, and live in a single place, and have set routines which they may follow for years. For this reason, memories are less distinct, and are often blurred together or consolidated. Upon recollection, it seems like time went by quickly because we can't remember what actually happened.</p>\n\n<p>In other words, it can be considered a special case of the <a href=\"http://en.wikipedia.org/wiki/Availability_heuristic\" rel=\"nofollow noreferrer\">availability heuristic</a>: people judge a time span to be longer in which there are more salient/unique events.</p>\n\n<p>Incidentally, (and to at least <em>mention</em> biology), episodic memory has been shown to be neurally distinct from semantic memory in the brain. In particular, a <a href=\"http://en.wikipedia.org/wiki/Double_dissociation\" rel=\"nofollow noreferrer\">double dissociation</a> has been shown for amnesics who suffer from semantic or episodic memory, but not both.</p>\n\n<p>My apologies for the lack of citations, but a good bit about autobiographical memories can be found in:</p>\n\n<blockquote>\n <p><a href=\"http://rads.stackoverflow.com/amzn/click/1841695408\" rel=\"nofollow noreferrer\">Eysenck, M.W., & Keane, M.T. (2010). Cognitive Psychology: A\n Student's Handbook.</a></p>\n</blockquote>\n\n<p>You may also be interested in some responses or references to a related question on the Cognitive Science StackExchange:</p>\n\n<p><a href=\"https://cogsci.stackexchange.com/q/129/55\">Perception of time as a function of age</a></p>\n"
}
] |
[
{
"answer_id": 713,
"pm_score": 3,
"text": "<p>There may be some clues in neurobiology.</p>\n\n<p>A possibility may be that a person's general emotional state may affect their perception of the passage of time, as argued in this <a href=\"http://www.robinson.cam.ac.uk/academic/robinson_rationality_luchini.pdf://\">article</a> and references within.</p>\n\n<p>Studies of people with damage to their orbitofrontal cortex (prefrontal cortex region) <a href=\"http://brain.oxfordjournals.org/content/126/7/1691.short\">can experience sustained altered emotional states when compared to control samples.</a> \nThese altered emotional states seemed to affect how they perceived future scenarios (specifically in a simulated gambling context) and the general passage of time compared to controls. </p>\n\n<p>In particular, emotions such as fear and anxiety tended to \"speed up\" the passage of time whereas positivity and excitement (particularly with regards to future events) lead to a subjective slowing down of time.</p>\n\n<p>Si it may be just that, as kids, we are just more \"excited\" in general which made for all those seemingly infinite long summers.</p>\n\n<p>Another possibility is that perhaps it is related to the aging process? As we live longer, I can imagine a scenario where our perception of time would alter (slow down?). It would be interesting to study the perception of the passage of time between long-lived and shorter lived populations in this context.</p>\n"
},
{
"answer_id": 1288,
"pm_score": 3,
"text": "<p>Maybe the passage of time is perceived as a function of heart rate.</p>\n\n<p>Waiting 5 minutes for a turn on the swings is 300 seconds for a 2 year old and 300 seconds for a 40 year old. But that same wait is <a href=\"http://www.ehow.com/about_5479822_normal-pulse-rate-children.html\">575 heart beats for the kid</a>, but only 300 heart beats for the adult.</p>\n"
},
{
"answer_id": 2832,
"pm_score": 3,
"text": "<p>Perception of time can change drastically during an <a href=\"http://www.livescience.com/2117-time-slow-emergencies.html\">emergency</a>.</p>\n\n<p>When we are younger, much like during an emergency, the brain hasn't activated very many filters for sensory data. The young have much to learn about the world and more detail is needed for the brain to make appropriate decisions. Sensory information is recorded in great detail, making time seem to relatively crawl. </p>\n\n<p>As we age, the brain learns to filter out more and more of what it considers inconsequential data. </p>\n\n<p>A good example of these filters at work is the morning commute. If the same route is driven at roughly the same time every workday, the brain begins to leave out much of the repetitive events and scenery from it's historical record of time. Given enough repetition, the record of the event will include so little detail in memory as to almost seem not to have occurred at all. A 30 minute commute will be perceived to have taken very little time -- if it's remembered at all.</p>\n\n<p>As Ferris Bueller so aptly put it, \"Life moves pretty fast... You don't stop and look around once in a while, you could miss it.\"</p>\n"
},
{
"answer_id": 14313,
"pm_score": 0,
"text": "<p>First:</p>\n\n<p>As a child, it could be that the brain is not encoded with a lot of experience. Thus, processing of new information is less complex, and conclusions are made much faster. These conclusions are then encoded into the brain, making future experiences more complex. </p>\n\n<p><em>A child may have concluded everything it is able to conclude within the first few seconds of arriving at that bus stop.</em></p>\n\n<p>Second:</p>\n\n<p>A brain with a lot of previous experiences, is able to occupy itself with \"trivialities\", such as watching snow flakes fall from the sky or thinking about what to have for dinner. Visualizing different tastes and smells.</p>\n\n<p><em>A grown individual might be slower to conclude, taking more factors into account. It may also have more to ponder on.</em></p>\n\n<p>Third:</p>\n\n<p>The brain is thinking all the time. It is unconsciously cross referencing every sound, smell and other sense with previous experiences and actually quite busy. If there is a limit to the amount of energy that goes into the brain for processing stuff, a larger and larger percentage of those electrons will be busy \"retriggering\" signals. Almost like a city road map. It will take a short time for a number of cars to travel every possible route in a small city, than in a big city. Possibly, this has to happen in the brain as well, to refresh old memories.</p>\n"
}
] |
757 |
<p>As far as I understand, various abilities like flying, sight, hearing etc. were caused by slow evolution, where those with a greater ability to to these things had better chance of survival. (If this assumption is wrong, then I am happy to delete this question). </p>
<p>Are there, however, any documented examples of by evolutionary leaps being made, over the course of just a few generations? I understand, that some abilities have a tipping point where one gets the ability suddenly, but there is not a lot of physiological change made. An example of this would be the ability to climb a tree, which could suddenly be possible if the body weight is reduced with just a few percent. What my question is about, are sudden changes to the characteristics of a creature.</p>
|
[
{
"answer_id": 7921,
"pm_score": 4,
"text": "<p>@kmm and @shigeta provided you with a nice observational account of sudden leaps in large organisms. However, if you want to look at where this is the norm and try to build a mathematical theory then you need to look at something much smaller; the prime candidate is <a href=\"http://en.wikipedia.org/wiki/Affinity_maturation\" rel=\"nofollow noreferrer\">affinity maturation</a>.</p>\n<p>In the human immune system, when exposed to an antigen B cells produce antibodies. If it is your first exposure to the antigen then the antibodies produced will probably have very low binding affinity. However, after some exposure time, your B cells will start to produce antibodies with much higher affinities for the antigen and thus you will be able to better fight off the disease. The cool part, is that <strong>the antigen produced is tuned via an evolutionary process</strong>!</p>\n<p>There is differential survival, with only antibodies with the highest affinity being able to survive. Variability is introduced by a very high mutation rate in the <a href=\"http://en.wikipedia.org/wiki/Complementarity-determining_regions\" rel=\"nofollow noreferrer\">complementarity determing region</a> (CDR). (Tonegawa, 1983). The length of this evolutionary process is very short, typically a local equilibrium is found after only 6-8 nucleotide changes in CDR (Crews et al., 1981; Tonegawa, 1983; Clark et al., 1985), so you need only a few point mutations to quickly develop a drastically better tuned antibody.</p>\n<p>The standard mathematical model for this is Kauffman's <a href=\"http://en.wikipedia.org/wiki/NK_model\" rel=\"nofollow noreferrer\">NK model</a>. With a protein sequence on <span class=\"math-container\">$N$</span> sites, we say that evolution is fast (and we have a sudden leap) if after our fitness landscape changes, we can get to a new local equilibrium in a number of generations that scales with <span class=\"math-container\">$\\log N$</span>. Kauffman & Weinberger (1989) showed how this model can be used to study affinity maturation, and showed that to achieve a sudden leap we need high <a href=\"http://en.wikipedia.org/wiki/Epistasis\" rel=\"nofollow noreferrer\">epistasis</a> and low correlations between pointwise mutants. In particular, their model suggests that typical epistasis in the CDR is on the order of 40 proteins (out of the total 112 proteins in the CDR).</p>\n<hr />\n<h2>References</h2>\n<p>Clark, S.H., Huppi, K., Ruezinsky, D., Staudt, L., Gerhard, W., & Weigert, M. (1985). Inter- and intraclonal diversity in the antibody response to influenza hemagglutin. <em>J. Exp. Med.</em> 161, 687.</p>\n<p>Crews, S., Griffin, J., Huang, H., Calame, K., & Hood, L. (1981). A single V gene segment encodes the immune response to phosphorylcholine: somatic mutation is correlated with the class of the antibody. <em>Cell</em> 25, 59.</p>\n<p>Kauffman, S. and Weinberger, E. (1989) The NK Model of rugged fitness landscapes and its application to the maturation of the immune response. <em>Journal of Theoretical Biology</em>, 141(2): 211-245</p>\n<p>Tonegawa, S. (1983). Somatic generation of antibody diversity. <em>Nature</em> 302, 575.</p>\n"
}
] |
[
{
"answer_id": 759,
"pm_score": 4,
"text": "<p><a href=\"http://rsbl.royalsocietypublishing.org/content/2/4/521.full?sid=36ce9d7f-9cc9-4c07-92f4-4808ec90f451\">Zuk et al. (2006)</a> document the rapid evolution of song-less crickets in a population of crickets that previously used song for courtship.</p>\n\n<p>In less that 20 generations, over 90% of male crickets of the species <em>Teleogryllus oceanicus</em> evolved to a novel morphology (\"flatwing\") that rendered them unable to call to females. They hypothesize that this shift resulted from the presence of an North American invasive \"acoustically orienting parasitoid fly.\" </p>\n\n<p>Basically the flies detect calling males and parasitize them, rendering them unable to reproduce. Were it not for the presence of the parasitoid fly, the flatwing flies would likely not have survived. Non-calling individuals rely on the presence of calling males to bring females near for mating.</p>\n"
},
{
"answer_id": 765,
"pm_score": 4,
"text": "<p>The ability to drink milk by the inheritance of lactase persistence via a single allele change. Sociology and genetic studies have shown that the immigration of a few lactose tolerant people into large non-lactose tolerant populations, the lactase persistence gene quickly spreads through the population, a sign of a dominant mutation and survival of the fittest at work. </p>\n\n<p>Not in the mood to dissect the papers but here are a few commentaries:</p>\n\n<ul>\n<li><a href=\"http://sciencelife.uchospitals.edu/2011/09/14/lactose-tolerance-in-the-indian-dairyland/\">http://sciencelife.uchospitals.edu/2011/09/14/lactose-tolerance-in-the-indian-dairyland/</a></li>\n<li><a href=\"http://news.discovery.com/human/got-milk-drinking-common-ancestor-india-and-europe-do-110914.html\">http://news.discovery.com/human/got-milk-drinking-common-ancestor-india-and-europe-do-110914.html</a></li>\n</ul>\n"
},
{
"answer_id": 838,
"pm_score": 2,
"text": "<p>I think that this might refer to evolution in <a href=\"http://www.scholarpedia.org/article/Punctuated_equilibria\" rel=\"nofollow\">punctuated equilibrium</a> as described by Stephen Gould et al way back in the 70s. If this is the case, it refers more to the idea that changes and speciations can be quite rapid in time and for long periods you don't see morphological changes or speciation events in the record. </p>\n\n<p>If so, then this is influenced by the study of evolution in cases where there are large changes in the environment very rapidly. The classic case is when there is a bare island and new animals arrive only rarely. This is all very much inspired by Darwin's observations in the Galapagos, but has since been studied quite a bit. In such cases you see just handful of sets of birds suddenly appear and you find a finch that can scrape bugs out of bark, another that can dig into narrow niches in the rock for food, where in a broader ecosystem two completely different species would be utilizing those 2 food sources. </p>\n\n<p>It should be said that no evolutionary leap should be understood as an acceleration or deceleration of evolution. Only a change in the rate of adoption of variations because of a wider set of possible advantages those variations can represent. </p>\n"
},
{
"answer_id": 21678,
"pm_score": 0,
"text": "<p>With all due respect, a few of these answers, although good examples of selection at work, were voted too high given the specific question asked: “documented examples of by evolutionary leaps being made, over the course of just a few generations?”</p>\n\n<p>Sometimes we’re better being honest and identifying something as an ‘unknown’ or ‘yet to be observed’ than to list (and have people up-vote) poor examples. <strong>We do evolution a dis-service when we promote poor examples as answers to questions like these.</strong> </p>\n\n<p>To expound:</p>\n\n<p>The cricket losing the ability to sing (communicate) examples does demonstrate mutation and natural selection at work, but really only shows the REDUCTION of a capability. It’s not a good example of evolutionary leaps. It only happens to be beneficial in one SPECIFIC context. This would be analogous to tanks on a battle-field which communicate via radio, vulnerable to radio-frequency tracking missiles. Any tank with a broken radio would not be vulnerable to these missiles. Although technically ‘beneficial’ in this context, it’s an example of a loss of capability, not a gain of capability. We need to promote examples of mutations that PRODUCE capabilities. </p>\n\n<p>Lactase persistence example likewise is an example of mutation and natural selection, but not a good example of a GAIN in functionality (as some have pointed out in the comments). It’s technically the loss of the normal switching-off mechanism of lactase production following weaning. So once again, a loss, that happens to have a beneficial side-effect. </p>\n\n<p>Regarding punctuated equilibrium, I’m not surprised that was mentioned but was surprised that it got some votes. It’s a hypothetical explanation for why we see gaps in the fossils, but not conclusive ‘evidence’, or in the case of the question asked not “documented examples”.</p>\n\n<p>Again: We do evolution a dis-service when we promote poor examples as answers to questions like these. Let’s focus on quality, not quantity when it comes to presenting evidence for evolution.</p>\n"
}
] |
762 |
<p>Humans have, in a relatively short amount of time, evolved from apes on the African plains to upright brainiacs with nukes, computers, and space travel. </p>
<p>Meanwhile, a lion is still a lion and a beetle is still a beetle.</p>
<p>Is there a specific reason for this? Do we have a particular part of brain that no other animal has?</p>
|
[
{
"answer_id": 766,
"pm_score": 6,
"text": "<p>We have the <a href=\"http://en.wikipedia.org/wiki/Human_accelerated_regions\">Human Accelerated Regions</a> (HARs) which are some of the most rapidly evolving RNA genes elements. While heavily conserved in vertebrates, they go haywire in humans and are linked with neurodevelopment.</p>\n\n<p>Thanks to @Nico, the following paper compares the human genome with that of the chimp and identifies genetic regions that show accelerated evolution. The most extreme, <a href=\"http://en.wikipedia.org/wiki/HAR1F\">HAR1</a> is expressed mainly in <a href=\"http://en.wikipedia.org/wiki/Cajal-Retzius_cell\">Cajal-Retzius</a> neuron cells which hints at its important role in human development.</p>\n\n<p><a href=\"http://dx.doi.org/10.1038/nature05113\"> <strong>Pollard KS, Salama SR, Lambert N, Lambot M-A, Coppens S, Pedersen JS, Katzman S, King B, Onodera C, Siepel A, et al.</strong>. 2006. An RNA gene expressed during cortical development evolved rapidly in humans. Nature 443: 167–72.</a></p>\n"
}
] |
[
{
"answer_id": 767,
"pm_score": 3,
"text": "<p>The ability to walk on two legs was hugely significant in human evolutionary development. This led to the hands being freed up to develop into precision tools rather than having to be durable for walking on rough terrain. Increased dexterity in the hands led <em>in part</em> to the leap forward in human development.</p>\n\n<p><em>~ <a href=\"http://en.wikipedia.org/wiki/The_Human_Body_%28TV_series%29\" rel=\"nofollow\">The Human Body</a> (Prof. Robert Winston - <a href=\"http://www.imdb.com/title/tt0200346/\" rel=\"nofollow\">BBC Documentary</a> 1998 (<a href=\"http://news.bbc.co.uk/1/hi/special_report/1998/05/98/the_human_body/114977.stm\" rel=\"nofollow\">BBC Text Summary</a>)</em></p>\n"
},
{
"answer_id": 779,
"pm_score": 1,
"text": "<p>I believe that it is significant that we spend so much of our brain-power on deciding who we want to mate with. For lions it seems like choosing a partner is much less based on rational thinking. The weakness of this theory is that I do not know how humans behaved earlier, and whether mating was strictly regulated by cultural rules to ensure that mating was not based upon convenience, but rational thinking about what who is the best partner in the long-term.</p>\n\n<p>The reason for me believing that this is so important, is that a well-functioning couple in a well-functioning community, will have the time and energy to educate their children, who again will make wiser decisions on who they will choose as their partner.</p>\n\n<p>I would love to get this theory tested (and hopefully rejected, as that is the way I learn the most) by this community.</p>\n"
},
{
"answer_id": 783,
"pm_score": 5,
"text": "<p>This question appears to address at least two distinct concepts:</p>\n<ol>\n<li>the "speed" of evolution</li>\n<li>whether there is some "end goal" that evolution seeks</li>\n</ol>\n<p>I will provide an explanation of each separately below:</p>\n<h2>The Speed of Evolution</h2>\n<p>The speed at which a species evolves—that is, the speed at which it acquires new heritable characteristics—can be affected by numerous factors. Among the most obvious which come to mind are:</p>\n<ul>\n<li>existing population size</li>\n<li>reproductive cycle rate</li>\n<li>number of offspring</li>\n<li>offspring survival rate</li>\n<li>environmental demands</li>\n</ul>\n<h3>That said, have humans evolved <em>faster</em> than other species?</h3>\n<p>On the whole, I do not feel that I could say without a doubt that humans have evolved significantly faster than other organisms. Considering the above factors (we have a slow reproductive cycle, few offspring, etc.), it seems unlikely but this is where a zoologist would know better. The answer provided by <a href=\"https://biology.stackexchange.com/a/766\">bobthejoe</a> may provide insight as well.</p>\n<p>I would just raise a word of caution before leaping to the conclusion that we have evolved rapidly without looking into it, because while we often study human evolution quite extensively in biology classes and thus are more <em><strong>aware</strong></em> of changes like upright walking and opposable thumbs and increased brain size, that doesn't mean other animals didn't evolve that much as well (we just don't learn about them in as much detail). Being a psychologist and not a zoologist, I do not have the knowledge to say with any surety that other species did not evolve in their own ways to the same magnitude as we have in the last 3-4 million years, so perhaps someone else can help you there.</p>\n<p>But you ask <strong>whether we have a particular part of our brain that no other animal has</strong>; the answer to this is no, but the parts of our brains which we do share with animals are often much larger than as seen in those other species.</p>\n<h2>The "Goal" of evolution</h2>\n<p>I would like to point out here that human technology has nothing to do with evolution. Not only have all of our notable technological achievements occurred in the last couple hundreds years when human evolution was at its slowest (early human evolution as we know it today dates back <em>at least</em> 5-7 million years, and it was during this several million year period when all the genetic evolution you speak of happened), I would argue that human spaceships and computers are no more sophisticated to us than a <a href=\"http://www.sciencedaily.com/releases/2009/11/091120000437.htm\" rel=\"noreferrer\">mushroom garden</a> and <a href=\"http://myportfolio.usc.edu/kentarom/2010/09/termites_friend_or_foe.html\" rel=\"noreferrer\">ventilation system</a> are to a termite. I could be wrong here but <strong>it seems as if you are under the impression that evolution is striving <em>towards</em> something</strong>... That humans are somehow intrinsically <em>better</em> than lions or sharks or beetles. On the contrary, each of these creatures is not significantly more or less adapted to their environments as we are to our own, and in many ways these creatures possess features which are beyond our own.</p>\n<p>I shall leave you with one of my favorite quotes:</p>\n<blockquote>\n<p>"We need a wiser and perhaps a more mystical concept of animals. We\npatronize them for their incompleteness, for their tragic fate having\ntaken form so far below ourselves. And therein we err, and greatly\nerr. For the animal shall not be measured by man. In a world older and\nmore complete than ours, they move finished and complete, gifted with\nextensions of the senses we have lost or never attained, living by\nvoices we shall never hear. They are not brethren, they are not\nunderlings. They are other nations caught with ourselves in the net of\nlife and time, fellow prisoners of the splendor and travail of the\nearth."</p>\n</blockquote>\n<p>–Henry Beston, in <em>The Outermost House</em></p>\n<p><sub>I don't have a dog in this fight, and I could very well be falsely assuming that you think this particular way when you in fact don't (you only wrote 4 lines after all, it's hard to glean much from that), but I wanted to make sure that these concepts were clear either way, particularly for any future visitors who might get the wrong impression. :)</sub></p>\n"
},
{
"answer_id": 787,
"pm_score": 4,
"text": "<blockquote>\n <p>It seems to me that humans have, in a relatively short amount of time evolved from apes on the African plains to upright brainiacs with nukes, computers, and space travel.</p>\n</blockquote>\n\n<p>The question covers changes of two sorts: biological evolution and cultural evolution. The other answers speak to biological evolution, but I want to point out that much of the most striking changes (\"nukes, computers...\") are due to the evolution of our culture.</p>\n\n<p>By 40,000 years ago most of our biological evolution to the present had happened (perhaps the most notable exception being changes related to our coevolution with disease organisms). Yet although we had achieved upright brainiac-hood by the apparent evidence, we were not strikingly different from other large animals. </p>\n\n<p>We had sharpened rocks and sticks, and made better use of the surroundings, particularly in non-food categories, than other animals. We had been successful enough to spread throughout much of the old world. Nevertheless, the overall contrast with other animals seems rather muted when viewed by the differences with the modern world.</p>\n\n<p>Most of the visible changes since then are due to evolution happening outside our genes and bodies in what can be called culture. Other animals have culture but our nature gives us many times the cultural capability. We build upon the culture we find ourselves in and make it more effective. The cultural presevation and advances come not just from aping ('monkey see, monkey do'), but from language, and from mechanisms of cultural distribution and preservation, most notably from the invention of written language. These things have driven the cultural evolution of the largest visible changes, those of the last few millenia. </p>\n"
},
{
"answer_id": 3542,
"pm_score": 2,
"text": "<p>Many animals have actually reached an optimal solution to their evolutionary path.\nThat means that from where their genome is right now, pretty much all changes are harmful to expected reproduction. Over time such species start to have less variability within their genome and start to evolve less. Evolving is simply not sensible anymore.</p>\n\n<p>Humans on the other hand are in an extremely open evolutionary path, that means there is much variability within the human genome that leads to greatly varied expected reproduction.</p>\n\n<p>That is why humans are evolving so fast.</p>\n"
},
{
"answer_id": 7383,
"pm_score": 2,
"text": "<p>What you are talking about is genetic vs memetic evolution. While both are important in our species, the memetic evolution is responsible for the changes you are citing (mostly technological advancements and \"culture\"). There are some interesting situations where memetic evolution is actually \"cancelling out\" genetic evolution. For example medical technology has largely allowed many (at least in the developed world) to survive in spite of genetic handicaps (lack of resistance to a pathogen, insulin, glasses, etc). \nDespite this I would argue we are still evolving rapidly in the genetic sense though not for the reasons you imply. In most vertebrates (any slow-reproducing creature), there is an ongoing selective pressure against pathogens. If their immune systems don't continually change (and antibiotics don't intervene), pathogens will wipe them out. While not as glorious as developing bipedalism, this is still evolution. We are also now a very transient species with people migrating extensively compared to the recent past. This leads to new genetic combinations and thus potential selection. \nIt could be argued (as others have) that the selective pressures for brain development (especially for language ala the FoxP2 gene) have brought about the rise of language, technology and culture. However I would argue that these evolutionary changes largely occurred, at minimum, the last few tens of thousands of years. \nAs others have also noted, crazy genius isn't <strong>THE</strong> end goal of evolution, it is merely <strong>ONE</strong> possible outcome. The real goal is genetic perpetuation (which we do seem to excel at) ;)</p>\n"
},
{
"answer_id": 13663,
"pm_score": 2,
"text": "<p>Interesting and thought provoking. Though I am curious why you wouldn't think plants and animals are conscious. Maybe they aren't self aware like you are, but if a lioness preserves herself to tend her cubs, is she not aware of the fact that things can exist or no longer exist? That life can be lost? No matter at what level you may perceive, this realization in her will trigger an emotion ( chemical reaction) which in turn will give her the fortitude to continue to survive, or as we sometimes see in nature, to not. How are we different? I hate this cut off that I see. \" if it doesn't do it on the level that we do it then it don't do it at all\". That's silly, if you believe in an evolutionary development of genetic material how can you not believe that emotions and awareness have levels of development too? Sounds a bit like the \"chosen one\" complex. Once you take that road, you're a hop skip and a jump from the creationist and 6000 year old earth.</p>\n"
},
{
"answer_id": 54608,
"pm_score": 1,
"text": "<blockquote>\n <p>Is there a specific reason for this? Do we have a particular part of\n brain that no other animal has?</p>\n</blockquote>\n\n<p>Because you are human. So every minor change in appears looks important from skin colour, to the length of a nose, to the sounds we regularly make. If you were a lion, such minor difference would be noted but hardly commented upon. Think about this, all male lions have manes right? That is the essential display of maleness in lions. However male Tsavo lions have no mane. this is the equivalent of a tribe of people where the women have no breast. </p>\n\n<p>There is no special part of the brain that is unique to humans. The structure of the brain in a mouse is essentially the same as the human. The big difference, is how big each section of the brain is. </p>\n\n<p>In fact elephants and dolphin come close to matching human in cerebrum complexity. And the long-finned pilot whale, has actually more neocortical neurons than any mammal studied to date including human. </p>\n\n<p>So why are us humans the guys with the guns? </p>\n\n<p>Environment... no matter how smart a dolphin is, they will never master fire, because living in water does that to you. (also no hands, imaging trying to make rope with only your mouth to work with.)</p>\n\n<p>And why elephant and man not waged war upon each other...(we have just not warfare were both sides used spears and swords) well them elephants have at best one hand with two fingers. No elephant, no matter how dexterous will ever learn how to knap a flint tool. Elephants never evolved hands... and us human got our hands from our ape ancestors that lived in the tree and needed limbs that could grasp.</p>\n\n<p>Humans are special... but not in the way you would think. It is not because we are the most brainy animal out there, the long-finned pilot whale is more brainy. No because we are talkative social animals.... elephants talk too and they do talk to herds tens of kilometers away, maintaining decade long relationship made as calves.. Not because we use tools, birds and dolphins use tools too. Not because we have hands... many animal have hands... even non primates... like raccoons. </p>\n\n<p>We are special because we can do all these things at the same time. We are brainy, have a pair of hands, tool using, social animals that live on dry land.</p>\n\n<p>But that said... even with all those features.. the human species have been around for about 200,000 years. Civilization for 10,000. </p>\n\n<p>Nukes, computers, and space travel.. strange as it is are very recent inventions. There are still people alive today who remembered the Wright brothers touring their new invention, the airplane. There are people alive today who saw the start of space race and the coming of the first PC (personal computer), the first nuke, the first mobile phone. </p>\n\n<p>Go back just 200 and an LED flash light is tech so beyond bleeding age technology, it might as well it be science fiction (first light bulb invented in 1801. First commercial light bulb 1879). </p>\n"
}
] |
832 |
<p>A student asked me this the other day and I thought that I would ask it again here. If one organism is said to be "more evolved" than another, what exactly does this mean?</p>
|
[
{
"answer_id": 833,
"pm_score": 6,
"text": "<p>\"More evolved\" is actually meaningless in all contexts. See terdon's answer for a good explanation.</p>\n\n<p>In the strictest sense, an organism can be said to be more divergent than another when comparing both to an outgroup, such that there is an inferred most common ancestor in reference to which to make the comparison. In this case, one organism is more divergent if there are more changes to this organism than the other, relative to the reference point.</p>\n\n<p>However, when speaking, many people get lazy, and use \"more evolved\" as shorthand, wishing it to mean something like \"more divergent\". Even \"more divergent\" is meaningless in the following contexts:</p>\n\n<ul>\n<li>when there is no outgroup understood</li>\n<li>when describing increasing complexity (obligate parasites have lost complexity and have had more evolutionary changes than their non-parasitic relatives) </li>\n<li>when the outgroup is poorly chosen. Mammal vs reptile comparisons should not, in general, use prokaryotes as the outgroup.</li>\n</ul>\n\n<p><strong>Edited 2013/12/06</strong> to reflect the precision in the answer by terdon. </p>\n"
}
] |
[
{
"answer_id": 834,
"pm_score": 4,
"text": "<p>I cannot improve on Thomas Ingalls' description of when \"more evolved\" is appropriately used, but the inappropriate/lazy use of the phrase is so prevalent that it deserves further comment. In my experience, the most common use of the phrase \"more evolved\" is when describing the increased complexity of one organism versus another. This usage is not just meaningless, but wrong and harmful, and springs from a misunderstanding of what evolution implies. Evolution is emphatically not the same as increased complexity. </p>\n\n<p>I try to avoid saying \"more evolved\" and tend to favor \"more complex\", \"less simple\" or \"less primitive.\" \"Primitive\" has its own problems, since it sometimes brings with it the connotation of evolution (a \"primitive eye\" or \"primitive nervous system\" are common phrases), but it at least avoids an explicit misuse of \"evolved.\"</p>\n"
},
{
"answer_id": 6974,
"pm_score": -1,
"text": "<p>I have mostly seen it used to mean \"possessing features that appeared most recently in the historical evolutionary record\". Thus a human is considered more evolved than a chimp because our bipedality, hairlessness and large brain appeared more recently than the features of chimps, and a chimp is more evolved than a fish because fish very similar to ones alive today appear in the record before anything resembling an ape, and so on.</p>\n\n<p>I think it's pretty poor use of language, frankly, since it suggests linearity and ordering to evolution that is simply not there, conflates gross morphological change with change in general and incorrectly implies that stabilising selection is not evolution.</p>\n"
},
{
"answer_id": 8623,
"pm_score": 3,
"text": "<p>There is no such thing as more or less evolved. At least not outside popular media. The only reasonable comparison one can make is comparing generation numbers. You <em>could</em> say that a species that has undergone X generations is less evolved than one that has undergone X*2 generations. It just doesn't mean much. </p>\n\n<p>Evolved is not a quantitative term, you cannot really be more or less evolved than something else. </p>\n"
},
{
"answer_id": 13862,
"pm_score": 0,
"text": "<p>It is a phrase in common parlance without scientific meaning, fitting in the same category as <em>devolved</em> or <em>devolution</em>. It is as @terdon said:</p>\n\n<blockquote>\n <p>There is no such thing as more or less evolved.</p>\n</blockquote>\n\n<p>In a scientific context you should always find the evolutionary measure in question and the methods for quantifying that measure.</p>\n\n<p>In a biological context the phrase would fail to find meaning, when evolution is a function of fitness. In such context fitness is inevitably tied to environmental parameters. The more complex these parameters, the more niches may be available for potential species, with temperature being one of the strongest factors (See: <a href=\"http://en.wikipedia.org/wiki/Effective_evolutionary_time\" rel=\"nofollow noreferrer\">Effective evolutionary time Hypothesis</a> ). Take this assertion with the necessary caution, as it is far outside my expertise.</p>\n\n<p>Mostly I have come across the phrase <em>more evolved</em> in reference to large, tangible species, and also in science fiction.</p>\n\n<p>Tell your student, to always be aware that in the end the unicellular species make life for us on this planet viable - we coevolved. But they also eventually consume/recycle us in one way or another, and surely will outlast us. It takes extreme effort and finesse for a large, energetic multicellular host to obtain, maintain and retain its niche on this planet. In all of the field of molecular biology there is nothing quite like Immunology.</p>\n\n<p><strong>For a mind experiment, let the student imagine soil with different pH, of the same plant species which equal seeding-times.</strong></p>\n\n<p><strong>The outcome may be something as shown below. The phrase \"more evolved\" clearly fails to describe such a scenario of one generation of plant species, and hence is not suitable in an objective description of evolution.</strong></p>\n\n<p><em>Sidenote: Al3+-ions are toxic to plants, stuning root growth and phosphate intake. With increased pH, more aluminum dissolves.</em>\n<img src=\"https://i.stack.imgur.com/bZHr4.jpg\" alt=\"enter image description here\"></p>\n"
}
] |
884 |
<p>This came up in a talk with a friend. I wanted to clear this doubt. I've read about it before and did again after her remark (my thoughts didn't change: her concept is Lamarck's, not Darwin's), but wanted to clarify.</p>
<p>Regarding Evolution, nothing, absolutely nothing, that a person does to herself in life can be genetically inherited. It does not matter how much this person drinks, the changes they do to their body, how dark their skin gets over life etc. Such changes can not be transmitted to their offspring in any way, correct?</p>
<p>*Summary:*Is the assertion "You can not change in life what will be genetically inherited in any possible way" true?</p>
|
[
{
"answer_id": 886,
"pm_score": 5,
"text": "<p>The assertion \"You cannot change in life what will be genetically inherited in any possible way\" is true, as you cannot (healthily) change the DNA in your germ cells.</p>\n\n<p>However, the assertion \"You cannot change in life what will be inherited in any possible way\" is wrong, because of <a href=\"http://en.wikipedia.org/wiki/Epigenetics\" rel=\"nofollow noreferrer\">epigenetics</a>. Parts of your DNA are marked (in different ways), and this can be inherited and have an effect. E.g. the only causal difference between these two mice is the diet of their mothers:</p>\n\n<p><img src=\"https://i.stack.imgur.com/1tmOP.jpg\" alt=\"Two mice of same genotype but different phenotype\"></p>\n\n<p>Image source and a further explanation: <a href=\"http://learn.genetics.utah.edu/content/epigenetics/nutrition/\" rel=\"nofollow noreferrer\">Nutrition and the epigenome</a>. </p>\n"
}
] |
[
{
"answer_id": 887,
"pm_score": 4,
"text": "<p>In general, Darwin's theory has been supported over and over again by experiments - our modern understanding of evolution is fundamentally what Darwin suggested. However, apart from appreciating many more details than Darwin ever could have, we also now know that Lamarck may not have been so crazy as he was later portrayed.</p>\n\n<p>Inheritance in the Darwinian sense involves the digital information of DNA, i.e the sequence of bases. But we also know that DNA can be altered structurally - i.e. in the way it folds, or whether bases are methylated - and that these structural alterations can affect the expression of genes. In some cases, these <a href=\"http://en.wikipedia.org/wiki/Epigenetics\">epigenetic modifications</a> can be trans-generational; they can be passed on to offspring.</p>\n\n<p>Here are the mechanisms that I know of (perhaps others can expand on this):</p>\n\n<ul>\n<li><a href=\"http://www.nature.com/scitable/topicpage/x-chromosome-x-inactivation-323\">X-chromosome inactivation</a> (XCI): this is when one of two copies of the X-chromosome in females is completely inactivated by being packed into heterochromatin, preventing the DNA from being transcribed. Which chromosome (the maternal or paternal) is deactivated initially is random, but the decision can be inherited by all daughter cells. <em>Skewed</em> x-inactivation is when a cell very early in the cell line passes on its XCI decision, and can result in a particular phenotype being activated in a whole organ or tissue (such as patches in tortoiseshell cats). It has been shown that in mice and in humans, the somatic cells can sometimes have their XCI decision influenced by the mother, and that this can lead to early skewing of the XCI in the offspring, thereby passing on a decision about which alleles are present without affecting the DNA sequence.</li>\n<li><a href=\"http://en.wikipedia.org/wiki/Genetic_imprinting\">Parental imprinting</a>: in this case, individual alleles derived from one parent are preferentially activated or deactivated by <a href=\"http://en.wikipedia.org/wiki/DNA_methylation\">methylation</a> or <a href=\"http://en.wikipedia.org/wiki/Histone_modification#Chromatin_regulation\">histone modification</a>. This change is passed on to the zygote, and alters expression in the offspring. Several human heritable diseases are associated with this kind of modification, such as <a href=\"http://en.wikipedia.org/wiki/Prader-Willi_syndrome\">Prader-Willi Syndrome</a>.</li>\n<li><a href=\"http://en.wikipedia.org/wiki/Paramutation\">Paramutation</a>: first discovered in maize, this is when the presence of one allele in a genome can affect another allele in a heritable way. I.e. if allele A is present in the same genome as allele B for a single generation, allele A is permanently inactivated so that if you breed out allele B, allele A will not be active in the offspring.</li>\n</ul>\n\n<p>Finally, there is also a phenomenon called <a href=\"http://en.wikipedia.org/wiki/Structural_inheritance\">structural inheritance</a>, whereby a structural feature of an organism is inherited in a non-genetic way. There is less written about this, so the mechanism is not entirely clear as far as I know, but an example is that the 'handedness' of the spiral pattern on the shell of a protozoan <em>Tetrahymena</em> is inherited without any genetic change (<a href=\"http://dev.biologists.org/content/105/3/447.long\">Nelsen et al., 1989</a>).</p>\n\n<p><strong>References:</strong></p>\n\n<p>Nelsen, E.M., Frankel, J. & Jenkins, L.M. (1989) Non-genic inheritance of cellular handedness. Development (Cambridge, England). 105 (3), 447–456.</p>\n"
},
{
"answer_id": 891,
"pm_score": 2,
"text": "<p>Infections by a retro-virus (such as HIV) can, at least in principle, be inherited.<br>\nThese viruses integrate their genome into the host's DNA, and these changes pass to next generations as the cells split. So if a germ cell is infected, all the cells in the child would be.<br></p>\n\n<p>The question is whether there's a retro-virus that infects germ cells. I don't think HIV does (it can certainly pass from mother to child, but as a \"normal\" infection, not through the DNA).</p>\n"
},
{
"answer_id": 899,
"pm_score": 3,
"text": "<blockquote>\n <p>Is the assertion \"You can not change in life what will be genetically inherited in any possible way\" true?\n No. Does not seems the case, as other people already replied.</p>\n</blockquote>\n\n<p>Here, I just want to point to two recent research articles showing evidence against your assertion.</p>\n\n<p>The first, published in Cell in 2010, is from Dr Oliver Rando, and suggests that <a href=\"http://www.sciencedaily.com/releases/2010/12/101223130149.htm\" rel=\"nofollow\">you are what your father ate, too.\n</a>\nThe second, published in Nature in 2011, is from Dr Anne Brunet, and argues that <a href=\"http://www.guardian.co.uk/science/2011/oct/19/worms-inherit-memory-longevity-parents\" rel=\"nofollow\">worms can inherit a 'memory of longevity'</a> from long-lived parents.</p>\n"
},
{
"answer_id": 1674,
"pm_score": 0,
"text": "<p>There's a related review paper: \"<a href=\"http://www.nature.com/nrg/journal/v12/n7/full/nrg3028.html\" rel=\"nofollow\">Beyond DNA: integrating inclusive inheritance into an extended theory of evolution</a>\" (<a href=\"http://champagnelab.psych.columbia.edu/docs/ChampagneNR.pdf\" rel=\"nofollow\">PDF</a>)</p>\n"
}
] |
1,228 |
<p>I am working with an Arabidopsis mutant with an F-box protein knocked out. It has been shown that F-box proteins targets must first be phosphorylated (<a href="http://www.sciencedirect.com/science/article/pii/S0092867400804031">Skowrya et al., 1997</a>). I have heard of phosphorylation sites, but I can't find out whether every protein has them. Can any protein be phosphorylated?</p>
<ul>
<li><a href="http://www.sciencedirect.com/science/article/pii/S0092867400804031">Skowyra, D., Craig, K.L., Tyers, M., Elledge, S.J. & Harper, J.W. (1997) F-Box Proteins Are Receptors that Recruit Phosphorylated Substrates to the SCF Ubiquitin-Ligase Complex. <em>Cell</em>. <strong>91</strong> (2), 209–219.</a></li>
</ul>
|
[
{
"answer_id": 1231,
"pm_score": 5,
"text": "<p>Phosphorylation can occur on specific amino acids only, what you have called phosporylation sites. These amino acids are Ser, Tyr, Asp, Thr and His. In theory any of these amino acids may be phosphorylated, but in reality it may not actually occur for a number of reasons. Some of these are because of the change in overall charge of the protein which can influence the 3D conformation, or the amino acids are not accessible to specific kinases, etc. If you ask for the purposes of doing a Western blot, then the antibody specification sheet should indicate whether a phosphorylated form exists and there should be a reference to the literature describing this modification.</p>\n"
}
] |
[
{
"answer_id": 1230,
"pm_score": 3,
"text": "<p>Phosphorylation requires exposed serine, threonine, tyrosine, or histidine residues (in eukaryotes). This is because the transfer of phosphate groups to proteins is mediated by a class of proteins called kinases. Kinases can have broad or specific activity. </p>\n\n<p>This review ought to have most of the answers to your questions :</p>\n\n<p><a href=\"http://www.cell.com/abstract/S0092-8674(06)01274-8\">http://www.cell.com/abstract/S0092-8674(06)01274-8</a> </p>\n"
},
{
"answer_id": 1241,
"pm_score": 3,
"text": "<p>One important thing is missing in the other answers: not only phosphorylation will happen only at selected aminoacids, but it will not happen at all of those.</p>\n\n<p>So, not all of the Ser/Thr/Tyr of a protein can be phosphorylated because they could be structurally unaccessible to protein kinase and because they need to be in a specific motif in order to be phosphorylated.</p>\n\n<p>The <a href=\"http://www.hprd.org/index_html\">Human Protein Reference Database</a>, for instance, lists the phosphorylation motifs for many <a href=\"http://www.hprd.org/tyrosine_motifs\">Tyr</a> and <a href=\"http://www.hprd.org/serine_motifs\">Ser/Thr</a> kinases.</p>\n"
},
{
"answer_id": 1248,
"pm_score": 3,
"text": "<p>I like Nico's response best +1. I did find an interesting <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/19751195\">review</a> on phosphoarginine and phospholysine - the list of possible phosphorylation sites grows. Not only is it the spatial context of the amino acid to be (or not) phosphorylated, as Nico writes and Leonardo implies, but also the temporal. Are the target protein and protein kinase co-expressed? If you're looking at specific tissues (root, flower, leaf) and the kinase in question is only produced in seedlings, maybe that potential phosphorylation won't really occur.</p>\n"
},
{
"answer_id": 5339,
"pm_score": 1,
"text": "<p>For one of the most comprehensive databases of protein post-translational modification (including phosphorylation, methylation, acetylation, ubiquitination, etc.), check out <a href=\"http://www.phosphosite.org\" rel=\"nofollow\">PhosphoSite</a>. You can find links to sequences, diseases, motifs, publications, antibodies, mass spec experiments, structures, you name it.</p>\n"
}
] |
1,446 |
<p>I don't know if this question applies to only humans but why can cones see much greater detail than rods? Is it possible to have a rod that can detect light intensity and color?</p>
|
[
{
"answer_id": 1461,
"pm_score": 6,
"text": "<p>The spectral sensitivity of photoreceptors expressed is the key to color vision. See figure below for the sensitivity of three-types of cone cells (S, M, L) and rod cell (R, dashed line).\n<img src=\"https://i.stack.imgur.com/fF2eT.png\" alt=\"Spectral sensitivity of photoreceptors\"></p>\n\n<p>From this figure, one can say rod cells provide information about the \"blue-greenness\" of vision, however, despite their spectral sensitivity, it seems that in human vision rod cells do not contribute to color vision, because they are <strong>highly sensitive to intensity</strong>, and thus they are mostly saturated in their response (does not induce firing of downstream bipolar cells) during normal daylight conditions. Rod cells specialize for night vision (<a href=\"http://en.wikipedia.org/wiki/Scotopic_vision\" rel=\"noreferrer\">scotopic conditions</a>) which is crucial for survival, and under this condition the cone cells are pretty much useless.</p>\n"
}
] |
[
{
"answer_id": 1454,
"pm_score": 4,
"text": "<p>Cone cells are each connected to their own neurone. This allows them a great deal of resolution as the brain can interpret the exact position of the cone cell that was stimulated by a light photon. However in order to improve low light vision, multiple rod cells are connected to a single neurone - this is called summation. Whilst it does allow for an action potential to be generated in low light conditions, it greatly reduces resolution as the brain can not know precisely which rod cell was stimulated:</p>\n\n<p><img src=\"https://i.stack.imgur.com/15SFw.gif\" alt=\"Anatomy of the human retina\"></p>\n\n<p>Rods can not detect colour as they only come in one variety - cone cells (in humans) come in a red, green and blue specific form to allow for the perception of colour by the brain due to the relative strength of these signals. </p>\n"
},
{
"answer_id": 1494,
"pm_score": 4,
"text": "<p>While the answers to date are correct regarding the wiring of rods and cones in the primate (specifically human) eye, they are also fundamentally wrong. Neither rods nor cones perceive color. The brain does. The rods and cones are just the receptors providing signals. The first answer in fact says this in its very last sentence.</p>\n\n<p>As one answer says, during the day the rods are saturated (overstimulated) so the brain ignores them. It uses the components of the cone responses to invent the sensation \"color\". At night the cones are usually only weakly stimulated, so the brain sees only with the more sensitive rods, and little or no color. This is why brightly colored stars such as Betelgeuse and Rigel still appear only faintly tinged (red and blue respectively).</p>\n\n<p>By the way, some primates have even better color perception than humans with four (or five) kinds of cones. It is speculated that color vision is so good in primates because of the need to judge fruit ripeness to eat. Many mammals have fewer cone types than primates.</p>\n"
},
{
"answer_id": 8122,
"pm_score": 3,
"text": "<p>All of the above answers are great, and very informative. But they are also <em>technically</em> wrong, in certain conditions. Once you understand them, you'll be able to understand this explanation of why.</p>\n\n<p>The canonical answer is that cones are used for color perception in bright light and rods are used in low light. But rods have a peak color sensitivity that is very distinct from the cones (see the chart posted above). And more importantly, <em>there are light levels at which both rods and cones are equally functional for color perception</em>. </p>\n\n<p>This is known as the \"Purkinje effect\" or \"Purkinje shift\". Basically, when light levels dim, your red color perception diminishes first, but your blue color perception is enhanced (or at least doesn't diminish nearly as fast). The specific effect is that red objects get darker much faster than blue ones. But the brain isn't yet just perceiving the blue objects as a brighter gray, so it seems there is some color perception built into the brain based on the rods. </p>\n\n<p><a href=\"http://en.wikipedia.org/wiki/Purkinje_effect\">http://en.wikipedia.org/wiki/Purkinje_effect</a></p>\n"
},
{
"answer_id": 51220,
"pm_score": 2,
"text": "<p>It has been proved that rods do add to color vision at certain conditions, especially at mesopic vision, Purkinje effect. Further testing showed that when only rods and L cones are excited, together they produce identifiable hues, although only two monochromatic lights are being used. One very faint blue light enough for rods to react but too dim for S and M cones to react, and one red strong enough to excite L cones, but too red to saturate rods. Rods may add some color information during phootopic vision as well, but only at low fotopic levels when rods are not being saturated yet. That part is still being investigated. </p>\n\n<p>I have found this article to be very informative...\n<a href=\"http://journal.frontiersin.org/article/10.3389/fpsyg.2014.01594/full\" rel=\"nofollow\">http://journal.frontiersin.org/article/10.3389/fpsyg.2014.01594/full</a></p>\n"
}
] |
1,448 |
<p><a href="http://www.uniprot.org/uniprot/P36659">CbpA</a> is DNA binding protein found in E. coli and binds non-specifically to curved DNA (<a href="http://dx.doi.org/10.1111/j.1365-2958.2010.07292.x">Cosgriff et al., 2010</a>), when the bacterium is in a static phase of growth. </p>
<p>The use of "curved DNA" confuses me. Is the term "curved DNA" essentially the same as "Circular DNA"?</p>
<hr>
<p><a href="http://dx.doi.org/10.1111/j.1365-2958.2010.07292.x">Cosgriff, S. et al. Dimerization and DNA-dependent aggregation of the Escherichia coli nucleoid protein and chaperone CbpA. Mol. Microbiol. 77, 1289–1300 (2010).</a></p>
|
[
{
"answer_id": 1461,
"pm_score": 6,
"text": "<p>The spectral sensitivity of photoreceptors expressed is the key to color vision. See figure below for the sensitivity of three-types of cone cells (S, M, L) and rod cell (R, dashed line).\n<img src=\"https://i.stack.imgur.com/fF2eT.png\" alt=\"Spectral sensitivity of photoreceptors\"></p>\n\n<p>From this figure, one can say rod cells provide information about the \"blue-greenness\" of vision, however, despite their spectral sensitivity, it seems that in human vision rod cells do not contribute to color vision, because they are <strong>highly sensitive to intensity</strong>, and thus they are mostly saturated in their response (does not induce firing of downstream bipolar cells) during normal daylight conditions. Rod cells specialize for night vision (<a href=\"http://en.wikipedia.org/wiki/Scotopic_vision\" rel=\"noreferrer\">scotopic conditions</a>) which is crucial for survival, and under this condition the cone cells are pretty much useless.</p>\n"
}
] |
[
{
"answer_id": 1454,
"pm_score": 4,
"text": "<p>Cone cells are each connected to their own neurone. This allows them a great deal of resolution as the brain can interpret the exact position of the cone cell that was stimulated by a light photon. However in order to improve low light vision, multiple rod cells are connected to a single neurone - this is called summation. Whilst it does allow for an action potential to be generated in low light conditions, it greatly reduces resolution as the brain can not know precisely which rod cell was stimulated:</p>\n\n<p><img src=\"https://i.stack.imgur.com/15SFw.gif\" alt=\"Anatomy of the human retina\"></p>\n\n<p>Rods can not detect colour as they only come in one variety - cone cells (in humans) come in a red, green and blue specific form to allow for the perception of colour by the brain due to the relative strength of these signals. </p>\n"
},
{
"answer_id": 1494,
"pm_score": 4,
"text": "<p>While the answers to date are correct regarding the wiring of rods and cones in the primate (specifically human) eye, they are also fundamentally wrong. Neither rods nor cones perceive color. The brain does. The rods and cones are just the receptors providing signals. The first answer in fact says this in its very last sentence.</p>\n\n<p>As one answer says, during the day the rods are saturated (overstimulated) so the brain ignores them. It uses the components of the cone responses to invent the sensation \"color\". At night the cones are usually only weakly stimulated, so the brain sees only with the more sensitive rods, and little or no color. This is why brightly colored stars such as Betelgeuse and Rigel still appear only faintly tinged (red and blue respectively).</p>\n\n<p>By the way, some primates have even better color perception than humans with four (or five) kinds of cones. It is speculated that color vision is so good in primates because of the need to judge fruit ripeness to eat. Many mammals have fewer cone types than primates.</p>\n"
},
{
"answer_id": 8122,
"pm_score": 3,
"text": "<p>All of the above answers are great, and very informative. But they are also <em>technically</em> wrong, in certain conditions. Once you understand them, you'll be able to understand this explanation of why.</p>\n\n<p>The canonical answer is that cones are used for color perception in bright light and rods are used in low light. But rods have a peak color sensitivity that is very distinct from the cones (see the chart posted above). And more importantly, <em>there are light levels at which both rods and cones are equally functional for color perception</em>. </p>\n\n<p>This is known as the \"Purkinje effect\" or \"Purkinje shift\". Basically, when light levels dim, your red color perception diminishes first, but your blue color perception is enhanced (or at least doesn't diminish nearly as fast). The specific effect is that red objects get darker much faster than blue ones. But the brain isn't yet just perceiving the blue objects as a brighter gray, so it seems there is some color perception built into the brain based on the rods. </p>\n\n<p><a href=\"http://en.wikipedia.org/wiki/Purkinje_effect\">http://en.wikipedia.org/wiki/Purkinje_effect</a></p>\n"
},
{
"answer_id": 51220,
"pm_score": 2,
"text": "<p>It has been proved that rods do add to color vision at certain conditions, especially at mesopic vision, Purkinje effect. Further testing showed that when only rods and L cones are excited, together they produce identifiable hues, although only two monochromatic lights are being used. One very faint blue light enough for rods to react but too dim for S and M cones to react, and one red strong enough to excite L cones, but too red to saturate rods. Rods may add some color information during phootopic vision as well, but only at low fotopic levels when rods are not being saturated yet. That part is still being investigated. </p>\n\n<p>I have found this article to be very informative...\n<a href=\"http://journal.frontiersin.org/article/10.3389/fpsyg.2014.01594/full\" rel=\"nofollow\">http://journal.frontiersin.org/article/10.3389/fpsyg.2014.01594/full</a></p>\n"
}
] |
1,495 |
<p>I know death and cancer doesn't hurt humans' reproductive success. It's not helping either.</p>
<p>Why do we die? Why dying humans (all of us) are common? What's the point of dying?</p>
|
[
{
"answer_id": 1496,
"pm_score": 6,
"text": "<p>Death is not only for humans. All 'complicated enough' organisms die (with a notable exception of <a href=\"http://en.wikipedia.org/wiki/Hydra_(genus)\" rel=\"nofollow noreferrer\">Hydra</a>, though you may argue when it comes to the complexity). It is is easier to create a new organism from scratch than to repair both internal factors (free radicals, metabolic by-products, ...) and external (physical damage, exposure to toxins, ...).</p>\n<p>Underlying causes of death actually can be evolutionary beneficial. For example, shortening of <a href=\"http://en.wikipedia.org/wiki/Telomere\" rel=\"nofollow noreferrer\">telomeres</a> offers protection against cancer (on a cellular level), but also bounds lifespan.</p>\n<p>So actually they may be evolutionary competition (within the same species) of young and old. Mutations helping young but harming older may be preferred to the opposite ones.</p>\n"
}
] |
[
{
"answer_id": 1497,
"pm_score": 3,
"text": "<p>Who is to say that having living Humans isn't hurting our reproductive success? Older non-reproducing humans cost the human network valuable resources and take up a sizeable portion of our living niche. Metabolically unstreamlined aged organisms are certainly not the most efficient and could potentially get in the way of better suited young'uns.</p>\n"
},
{
"answer_id": 6997,
"pm_score": 2,
"text": "<p>From a systemic point of view, if we wish to evolutionarily induce our descendants (descendants of the current human race on the whole) to live longer lives, we would need to pro-create later.</p>\n\n<p>If the whole of human race enforced a statute that prohibits pro-creation before the age of 40, then two pronged dynamics would happen</p>\n\n<ul>\n<li>only adults fit enough to pro-create after 40 would produce off-springs.</li>\n<li>only off-springs born to parents older than 40 who are fit enough would survive.</li>\n</ul>\n\n<p>Since, there is a high tendency of abnormality and low survival of off-springs born to parents of older ages, absence of resource contention and genetic dynamics would encourage the initial propagation of the rare few fit off-springs.</p>\n\n<p>Hence, unnatural \"natural selection\" would encourage the propagation of humans of longer life-spans. Perhaps, a natural disaster or viral outbreak could discourage humans from pro-creating before age 40. Perhaps, high rates of abortion. So long as the human race does not die out due to such restrictions. Perhaps, to the satisfaction of conspiracy lovers, a secretive organisation carries out a plan every 100K years to raise the bar for child-bearing age.</p>\n\n<p>Therefore, it might be less of a question of advantage and more of the effects of motivation. That current status where</p>\n\n<ul>\n<li>high motivation for humans to pro-create early in life.</li>\n<li>low motivation for humans to have more children as they wise-up by being tired of raising kids too early.</li>\n</ul>\n\n<p>Therefore, since no such secret organisation exists, there is infinitesimally little motivation for the existence of a \"super-virus\" type of humans to exist. </p>\n\n<p>There is no motivation for super-humans to exist, because the distribution of life-spans have crowded out the food and survival resources of any possible primeval super-human.</p>\n"
},
{
"answer_id": 54418,
"pm_score": 2,
"text": "<p>There is no evolutionary advantage to dying. </p>\n\n<p>So you question should be rephrased as to why organism die at all? Why hasn't evolution come up with an immortal animal that lives forever?</p>\n\n<p>Well nature has actually done that <a href=\"https://en.wikipedia.org/wiki/Turritopsis_dohrnii\" rel=\"nofollow noreferrer\">https://en.wikipedia.org/wiki/Turritopsis_dohrnii</a> Behold the immortal jellyfish.</p>\n\n<p>So if we do have immortal jellyfish.. why aren't there immortal mice?</p>\n\n<p>A possible answer is because mice get eaten by cats (and wolves, foxes, owls, toads, humans, etc) The idea goes like this... there is no point having genes that makes you immortal if the probability of you being eaten within 1 year approaches 100%. In fact, in such a situation, you would want genes that will allow you to have as many babies as possible before that one year is up, even if those genes result in your death (ie cancer from cells that are growing too fast in that rush to be an adult, heart problem, muscle degeneration, poor immune system.. because the body has redirected all energy from repair to reproduction). Such a trade off is worth while, as you aren't going to be alive long enough to see the downside of those bad genes. </p>\n\n<p>So if this idea is correct... if an animal has fewer predators (or none at all), the animal would live longer. And yes, we actually do see such examples. </p>\n\n<p>A famous example are the Opossums of Sapelo Island. The Possums were isolated on a predator free island 9000 years ago and now live 25%-50% longer than their mainland cousins. The difference is hereditary. </p>\n\n<p><a href=\"https://books.google.com/books?id=yYwHDAAAQBAJ&pg=PT62&lpg=PT62&dq=Sapelo+Island+opossum+long+lived&source=bl&ots=4AHZcnd8_L&sig=9Wgka1-bVl1xzJTX2F-AJhF0Y-g&hl=en&sa=X&ved=0ahUKEwi506Kq7_7QAhUI6YMKHS3FBQ84ChDoAQgZMAA#v=onepage&q=Sapelo%20Island%20opossum%20long%20lived&f=false\" rel=\"nofollow noreferrer\">https://books.google.com/books?id=yYwHDAAAQBAJ&pg=PT62&lpg=PT62&dq=Sapelo+Island+opossum+long+lived&source=bl&ots=4AHZcnd8_L&sig=9Wgka1-bVl1xzJTX2F-AJhF0Y-g&hl=en&sa=X&ved=0ahUKEwi506Kq7_7QAhUI6YMKHS3FBQ84ChDoAQgZMAA#v=onepage&q=Sapelo%20Island%20opossum%20long%20lived&f=false</a></p>\n\n<p>Another possible example is that between bats and mice. Both are small animals of similar weight. And in general the smaller the animal, the faster it breeds and the shorter its life span. Bats are a noted exception from this the rule. Bats live a very long life span or their mass. Lifespan in the wild rangers from 10 years to 40 years depending on species. Compare that to 1 year for a mouse. The difference? Not metabolism... Not mass.. Not climate. But predators. Mice have many predators. Bats very few. </p>\n"
},
{
"answer_id": 89879,
"pm_score": -1,
"text": "<p>The evolutionary explanation is quite simple. Without death, evolution couldn't take place in the first place at all.</p>\n\n<p>Who knows that jellyfish are immortal? Did they continuously evolve from one cell (without reproduction)? I don't think so. Who knows if today present jellyfish were already alive 1000 000 years ago (i.e. without parents)? I think this is the case for any living creature.</p>\n\n<p>That's why telomeres get shorter and shorter when growing older. In the case of cancer, these telomeres stay the same with each division of the parent cell, so it grows wildly. Which all species would probably do so too.</p>\n"
},
{
"answer_id": 95096,
"pm_score": 0,
"text": "<p>One key concept to bear in mind is "mutational load". Over time, individuals accumulate mutations - for example, <a href=\"https://www.llnl.gov/news/study-shows-genetic-quality-sperm-deteriorates-men-age\" rel=\"nofollow noreferrer\">older fathers pass on more mutations</a> than younger ones. Undesirable mutations need to be removed by natural selection each generation at at least the same rate as they accumulate, or a "mutational meltdown" occurs. The length of time between generations needs to be set so that the number of mutations purged by deaths is equal to the number that are introduced by mutation. Here is <a href=\"https://www.sciencedirect.com/science/article/pii/S0092867419306324\" rel=\"nofollow noreferrer\">a rather interesting study</a> providing some evidence for this point of view.</p>\n<p>Note that infertility is "lethal" in genetic terms, so this concept in and of itself does not explain why a woman who passes menopause needs to die at any age. It seems easy to add further speculation here, so I'll leave that to the reader.</p>\n"
}
] |
1,515 |
<p>This is my first post here, so please be gentle. I recently learned that I have Rh- blood (I'm A-), and was idly looking into blood types on Wikipedia. I was surprised to find that relatively few (~15% of all) humans have it, and most of those seem to be European. Looking just a little further, I found a bunch of crackpot-looking sites that try to explain how people got Rh- blood, and what weird abilities they possess as a result.</p>
<p>I managed to find one site that seemed at least less laughable, which suggested that interbreeding with <em>Homo neanderthalensis</em> (or possibly <em>Homo sapiens neanderthalensis</em>, since the site seemed to indicate that there was some question about how different <em>H. s. sapiens</em> were from <em>H. neanderthalensis</em>) might have accounted for the introduction of the condition.</p>
<p>It seems that from more reputable (medical) sources, the only difference between Rh+ and Rh- is that complications can arise during pregnancy if the mother is Rh- and the fetus is Rh+. Indeed, most sites (e.g., WebMD) seem to explicitly state that there are no other differences of note.</p>
<p>I am not a biologist, or an anthropologist, or a life-science kind of guy at all. However, as a computer scientist, I like to think that I have both an open mind but one which demands scientific and/or logico-mathematical evidence for claims. Lots of the pseudo-scientific, paranormal, etc. theories on the web I basically dismiss out of hand, as explanations which are almost certainly fantasies, but most definitely baseless and untestable.</p>
<p>My question:</p>
<blockquote>
<p>What, if any, is the current scientific understanding of the origin, or source, of rhesus negative blood in human beings? Do individuals with Rh- blood have any common (in a statistically significant sense) characteristics or health issues, aside from the issue with pregnancy and tending to be more European than not? Is there anything to continuing to look into this?</p>
</blockquote>
<p>For context, I got started down this rabbit hole while looking into different dieting strategies, and found the "blood type diet". Just as an aside, I don't think there's a lot of merit to that diet... sounds like a fad thing. Any sources or information or help on this subject are appreciated.</p>
<p>EDIT:</p>
<p>I have been looking a little more, and I stumbled across a paper entitled, "The influence of RhD phenotype on toxoplasmosis and age-associated changes in personality profile of blood donors" which looks at the effect of the Rh- trait on personality changes caused by toxoplasmosis (if you Google the title, you should be able to download). Using Cloninger's and Cattel's personality factors, they seem to show a variety of things, including (a) personality differences between Rh+ and Rh- individuals not affected by toxoplasmosis, and (b) different reactions to prolonged toxoplasmosis affection in Rh+ and Rh- individuals.</p>
<p>I didn't even know that parasites could affect your behavior; that seems frightening on the one hand, but on the other, it's fascinating if it's for real, especially since the incidence of toxoplasmosis is not insignificant in most people. Anybody who knows anything about this or who reads the paper and can help me understand what it's saying would be doing me a great favor to answer/comment/chat. Thanks!</p>
|
[
{
"answer_id": 1539,
"pm_score": 4,
"text": "<p>Your question has many questions in it. </p>\n\n<p>As for the evolution of Rh factor, <a href=\"http://jhered.oxfordjournals.org/content/91/3/205.abstract\">Blancher and Apoil (2000)</a> attribute the high level of sequence similarity (92%) of the two <em>RH</em> locus genes, <em>RHD</em> and <em>RHCE</em> to a gene duplication event in the common ancestor of human, chimps, and gorillas. Their analysis of the cDNA from these genes revealed \"complex recombination events\" after the lineages split.</p>\n\n<p>Basically the most recent common ancestor of apes had the \"human\" <em>RH</em> genes, which then differentiated after the lineages diverged. Duplicate and differentiate is a common theme in evolution.</p>\n\n<p>As for why it's called rhesus antigen, that's just as experimental artifact:</p>\n\n<blockquote>\n <p>The term \"Rhesus antigen\" was introduced by Landsteiner and Wiener,\n who found that rabbits (and later, guinea pigs) immunized with red\n blood cells (RBCs) from a rhesus monkey produced antibodies which\n agglutinated 85% of Caucasian blood samples (Landsteiner and Wiener\n 1940, 1941).</p>\n</blockquote>\n\n<p>They probably weren't even correct about the antibodies being rhesus:</p>\n\n<blockquote>\n <p>In conclusion, if the term \"Rh\" was coined by Landsteiner and Wiener\n because of the source of antigens (the rhesus monkey) they used to\n obtain anti-Rh in rabbits, it is highly probable that, in fact, they\n produced anti-LW antibodies.</p>\n</blockquote>\n"
}
] |
[
{
"answer_id": 9033,
"pm_score": -1,
"text": "<p>It's my opinion the rh antigen developed from toxoplasmosis infection. I only recently learned that this protozoan can actually insert its genes into a host's genome. Once it's in the genes, it can be passed in the germline. Toxoplasmosis can infect all primates, human and otherwise. Monkeys get it, and so do humans living in toxoplasmosis endemic places. The life cycle of toxoplasmosis is connected with mice and cats as an evolved survival strategy for the toxoplasmosis protozoan. There never were cats in northwest Europe, and that would explain why the people with ancestry from that area were never exposed to toxoplasmosis. I look for the rational biological explaination. One great clue to my thinking is I found a term used in some research writings, the text read \"RH strain of toxoplasmosis\". Yes they seemed to be doing experiments with the toxoplasmosis found in rhesus monkey.</p>\n"
},
{
"answer_id": 10939,
"pm_score": 0,
"text": "<p><a href=\"http://www.frozenevolution.com/origin-rh-blood-group-polymorphism\" rel=\"nofollow\">http://www.frozenevolution.com/origin-rh-blood-group-polymorphism</a></p>\n\n<blockquote>\n <p>The high proportion of Rh-negative persons in the European population\n could be connected with the fact that, until recently, big cats (the\n definitive host of Toxoplasma gondii) were practically not present\n here and thus toxoplasmosis was rare (and Rh-negative persons were at\n an advantage compared to the rest of the population). The low\n percentage of Rh-negative persons in Africa (less than 1%) could be\n related to the high prevalence of toxoplasmosis there, which often\n approaches 100%.</p>\n</blockquote>\n"
},
{
"answer_id": 10940,
"pm_score": 0,
"text": "<p><a href=\"http://www.sott.net/article/228188-Toxoplasma-gondii-Cat-parasite-may-affect-cultural-traits-in-human-populations\" rel=\"nofollow\">http://www.sott.net/article/228188-Toxoplasma-gondii-Cat-parasite-may-affect-cultural-traits-in-human-populations</a></p>\n\n<blockquote>\n <p>Lafferty suggested that because climate affects the persistence of\n infectious states of Toxoplasma in the environment, it helps drive the\n geographic variation in the parasite's prevalence by increasing\n exposure risk. The parasite's eggs can live longer in humid,\n low-altitude regions, especially at mid latitudes that have infrequent\n freezing and thawing. Cultural practices of food preparation such as\n rare or undercooked meats, or poor hygiene, can increase exposure to\n infection, as can having cats as pets. Lafferty added, \"Toxoplasmosis\n is one of many factors that may influence personality and culture,\n which may also include the effects of other infectious diseases,\n genetics, environment and history. Efforts to control this infectious\n pathogen could bring about cultural changes.\" / this is why I feel\n rh- is a newer blood grouping due to the last ice age conditions.\n these were the conditions in nw Europe back then and the rh- trait has\n persisted in that area. it just all makes sense . you may also search\n out \" congenital toxoplasmosis infection \" and I believe you will find\n when a pregnant woman gets toxo infection the baby comes out with the\n same symptom ology as erythroblastosis fetalis, rhesus disease.this is\n why all pregnant women are cautioned to avoid cat feces and stay away\n from cat boxes where they defecate.</p>\n</blockquote>\n\n<p>OPINION ? i'll have you know i'm 61 y old retired medical worker who has studied biology and etc my whole life . this opinion is not just anyone's . btw i'm o- myself /</p>\n"
},
{
"answer_id": 10942,
"pm_score": 0,
"text": "<p><a href=\"http://www.ncbi.nlm.nih.gov/pubmed/18766148\" rel=\"nofollow noreferrer\">http://www.ncbi.nlm.nih.gov/pubmed/18766148</a></p>\n<blockquote>\n<p>RESULTS:</p>\n<p>RhD-positive subjects have been confirmed to be less sensitive to the influence of latent toxoplasmosis on reaction times than Rh-negative subjects. While a protective role of RhD positivity has been demonstrated previously in four populations of men, the present study has shown a similar effect in 226 female students. Our results have also shown that the concentration of testosterone in saliva strongly influences (reduces) reaction times (especially in men) and therefore, this factor should be controlled in future reaction times studies.</p>\n<p>CONCLUSIONS:</p>\n<p>The observed effects of RhD phenotype could provide not only a clue to the long-standing evolutionary enigma of the origin of RhD polymorphism in humans (the effect of balancing selection), differences in the RhD+ allele frequencies in geographically distinct populations (resulting from geographic variation in the prevalence of Toxoplasma gondii), but might also be the missing piece in the puzzle of the physiological function of the RhD molecule.</p>\n</blockquote>\n"
}
] |
1,838 |
<p>On news, articles etc. experts talking about <strong>Genetically Modified Foods and Organisms</strong> often mentions about their disadvantages like, </p>
<ul>
<li>their potential to harm human health</li>
<li>allergies may become more intense, new allergy types may develop</li>
<li>possible damages to the environment</li>
</ul>
<p>So I wonder, what's the aim of genetically modifying of foods/organisms? In other words, what are advantages of that? </p>
|
[
{
"answer_id": 1844,
"pm_score": 5,
"text": "<p>GMO foods have a huge potential to make food cheaper to produce and more nutritious.</p>\n\n<p>The most common GMO foods have at least one gene added to them - an enzyme that makes the plant resistant to RoundUp - an herbicide made by the same company (Monsanto). this makes the farmers able to grow their crops with much less intensive labor to keep the plants healthy. It does cost some money and people wonder whether using so much roundUp is good. I won't come down on the benefits of this, but you can see how it might be more economical way to grow crops. roundUp is biodegradable and does break down in about 3 weeks, just FYI. </p>\n\n<p>Other GMO foods can make the crops more resistant to drought, disease or insects. This might enable crops to be grown in areas and or with longer growing seasons - a big advantage for thirsy crops like tomatos or rice. Other GMO project may allow us to make the crops more nutritious. A famous example of this is <a href=\"http://www.goldenrice.org/\">golden rice</a>, which has been enhanced to produce pro-vitaminA, which will help malnutrition in millions of children who can die annually because of a lack of vitamins in their diet. </p>\n\n<p>There is also an effort in nutriceuticals, where vaccines and common drugs maybe produced by edible plants for easily processing or even direct distribution of pharmaceuticals. </p>\n\n<p>For people who can afford organic food and free range beef, I think its great that its available, but at for a hungry world, GMO foods can help solve some vital problems. </p>\n"
}
] |
[
{
"answer_id": 1840,
"pm_score": 2,
"text": "<p>In terms of crops, plants that are grown for food, one advantage is the targeted modification of a single gene. Classical plant breeding is slow, imprecise and carries many traits of negative benefit. For example, if you cross plant variety A with variety B for the purpose of obtaining one of B's traits (say oil content of the seed), the resulting progeny will have half of the B genome (which half? each offspring a different half of all possible alleles, and many of the hybrids may carry less desirable traits of B like altered germination and maturation times, which would be quite problematic for a farmer). Back-crosses to variety A are then necessary in order to make, in successive generations, offspring that are 75% A, then 87% A, then 93% A and so on. This takes time - to do those back-crosses and to test that the trait of interest remains. Knowing the gene for oil content, or a set of genes, can speed this process by modifying that gene alone while maintaining all the other advantageous traits of variety A.</p>\n\n<p>This is but one example. If I think of others and find the time to describe those, I'll add such information here.</p>\n"
},
{
"answer_id": 1846,
"pm_score": 3,
"text": "<p>On the example of \"golden rice\" already raised here I took the liberty of looking up some literature about this GMO varietal. <a href=\"http://jn.nutrition.org/content/132/3/506S.short\">This article</a> by Beyer et al. describes the introduction of the beta-carotene biosynthetic pathway into the strain of rice. About a decade later, <a href=\"http://www.ajcn.org/content/89/6/1776.short\">Tang et al.</a> followed this up with a clinical trial to measure how much beta-carotene a population defined to be clinically low in vitamin A are able to obtain. They found that there is efficient and significant conversion of beta-carotene into vitamin A within this population, providing evidence that the theoretical goal to reduce the vitamin deficiency is actually achievable.</p>\n\n<p>As Larry pointed out, lab modified GMO plants allow a very specific gene or set of genes to be targeted, rather than crossing two plants together and screening the offspring for more desirable than undesirable characteristics. It is important to know that ever since <em>homo sapiens</em> created the primitive form of agriculture called farming, we have been engaged in producing GMO plants. Every time a farmer select seeds form the plants that grew a little heartier in cold weather, or produced fruit just a little more juicy, it was a deliberate act to produce a higher quality crop (for some trait) the next season. The only difference between what we called and still call farming and GMO agricultural practices, is how finely controlled the individual genes are manipulated. The obvious by product from being able to sequence and manipulate a genome is that we can much more rapidly and broadly create and test new varietals at a pace that could have taken decades or generations earlier. This represents a very important opportunity to improve our quality of food and robustness of crops, and is just as \"natural\" as what has happened for 10,000 or so years.</p>\n"
},
{
"answer_id": 1849,
"pm_score": 2,
"text": "<p>I'd like to add that most of the GMOs that might most dramatically improve human condition (ie via drought/salt resistance, greatly increased yield or nutritional value) are all unfortunately still under development (or not even that), partially because of the general public resistance to GMO in some regions of the world (like Europe; anyone remembers the tomatoes?) and organized campaigns against GMO (not really fact-based; ie Greenpeace & Co).</p>\n\n<p>So yes, GMO can lead to development of crops with increased nutritional value, better resistance to environmental conditions or changes and/or increased yield, but we're not there (yet).</p>\n\n<p>The above should not mean that what we have so far (insect resistant crops, disease-reducing GM insects or the golden rice) is not important, because it is, and it should not mean that the current legal/political context of GMO is fine, because it isn't.</p>\n"
},
{
"answer_id": 38884,
"pm_score": 0,
"text": "<p>Imagine an apple which won't get brownish (oxidised) after being cut..\n<a href=\"https://i.stack.imgur.com/86bim.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/86bim.jpg\" alt=\"enter image description here\"></a>\nImagine a tomato which will not get wrinkles and will not perish for a long time<a href=\"https://i.stack.imgur.com/Ye48o.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/Ye48o.jpg\" alt=\"enter image description here\"></a></p>\n\n<p>Imagine a chicken and fish which gives more flesh in short incubation time \n<a href=\"https://i.stack.imgur.com/BE301.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/BE301.jpg\" alt=\"enter image description here\"></a><a href=\"https://i.stack.imgur.com/NAChX.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/NAChX.jpg\" alt=\"enter image description here\"></a><a href=\"https://i.stack.imgur.com/fcOWC.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/fcOWC.jpg\" alt=\"enter image description here\"></a></p>\n\n<p>In endocrinology to get one unit of growth hormone one have to get 1000 pituitaries from cadavers.\nImagine a bacteria which produces growth hormone and other hormones like insulin for therapeutic and research purposes</p>\n\n<p>Imagine a vaccine against flu in cow's milk and hepatitis in Banana. Eat it earn the protection<a href=\"https://i.stack.imgur.com/c2aty.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/c2aty.jpg\" alt=\"enter image description here\"></a></p>\n\n<p>Imagine a iron rich rice ( fortified ) maize with complete nutrition without any amino-acid lag<a href=\"https://i.stack.imgur.com/lG0z7.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/lG0z7.jpg\" alt=\"enter image description here\"></a>\nImagine glowing trees by the road side in night which prevent accidents<a href=\"https://i.stack.imgur.com/m9MZN.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/m9MZN.jpg\" alt=\"enter image description here\"></a></p>\n\n<p>And there are much more and most advantages are coming out from GMO's.\nThe only problem is ethics i.e if we change our ecosystem to our wish it may collapse and either we may become extinct or else we may lead other species to it's extinction. But it's only a chance and it's a pointless fear. In the view of science logic is the prime and we can even bring the extinct alive. So we have got the power and we gotta use it and not waste it</p>\n"
}
] |
2,075 |
<p>A number of companies have started marketing LED lamps that can be switched to a red mode. The claim is that red light is less harmful to one's night vision. Given that our eyes are less sensitive to red light, though, I'm not convinced that that red light is any better than dim white light. So if "equivalent" luminosity is defined where it's equally easy to, say, read a book in both light types, is there some physiological reason that red light is better than the equivalent white light? </p>
|
[
{
"answer_id": 3471,
"pm_score": 5,
"text": "<p>This is a very good question. Red light is routinely used by scientific laboratories to do low light dissections of retinas, and of course it is used in other low light contexts such as printing plate development.</p>\n\n<p>In both of the above contexts, you have a clear subject: the retina being dissected or the printing plate being developed. In the case of the printing plate the film has been designed to be specifically non-reactive to red light, so red light is used because <strong>your eyes can see it, but the film doesn't react to it</strong>. Similarly in some scientific settings it makes sense to use red light during dissections. Mice lack a long wavelength opsin, and therefore using a dim red light allows the experimenter to have a <strong>relative sight advantage compared to the mouse</strong> when keeping the mouse dark adapted.</p>\n\n<p>But in the case you're asking about, there is no film or animal to serve as a second party. So is there any intrinsic advantage to using red light? As it turns out, there is. The fovea, which is in the center of our eye and used for high acuity vision, has no rods and primarily L- or red sensitive cones. Note the high density center area which lacks blue sensitive cones and has <a href=\"http://www.psych.ndsu.nodak.edu/mccourt/Psy460/Color%20Vision/Color%20Vision.html\" rel=\"noreferrer\">2:1 red to green cones</a>. </p>\n\n<p><img src=\"https://i.stack.imgur.com/wIbcE.jpg\" alt=\"retinal mosaic\"></p>\n\n<p>So by having red light present, you stimulate this area. But red light is present in white light, too, why not just use that? Leonardo's answer comes the closest, but it's a little off. <strong>Red light is used because it preferentially stimulates L cones more than rods</strong>, but you are definitely not able to preserve night vision by using red light. Why not? Well it may look like it is possible to exclusively stimulate cones from the chromatic sensitivity figure </p>\n\n<p><img src=\"https://i.stack.imgur.com/UvNmc.png\" alt=\"chromatic sensitivity\"></p>\n\n<p>But that figure is 1) normalized and 2) not indicative of synaptic signal processing. 1000's of rods can converge onto a single ganglion cell, where cone convergence in the fovea can be on the order of a single cone per ganglion cell. When it comes to perception, in order to compare the black rod line above with the red L-cone line you'd have to magnify it dramatically in size. Practically speaking, it is nearly impossible to stimulate cone pathways without stimulating rod pathways when using a relatively broad spectrum LED that you're powering with a battery. Maybe with a high power infrared laser. </p>\n\n<p>So <strong>the purpose of using red light is to attempt to balance the activation of high sensitivity (red insensitive) rods with that of the low sensitivity (but red sensitive) cones in the fovea.</strong> While using a similar level of rod activation with blue light, you would perceive a \"blind spot\" where your fovea is.</p>\n\n<p>Finally, instrinsically photosensitive cells (the melanopsin cells brought up) do not factor into this processing. These cells are activated only with extraordinarily bright levels of light, and the therefore do not enter into conversations dealing with night vision.</p>\n"
}
] |
[
{
"answer_id": 2083,
"pm_score": 3,
"text": "<p>Another reason why red lights are now sponsorized for night illumination is because they are supposed to be safer in terms of interference on the circadian cycle. This is not related to better vision, but better health.</p>\n\n<p>The mammalian eye senses the light by the conventional rode and cone cells. However, a third light-sensing cell type <a href=\"http://dx.doi.org/10.1038/nature01761\" rel=\"nofollow noreferrer\">has been recently identified</a>. This third light-sensor is based on <strong>melanopsin</strong>-positive cells. While rod and cone cells respond best to white, full spectrum light, melanopsin cells only respond to a specific bandwidth of blue light, in the range of 446-477 nanometers. These cells connect and regulate brain centers responsible for circadian rhythms. Therefore, during the night, blue-light exposure <a href=\"http://dx.doi.org/10.1289/ehp.118-a22\" rel=\"nofollow noreferrer\">might interfere</a> with circadian rhytms facilitating the onset of depression and other metabolic derangements associated with circadian cycle <a href=\"https://biology.stackexchange.com/questions/1659/why-is-maintaining-a-circadian-rhythm-important\">see another SE question</a>. White light contains also blue light, while red light does not. This is apparently the rationale to claim that red light is less harmful. However, no clinical evidence is available to my knowledge, and the threshold of blue light required to stimulate melanopsin receptors is probably over the common night illumination. </p>\n\n<p><strong>References:</strong></p>\n\n<ol>\n<li><a href=\"http://dx.doi.org/10.1038/nature01761\" rel=\"nofollow noreferrer\"> <strong>Hattar S, Lucas RJ, Mrosovsky N, Thompson S, Douglas RH, Hankins MW, Lem J, Biel M, Hofmann F, Foster RG, et al.</strong>. 2003. Melanopsin and rod-cone photoreceptive systems account for all major accessory visual functions in mice. Nature 424: 76–81.</a></li>\n<li><a href=\"http://dx.doi.org/10.1289/ehp.118-a22\" rel=\"nofollow noreferrer\"> <strong>Holzman DC</strong>. 2010. What’s in a color? The unique human health effect of blue light. Environmental health perspectives 118: A22–7.</a></li>\n</ol>\n"
},
{
"answer_id": 2120,
"pm_score": 3,
"text": "<p>Here is a comparison of the range of wavelength sensitivities for both rod cells (labelled R) to the 3 subtypes of cones cells (labelled S, M and L) from <a href=\"http://en.wikipedia.org/wiki/Rod_cell\" rel=\"noreferrer\">Wikipedia</a>.</p>\n\n<p><img src=\"https://i.stack.imgur.com/qrlth.png\" alt=\"Cone and rod wavelength sensitivities.\"></p>\n\n<p>If one is exposed to red light (above ~650 nm), it would activate the L-type cones mainly (possibly some M-type activation), but no rod activation. Rods are the low light receptor cells in our eyes, and as such, are very sensitive to the photon density, or brightness, entering the eye.</p>\n\n<p>This is just my speculation, but I think it's plausible that if you were in a completely dark environment with just a red light, filtering out the higher frequencies, night vision could be spared in the sense that we don't activate the rod cells.</p>\n"
},
{
"answer_id": 2166,
"pm_score": 3,
"text": "<p>As mentioned in the other answer, red light does not affect the melanopsin receptors in eyes. These receptors not only regulate body rhythm but also <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/12808468\" rel=\"nofollow\">regulate the diameters of the eye pupils</a>. Once they are stimulated, the eye thinks that there is enough light around and the pupils get smaller to protect the eye against over-exposition, which reduces sensitivity.</p>\n"
},
{
"answer_id": 9294,
"pm_score": 1,
"text": "<p>Yes red light is useful IF and only if >650 nm. Some of the answers above are close, but they miss the issue because they used the same scale for rods and cones which they are not on. Rods are several orders of magnitude more sensitive than cones and hence why the graphs above make it look like they have no sensitivity out to 700nm, they actually do, just not nearly as much.</p>\n\n<p>Look up photochromatic step. It explains why >650nm works and it is well documented.</p>\n"
},
{
"answer_id": 67000,
"pm_score": 1,
"text": "<p>When I was in the Navy in 1957, I was an ECM sensor operator on a P-2 Neptune maritime patrol aircraft, originally built in 1941. We flew 11-hour patrols low over the ocean. At night all the pilot's Gage's and controls were illuminated with red light. The flashlights we had were equipped with red lenses. Most WWII aircraft were equipped the same way! For some reason, the red light-night vision theory was obviously the belief back then. Lieutenant Rudy Jopp, USN, Retired.</p>\n"
},
{
"answer_id": 76126,
"pm_score": 0,
"text": "<p>I think the most logical and simplistic scientific test in this situation would be application. Buy red yard lamps and white yard lamps. Set up a various objects in the yard that would be increasingly harder to see in the dark (like a vision test where the letters get small but your distance is static.)</p>\n\n<p>Sit outside with no light for an hour, more if you want, and then pick out the objects. This is your constant, what you will compare your results to. Repeat at least three times making note of which objects you can see.</p>\n\n<p>Repeat this with each lamp, exposure for the exact amount of time as you waited in the dark. Both lamps should give you the same level of visibility, for accuracy. Take note of how long it took to be able to clearly see each object. I recommend a buddy out of your vision to keep track of time so you don't spoil the excitement by introducing light source.</p>\n\n<p>Compare the results and you will know which light source affects your night-vision more.</p>\n"
}
] |
2,246 |
<p>I have a gene of of interest that I would like to compare between homologues. How does one go about finding a gene from known coding sequences across phyla? Afterwards I imagine I could do a Clustal sequence alignment to see how the sequences match.</p>
|
[
{
"answer_id": 2258,
"pm_score": 4,
"text": "<p>There are various databases of homologs, for example:</p>\n\n<ul>\n<li><a href=\"http://eggnog.embl.de\">eggNOG</a></li>\n<li>Ensembl Compara (accessible via <a href=\"http://www.ensembl.org/biomart/martview\">BioMart</a>, I think)</li>\n<li><a href=\"http://www.ncbi.nlm.nih.gov/homologene\">Homologene</a></li>\n<li><a href=\"http://omabrowser.org/\">OMA</a></li>\n<li><a href=\"http://www.treefam.org/\">TreeFam</a></li>\n</ul>\n\n<p>The advantage of using an existing database is that more sophisticated methods for detecting orthologs than simple BLAST searches have been used (see \"<a href=\"http://doi.org/cxwqpk\">Computational methods for Gene Orthology inference</a>\" for a review), and everything is already precomputed, so it's much faster. The downside is that all precomputed methods need to use a snapshot of the genomes from the past, so not all currently available genomes will be there. </p>\n"
}
] |
[
{
"answer_id": 2247,
"pm_score": 3,
"text": "<p>If I understand your question adequately, the <a href=\"http://genome.ucsc.edu\">Genome Browser</a> at UCSC is a great place to start. If you know the name of the gene, you can search for it. For example, <a href=\"http://genome.ucsc.edu/cgi-bin/hgTracks?position=chr2:227659726-227663454&hgsid=265444947&knownGene=pack&hgFind.matches=uc021vxn.1,\">here is the page for human insulin receptor 1</a>. From there you can compare 46 genomes, with alignments. </p>\n"
},
{
"answer_id": 2248,
"pm_score": 2,
"text": "<p>maybe you'd like NCBI/Homologene instead. <a href=\"http://www.ncbi.nlm.nih.gov/homologene\" rel=\"nofollow\">http://www.ncbi.nlm.nih.gov/homologene</a></p>\n\n<p>or just using psiblast against NR if you have a nucleotide or protein sequence.</p>\n\n<p><a href=\"http://blast.ncbi.nlm.nih.gov/Blast.cgi\" rel=\"nofollow\">http://blast.ncbi.nlm.nih.gov/Blast.cgi</a></p>\n"
},
{
"answer_id": 2249,
"pm_score": 3,
"text": "<p>If you don't have any idea where your gene will have a match with other genes, try something like <a href=\"http://blast.ncbi.nlm.nih.gov/Blast.cgi\" rel=\"nofollow\">Blast at the NCBI website</a>.</p>\n\n<p>This will give you a list of hits that you can then use to align with a multiple sequence aligner (MSA). The same NCBI page can give you a tree reconstructed from the results of the searching process, although there is a variety of methods that can be used if you just download the sequences and attempt to build the gene family alignment yourself using \"[x] Select All -- Get selected sequences\" in the NCBI blast results page, then downloading them in FASTA or other format with \"Send to -- File -- Format FASTA -- Create File\".</p>\n\n<p>If what you want instead is to include your gene sequence into the best aligning place in an existing gene family alignment, you can try <a href=\"http://code.google.com/p/pagan-msa/wiki/PAGAN\" rel=\"nofollow\">PAGAN</a>.</p>\n"
},
{
"answer_id": 4954,
"pm_score": 2,
"text": "<p>Just adding my 5 cents, there is a recent database called <a href=\"http://orthology.phylomedb.org/\" rel=\"nofollow\">metaphors</a>:</p>\n\n<blockquote>\n <p>MetaPhOrs is a public repository of phylogeny-based orthology and\n paralogy predictions that were computed using resources available in\n seven popular homology prediction services (PhylomeDB, EnsemblCompara,\n EggNOG, OrthoMCL, COG, Fungal Orthogroups, and TreeFam). Currently\n above 306 millions of unique homologous protein pairs are deposited in\n MetaPhOrs database. These predictions were retrieved from 705 123\n phylogenetic trees for 829 genomes. For each prediction, MetaPhOrs\n provides a Consistency Score and Evidence Level describing its\n goodness, together with number of trees and links to their source\n databases.</p>\n</blockquote>\n\n<p>It is particularly good because:</p>\n\n<ul>\n<li><p>It is the only homology database I know of that gives information on paralogy vs orthology.</p></li>\n<li><p>It is linked to UniProt names</p></li>\n<li><p>It provides a pretty good python API for batch queries</p></li>\n</ul>\n"
}
] |
2,574 |
<p>The main paper for the <em>Plasmodium palciparum</em> genome project (Gardner et al., 2002) repeatedly mentioned that the unusually high A+T content (~80%) of the genome caused problems. For example they imply that it prevented them using a clone-by-clone approach:</p>
<blockquote>
<p>Also, high-quality large insert libraries of (A + T)-rich P. falciparum DNA have never been constructed in Escherichia coli, which ruled out a clone-by-clone sequencing strategy.</p>
</blockquote>
<p>And that it made gene annotation difficult:</p>
<blockquote>
<p>The origin of many candidate organelle-derived genes could not be conclusively determined, in part due to the problems inherent in analysing genes of very high (A + T) content. </p>
</blockquote>
<p><strong>Question:</strong><BR>
What is the biological significance of high A+T content, and why would it cause problems in genome sequencing?</p>
<p><strong>Ref:</strong><br>
<a href="http://dx.doi.org/10.1038/nature01097">Gardner, M.J., Hall, N., Fung, E., White, O., Berriman, M., Hyman, R.W., Carlton, J.M., Pain, A., Nelson, K.E., Bowman, S., Paulsen, I.T., James, K., Eisen, J.A., Rutherford, K., et al. (2002) Genome sequence of the human malaria parasite Plasmodium falciparum. Nature. 419 (6906), 498–511.</a></p>
|
[
{
"answer_id": 2612,
"pm_score": 4,
"text": "<p>The sequencing technologies that were developed in the last 20 years have a range of optimal use at an average A+T/G+C rate. Both highly AT-rich and GC-rich regions are complicated to process by the different sequencing technologies. Each technology has different ranges of usage, but to name one, <a href=\"http://www.illumina.com/technology/sequencing_technology.ilmn\">Illumina technology</a> prefers sequences in the middle range. If you try to sequence an AT-rich genome with the Illumina standard protocol, you will sequence an incomplete genome, the fragments of which are not a perfect reflection of the original complete genome. Other technologies claim to be completely unbiased to nucleotide content. <a href=\"http://www.pacificbiosciences.com/products/\">Pacific Biosciences</a> is one of them, and people seem to agree on that claim, after having analyzed the data that is produced by their machines. <a href=\"http://www.nanoporetech.com/\">Oxford Nanopore Technologies</a> claims that they have almost no biases, but as of today (2012-06-13), there is no confirmation of that by external analyses. </p>\n\n<p>Beyond sequencing problems, the software used to assemble and annotate the sequences may also be prone to errors in AT-rich and GC-rich regions. But many of those problems stem from the incompleteness of the sequencing.</p>\n"
}
] |
[
{
"answer_id": 2575,
"pm_score": 3,
"text": "<p>I can't comment on how A+T richness complicates the sequencing process itself, but I can comment on complications that arise when annotating the sequence. <em>Ab initio</em> gene predictors are often based on hidden Markov models that are very sensitive to base composition in the genome (di-nucleotides, tri-nucleotides, etc). These gene finders typically perform very poorly if they are run on a genome that has a much different base composition than the one on which it was trained. This could explain some of the difficulty they has with analyzing genes in the genome.</p>\n"
},
{
"answer_id": 2697,
"pm_score": 2,
"text": "<p>Often sequencing involves a step of amplification of genomic material. The standard way to perform this is with PCR, but PCR is biased and does not amplify very AT-rich regions well. With multiple rounds of PCR, even low-abundance regions that are not as AT-rich might come to dominate the sample and hide the AT-rich sequences.</p>\n\n<p>This is not only a problem for de novo sequencing, but for many sequencing-based techniques (RNA-seq, ChIP-seq, your-favorite-seq...). Alternative methods have been employed in plasmodium, but they are not as standard (yet?).</p>\n\n<p>See, for example, <em>H2A.Z Demarcates Intergenic Regions of the Plasmodium falciparum Epigenome That Are Dynamically Marked by H3K9ac and H3K4me3</em> at <a href=\"http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1001223\" rel=\"nofollow\">http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1001223</a></p>\n"
},
{
"answer_id": 2831,
"pm_score": 1,
"text": "<p>In the past, before massively parallel sequencing, they made a library of cloned sequences and transformed these into <em>E. coli</em>. High AT sequences are difficult to maintain in <em>E. coli</em> (perhaps due to similarity to promoters?).</p>\n"
},
{
"answer_id": 43362,
"pm_score": 1,
"text": "<p>A lot has already been said in previous answers so I am just gonna add briefly two potential issues with strong AT/CG bias:</p>\n\n<p>1) Potential for polymerase slippage due to homopolymers: this introduces errors in general because you may have unwanted indels in the reads as well as purely incorrect bases being incorporated. This is a problem that can happen even with PCR (although there's a lot of choices now if u want to spend). So in general higher error rates and higher read failure.</p>\n\n<p>2) Difficulty of the machine to separate the signals of individual nucleotides for SANGER (it gets all blurred) or calibration errors with next gen sequencing. So higher read failure (bad quality).</p>\n\n<p>3) Assuming everything is now fine, still lower complexity regions can be VERY hard to map, let alone assemble a complete genome from scratch.</p>\n\n<p>Hope this helps!</p>\n"
}
] |
2,602 |
<p>I'm curious how much damage is potentially inflicted by shear stress by pipetting. I know that syringes used for stem cell injection can cause a lot of damage. However, to what extent does this happen with P20 and P200 pipette tips? Understandably the shear modulus of bacterial cells is significantly different from that of cancer cells, which will be different from that of stem cells.</p>
|
[
{
"answer_id": 20890,
"pm_score": 5,
"text": "<p>This is an excellent question, I have been training people to culture cells for about 12 years and students have a hard time grasping this and appreciating the importance etc.</p>\n\n<p>What cells are usually experiencing during pipetting is analogous to a crowd of people trying to fit through the doorway of a building. Shearing during pipetting is certainly a legitimate concern in cell culture. You will notice its negative effect on viability most explicitly when pipetting cells in freezing\n medium (containing DMSO) following a thaw. Until their DMSO concentration drops their membranes are weaker & more fluid. That's why you pipette the frozen cells drop-wise to the fresh medium, to be especially gentle at this point.</p>\n\n<p>Prokaryotic cells such as the above mentioned TOP10 cells are treated with Calcium chloride and glycerol which has essentially the same effect on their walls and membranes. Hence pipetting should be delicately performed after thawing these cells as well. </p>\n\n<p>With that being said, if you compare the sensitivity of prokaryotic and eukaryotic cells to shearing, eukaryotic cells are profoundly more sensitive.</p>\n\n<p>For individuals using competent bacteria for sub-cloning and other routine uses, killing a small percentage of of your cells is not that important. However if you are using the transformation to generate cDNA libraries it's very important that you have a titer sufficiently representing the transcriptome the library is composed of. </p>\n\n<p>In these instances using a more premium competent cell, adhering to correct temperatures and minimizing pipetting is essential. This is why many are taught to swirl the DNA the with the competent cells, rather than the harsher alternative: pipetting up-and-down.</p>\n\n<p>The four most important factors that contribute to cellular shearing are, and in order form most to least contributory:</p>\n\n<ol>\n<li>Diameter of the bore in the pipette tip, the smaller the more shearing. </li>\n<li>Speed at which the suspension is passing through the opening of the tip. The faster the more damaging. </li>\n<li>Size and rigidity of the cell. Larger cells are more prone to damage. Cells with a murein wall are less prone to damage. </li>\n<li>Concentration of cells. Cultures that are more concentrated are more prone to damage.</li>\n</ol>\n\n<p>Because the make up if the cell itself is so influential on the amount of damage, and because of the enormous variety of cells; designing a representative experiment to assess damage would be very difficult and laborious.</p>\n\n<p>Finally, the variety of tips and seriologicals is also enormous. However if one were to attempt to assess this it could be done:</p>\n\n<p>Choose a representative variety of cell lines, choose a representative variety of pipettes. One would probably want to use a robotic pipette to be able to evaluate incrementally assigned speeds and pressures. Look at different culture concentrations, phases of the growth curve, time between pipetting and analysis, distance between the exiting fluid and the culture etc, etc.</p>\n\n<p>I think a very successful analysis method would be using propidium iodide and FACS.</p>\n\n<p>After your experiment which will cost a lot of time and $, I think you will find common sense rules: keep pipetting to a minimum and use wider tips whenever possible.</p>\n"
}
] |
[
{
"answer_id": 2603,
"pm_score": 4,
"text": "<p>It's an easy experiment to do. Take your cells aliquot them into 10 microfuge tubes, and pipette each suspension increasing amount of times, stain with trypan blue and count.</p>\n\n<p>The most important factors will be which pipette-type you use; I would expect a p1000 to cause more damage then a p200 then a p20 due to velocity of the fluid. Also the most important factor will be the skill of the scientist, if you pipette slowly it should decrease stress as opposed to pipetting quickly.</p>\n\n<p>In my experience it depends on the pipette-type and the skill of the operator. The only way to answer this for you is to try it empirically. </p>\n"
},
{
"answer_id": 2604,
"pm_score": 3,
"text": "<p>Anecdotally I have not observed any cell death upon pipetting of <em>E. coli</em> DH5alpha or TOP10, however as competent cells, mixing by pipetting up and down is discouraged due to the compromised cell wall.</p>\n"
},
{
"answer_id": 20903,
"pm_score": 2,
"text": "<p>This question would be better served in the physics se or chemistry. I don't think we have a generic engineering where fluid dynamics could be described in a different method than physics but if we did it should also be answered there.</p>\n<p>Indeed the osmotic or liquid pressure in and of itself would cause changes possibly damages to the cell. Then other eexothermic and endothermic reactions to the chemicals due to force of impact like a chem or friction burn.</p>\n<p>I'm sure the other requirements of conservation of energy which I half-hazardly ignored.</p>\n<p>I found this interesting paper which focuses on the shear stress in general.</p>\n<blockquote>\n<p><a href=\"http://www.ncbi.nlm.nih.gov/pubmed/17492777\" rel=\"nofollow noreferrer\">Pipetting causes shear stress and elevation of phosphorylated stress-activated protein kinase/jun kinase in preimplantation embryos.</a></p>\n<p>Xie Y1, Wang F, Puscheck EE, Rappolee DA.</p>\n<p>Shear stress at 1.2 dynes/cm(2) induces stress-activated protein kinase/jun kinase phosphorylation that precedes and causes apoptosis in embryos (Xie et al., 2006b, Biol Reprod). Pipetting embryos is necessary for many protocols, from in vitro fertilization to collecting embryos prior to analyzing gene expression by microarrays. We sought to determine if pipetting upregulates phosphorylated MAPK8/9 (formerly known as stress-activated protein kinase/jun kinase/SAPK/JNK1, 2). We found that phosphorylated MAPK8/9, a marker of MAPK8/9 activation, is upregulated in a dose-dependent manner by pipetting. Whereas embryos with the zona pellucida removed were more sensitive to stress-induced lethality mediated by 1.2 dynes/cm(2) shear force, phosphorylated MAPK8/9 was induced at lower numbers of pipet triturations in hatched embryos at E4.5. E4.5 embryos were more sensitive to induction of MAPK8/9 than unhatched embryos at E2.5 or E3.5. E3.5 embryos also showed a pipetting dose-dependent induction of FOS protein (formerly known as c-fos), a marker of shear stress in many cell types. Phosphorylated MAPK8/9 measured in ex vivo embryos from E1.5 to E4.5 were expressed at low levels. Embryos that had been pipetted sufficiently to induce phosphorylated MAPK8/9 and FOS had the same number of cells as untreated embryos 24 hr later. This suggests that rapid phosphorylation of MAPK8/9 due to transient shear stress does not mediate long-term negative biological outcomes. But, it is possible that techniques requiring multiple handling events would induce MAPK8/9 and cause biological outcomes or that other biological outcomes are affected by low amounts of transient shear stress. This study suggests that embryo handling prior to experimental measurement of signal transduction phosphoproteins, proteins and mRNA should be performed with care. Indeed, it is likely that shear stress may cause rapid transient changes in hundreds of proteins and mRNA.</p>\n</blockquote>\n"
},
{
"answer_id": 23394,
"pm_score": 2,
"text": "<p>Shear stress $\\tau$ in this small sizes is usually measured in dyne/cm2 or N/m2 = Pa. The equations betweeen them: $1dyn/cm^2 = 10^{-5}N/cm^2 = 0.1N/m^2 = 0.1Pa$.</p>\n\n<p>What kind of damages zygotes can suffer by pipetting?</p>\n\n<blockquote>\n <p>Using scanning electron microscopy, we found open holes on the surface\n of lysed eggs, indicating failure of the plasma membrane to reseal\n after microinjection. No holes were seen in unlysed eggs, but many of\n them had membrane alterations suggestive of healed punctures.</p>\n</blockquote>\n\n<ul>\n<li>1987 - <a href=\"http://www.biolreprod.org/content/37/4/957.short\" rel=\"nofollow\">Zygote viability in gene transfer experiments</a></li>\n</ul>\n\n<p>Even a small 1.2 dyn/cm2 shear stress induces apoptosis by pipetting zygotes. So zygotes have their critical shear stress level by 1.2 dyn/cm2 and pipetting involves greater forces than 1.2 dyn/cm2.</p>\n\n<blockquote>\n <p>Shear stress at 1.2 dynes/cm2 induces stress-activated protein\n kinase/jun kinase phosphorylation that precedes and causes apoptosis\n in embryos (Xie et al., 2006b, Biol Reprod). Pipetting embryos is\n necessary for many protocols, from in vitro fertilization to\n collecting embryos prior to analyzing gene expression by microarrays.\n We sought to determine if pipetting upregulates phosphorylated MAPK8/9\n (formerly known as stress-activated protein kinase/jun\n kinase/SAPK/JNK1, 2). We found that phosphorylated MAPK8/9, a marker\n of MAPK8/9 activation, is upregulated in a dose-dependent manner by\n pipetting.</p>\n</blockquote>\n\n<ul>\n<li>2007 - <a href=\"http://onlinelibrary.wiley.com/doi/10.1002/mrd.20563/abstract\" rel=\"nofollow\">Pipetting causes shear stress and elevation of phosphorylated stress-activated protein kinase/jun kinase in preimplantation embryos</a></li>\n</ul>\n\n<p>The critical shear stress level is somewhere between 0.01 and 1000 dyn/cm2 by animal cells depending on the cell type and species. (I think the average is somewhere about 50 dyn/cm2, but it is very hard to differentiate between articles mentioning critical shear levels and most lethal shear levels, so the range and the average might be lower.) The death constant (1/h) increases exponentially by increasing the shear stress.</p>\n\n<blockquote>\n <p>An apparatus for the detailed investigation of the influence of shear\n stress on adherent BHK cells was developed. Shear forces between 0.0\n and 2.5 N m−2 were studied. The influence on cell viability, cell\n morphology, cell lysis, and cell size was determined. Increasing shear\n forces as well as increasing exposure duration caused increasing\n changes in cell morphology and cell death. A “critical shear stress\n level” was determined.</p>\n</blockquote>\n\n<ul>\n<li>1992 - <a href=\"http://www.sciencedirect.com/science/article/pii/014102299290068Y\" rel=\"nofollow\">Determination of a “critical shear stress level” applied to adherent mammalian cells</a></li>\n</ul>\n\n<blockquote>\n <p>Shear stress related damage to a mouse hybridoma was examined by\n Abu-Reesh and Kargi under laminar and turbulent conditions in a\n coaxial cylinder Searle viscometer. Cells were exposed to 5 to 100\n N/m2 shear stress levels for 0.5 to 3.0 h. At a given shear stress and\n exposure time, turbulent shear was much more damaging than laminar\n shear as also reported in the past for protozoa and plant cells. Under\n turbulent conditions, damage occurred when shear stress exceeded 5\n N/m2. Respiratory activity of the cells was damaged earlier than the\n cell membrane, thus implying transmission of the stress signal to the\n interior of the cell. Cell damage followed first-order kinetics both\n in laminar and turbulent environments. For turbulent shear stress\n levels of 5 to 30 N/m2, the death rate constant (kd) increased\n exponentially with increasing stress level; the kd values varied over\n 0.1 to 1.0 1/h.</p>\n</blockquote>\n\n<ul>\n<li>2001 - <a href=\"http://www.massey.ac.nz/~ychisti/HydroD.pdf\" rel=\"nofollow\">Hydrodynamic Damage to Animal Cells</a></li>\n</ul>\n\n<blockquote>\n <p>Subconfluent endothelial cultures continuously exposed to 1–5\n dynes/cm2 shear proliferate at a rate comparable to that of static\n cultures and reach the same saturation density (≃ 1.0–1.5 × 105\n cells/cm2 ). When exposed to a laminar shear stress of 5–10 dynes/cm2\n , confluent monolayers undergo a time-dependent change in cell shape\n from polygonal to ellipsoidal and become uniformly oriented with flow.\n Regeneration of linear “wounds” in confluent monolayer appears to be\n influenced by the direction of the applied force. Preliminary studies\n indicate that certain endothelial cell functions, including fluid\n endocytosis, cytoskeletal assembly and nonthrombogenic surface\n properties, also are sensitive to shear stress. These observations\n suggest that fluid mechanical forces can directly influence\n endothelial cell structure and function.</p>\n</blockquote>\n\n<ul>\n<li>1981 - <a href=\"http://biomechanical.asmedigitalcollection.asme.org/article.aspx?articleid=1395402\" rel=\"nofollow\">The Dynamic Response of Vascular Endothelial Cells to Fluid Shear Stress</a></li>\n</ul>\n\n<blockquote>\n <p>Shear stress above 0.25 dyne/cm(2) resulted in dramatic loss of\n podocytes but not of proximal tubular epithelial cells (LLC-PK(1)\n cells) after 20 h.</p>\n</blockquote>\n\n<ul>\n<li>2006 - <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/16684926\" rel=\"nofollow\">Podocytes are sensitive to fluid shear stress in vitro</a></li>\n</ul>\n\n<blockquote>\n <p>A series of careful studies has been made on blood damage in a\n rotational viscometer. Specific attention has been focused on the\n effects of solid surface interaction, centrifugal force, air interface\n interaction, mixing of sheared and unsheared layers, cell-cell\n interaction, and viscous heating. The results show that there is a\n threshold shear stress, 1500 dynes/cm2, above which extensive cell\n damage is directly due to shear stress, and the various secondary\n effects listed above are negligible.</p>\n</blockquote>\n\n<ul>\n<li>1972 - <a href=\"http://www.sciencedirect.com/science/article/pii/S0006349572860855\" rel=\"nofollow\">Red Blood Cell Damage by Shear Stress</a></li>\n</ul>\n\n<blockquote>\n <p>The shear stress threshold of some dinoflagellates (microalgae) is\n even lower than that of erythrocytes (0.029 N/m2). For example, a\n continuous laminar shear stress level of only 0.0044 N/m2 (equivalent\n to a shear rate of 2.2 1/s) has proved lethal to the dinoflagellate\n Gonyaulax polyedra.</p>\n</blockquote>\n\n<ul>\n<li><a href=\"http://books.google.hu/books?id=aaEeAAAAQBAJ&printsec=frontcover&hl=hu#v=onepage&q&f=false\" rel=\"nofollow\">Upstream Industrial Biotechnology</a></li>\n</ul>\n\n<p>Other cell types are not necessary as sensitive as animal cells and they don't necessary react with apoptosis (about 10 dyn/cm2) to shear stress, so you have to use necrotic (about 5000 dyn/cm2) forces to destroy them :</p>\n\n<pre><code>cell type size shear sensitivity\nmicrobial cells 1-10μm low\nmicrobial pellets/clumps up to 1cm moderate\nplant cells 100μm moderate/high\nplant cell aggregates up to 1-2cm high\nanimal cells 20μm high\nanimal cells on microcarriers 80-200μm very high\nfungi cells 2-10μm moderate/high\n</code></pre>\n\n<ul>\n<li>Table 1 - shear sensitivity by cells types </li>\n<li><a href=\"http://books.google.hu/books?id=Z-N4SNmsYnMC&printsec=frontcover&hl=hu&source=gbs_ge_summary_r&cad=0#v=onepage&q&f=false\" rel=\"nofollow\">Bioprocess Engineering Principles: table 8.6 - Pauline M. Doran</a></li>\n<li>1996 - <a href=\"http://www.sciencedirect.com/science/article/pii/092304679503062X\" rel=\"nofollow\">Role of hydrodynamic shear in the cultivation of animal, plant and microbial cells</a></li>\n<li>1988 - <a href=\"http://www.sciencedirect.com/science/article/pii/0141022988900166\" rel=\"nofollow\">Effect of shear on the viability of plant cell suspensions</a></li>\n<li>2004 - <a href=\"http://onlinelibrary.wiley.com/doi/10.1002/bit.260440512/abstract\" rel=\"nofollow\">A quantitative analysis of shear effects on cell suspension and cell culture of perilla frutescens (plant) in bioreactors</a></li>\n<li>2009 - <a href=\"http://onlinelibrary.wiley.com/doi/10.1002/9780470054581.eib543/abstract\" rel=\"nofollow\">Shear Sensitivity</a> - the full text probably contains all the numbers</li>\n</ul>\n\n<blockquote>\n <p>Results show that Chinese Hamster Ovaries and Human Embryonic Kidney\n cells will enter the apoptotic pathway when subjected to low levels of\n hydrodynamic stress (around 2.0 Pa) in oscillating, extensional flow.\n In contrast, necrotic death prevails when the cells are exposed to\n hydrodynamic stresses around 1.0 Pa in simple shear flow or around\n 500 Pa in extensional flow.</p>\n</blockquote>\n\n<ul>\n<li>2009 - <a href=\"http://onlinelibrary.wiley.com/doi/10.1002/bit.22405/abstract\" rel=\"nofollow\">Induction of mammalian cell death by simple shear and extensional flows</a></li>\n</ul>\n\n<p>The shear sensitivity is not determined only by cell type and species, there are many other factors involved: </p>\n\n<ul>\n<li>type of cell and species</li>\n<li>composition and thickness of cell wall when present</li>\n<li>size and morphology of cell</li>\n<li>the intensity and nature of shear stress, whether turbulent or laminar, or associated with interfaces (e.g. during bubble rise and rupture)</li>\n<li>growth history, both short-term (e.g. starvation) and long term adaptation</li>\n<li>growth medium (trace elements, vitamins, carbon and nitrogen sources)</li>\n<li>growth rate</li>\n<li>growth stage</li>\n<li>type and concentration of shear protective agents if present</li>\n</ul>\n\n<p>Cells can be very sensitive to shear stress caused by turbulent flow, while not so sensitive to shear stress caused by laminar flow.</p>\n\n<blockquote>\n <p>On the basis of laminar flow viscometriy measurements, a critical\n shear stress level of 80-200 N/m2 has been suggested for Morindata\n citrifolia cells.</p>\n \n <p>... while for Daucus carota a shear stress level of 50 N/m2 has been\n associated with cell damage. In other study, carrot cells in a laminar\n flow Couette viscosimeter lost the ability to grow and divide in the\n shear stress range of 0.5-100 N/m2. The intracellular enzyme activity\n was impaired at shear stress levels above 3000N/m2, but significant\n lysis did not occur until a shear stress level of 10.000 N/m2 applied\n over a prolonged perioud (>1h).</p>\n \n <p>In contrast to the behavior in laminar flow, the cells were quite\n sensitive to turbulent impeller agitation. Impeller tip speeds of ~1.1\n m/s lysed a significant proportion of the cells within 40min.</p>\n</blockquote>\n\n<ul>\n<li><a href=\"http://books.google.hu/books?id=-HDQZc_OftoC&printsec=frontcover&hl=hu#v=onepage&q&f=false\" rel=\"nofollow\">Cell and Tissue Reaction Engineering</a></li>\n<li><a href=\"http://books.google.hu/books?id=aaEeAAAAQBAJ&printsec=frontcover&hl=hu#v=onepage&q&f=false\" rel=\"nofollow\">Upstream Industrial Biotechnology</a></li>\n</ul>\n\n<p>The bubble damage is severe (1000 cells by a single 3.5mm size bubble) because of the cell adherence to the interface of the bubble and the strong forces involved (>1000 dyn/cm2 by stirred bioreactors). The adhesion and so the damage can be reduced with surfactants. </p>\n\n<ul>\n<li>2004 - <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/15296446\" rel=\"nofollow\">Quantitative studies of cell-bubble interactions and cell damage at different pluronic F-68 and cell concentrations.</a></li>\n<li>2004 - <a href=\"http://journals.lww.com/anesthesiology/Abstract/2004/07000/Surfactant_Reduction_in_Embolism_Bubble_Adhesion.16.aspx\" rel=\"nofollow\">Surfactant Reduction in Embolism Bubble Adhesion and Endothelial Damage</a></li>\n</ul>\n\n<blockquote>\n <p>It is proposed that when cells are either attached to, or very near, a\n rupturing bubble, the hydrodynamic forces associated with the rupture\n are sufficient to kill the cells.</p>\n \n <p>All experiments were conducted with Spodoptera frugiperda (SF-9)\n insect cells, in TNM-FH and SFML medium, with and without Pluronic\n F-68. Experiments indicate that approximately 1050 cells are killed\n per single, 3.5-mm bubble rupture in TNM-FH medium and approximately\n the same number of dead cells are present in the upward jet. It was\n also observed that the concentration of cells in this upward jet is\n higher than the cell suspension in TNM-FH medium without Pluronic F-68\n by a factor of two. It is believed that this higher concentration is\n the result of cells adhering to the bubble interface. These cells are\n swept up into the upward jet during the bubble rupture process.\n Finally, it is suggested that a thin layer around the bubble\n containing these absorbed cells is the “hypothetical killing volume”\n presented by other researchers.</p>\n</blockquote>\n\n<ul>\n<li>1994 - <a href=\"http://onlinelibrary.wiley.com/doi/10.1002/bit.260430106/abstract\" rel=\"nofollow\">Quantification of damage to suspended insect cells as a result of bubble rupture</a></li>\n</ul>\n\n<blockquote>\n <p>For a hybridoma line, reported that exposure to laminar shear stress\n (208 N/m2) in unaerated flow in a cone and plate viscometer led to\n substantial loss in cell count and viability within 20 min. At a\n constant 180 s exposure, increasing shear stress over 100-350 N/m2\n linearly enhanced cell disruption, with >90% of the cells being\n destroyed at 350 N/m2 stress level. Shear stres levels associated with\n bubble rupture at the surface of a bioreactor may range over 100-300\n N/m2. These values are remarkably consistent with shear rates that\n damaged hybridomas in unaerated laminar flow experiments.</p>\n</blockquote>\n\n<ul>\n<li><a href=\"http://books.google.hu/books?id=aaEeAAAAQBAJ&printsec=frontcover&hl=hu#v=onepage&q&f=false\" rel=\"nofollow\">Upstream Industrial Biotechnology</a></li>\n</ul>\n\n<p>Smaller hole pipettes cause more damage.</p>\n\n<blockquote>\n <p>We also examined aspects of the gene transfer procedure that might\n influence survival such as the size of injection pipettes and their\n taper relative to zygote diameter, possible toxicity of the injection\n medium, the timing of injection, and immediate vs. delayed pipette\n withdrawal. The only factors that significantly affected cell\n viability were pipette size and taper, and timing of injection in\n relation to first cleavage. This suggests that zygote viability\n correlates inversely with the size of the hole produced by the\n injection pipette and that damage to the membrane is less successfully\n repaired as the fertilized egg readies itself for division.</p>\n</blockquote>\n\n<ul>\n<li>1987 - <a href=\"http://www.biolreprod.org/content/37/4/957.short\" rel=\"nofollow\">Zygote viability in gene transfer experiments</a></li>\n</ul>\n\n<p>It is hard to find anything about the level of shear stress by pipetting. It can be certainly more than 1 dyn/cm2. It has a short duration (at most a few seconds). I think the following factors can influence the shear stress levels by pipetting:</p>\n\n<ul>\n<li>pipette type</li>\n<li>flow speed (faster flow can be more likely turbulent)\n<ul>\n<li>negative pressure by suction</li>\n<li>hole size (<a href=\"http://en.wikipedia.org/wiki/Venturi_effect\" rel=\"nofollow\">bigger hole can reduce flow speed</a>)</li>\n<li>liquid viscosity</li>\n</ul></li>\n<li>bubble formation</li>\n</ul>\n\n<p>Probably more factors are involved but I am not a pipetting expert. ;-) I agree with the others, it surely depends on the personal skills e.g. an amateur can create huge bubbles by pipetting, which can kill a lot of cells by formation and disruption...</p>\n\n<p>I agree with Artem that this is an experiment to do especially if the result is important for you. What you need to create a model about pipette damage, are the shear stress levels by pipetting and the critical shear stress levels of the cells. I think it is hard to design and experiment in which you can measure the shear stress levels in your pipettes and there is no flow model for pipetting as far as I know, so it can be a good topic for a thesis or a diploma work. </p>\n"
},
{
"answer_id": 55085,
"pm_score": 2,
"text": "<p>I know this is a two-year-old thread, but I though I would post this anyway in case someone else is searching for this answer like I was tonight. This article cited below doesn't discuss pipette tips vs needles specifically, but it does discuss the difference in effects of tapering vs cylindrical needles on cell damage. Unfortunately, the math in the paper is a bit beyond me (I'm a doctor, not an engineer, and they didn't cover this stuff in medical school), but they found that with cylindrical needles result in approximately 5x the amount of cell death compared to a tapered needle at any given flow rate, and approximately 6-8x the amount of cells damaged. This was likely due in part to the need for higher pressures to increase flow rates in cylindrical needles compared to tapered needles and variations in shear due to the geometries. While a tapered needle is not identical to a plastic pipette tip, the geometries are comparable.</p>\n\n<p>Biotechnol Prog. 2011 Nov-Dec;27(6):1777-84. Effect of needle geometry on flow rate and cell damage in the dispensing-based biofabrication process. Li M1, Tian X, Schreyer DJ, Chen X.</p>\n\n<p><a href=\"http://onlinelibrary.wiley.com/doi/10.1002/btpr.679/full\" rel=\"nofollow noreferrer\">http://onlinelibrary.wiley.com/doi/10.1002/btpr.679/full</a></p>\n"
},
{
"answer_id": 64728,
"pm_score": 1,
"text": "<p>I have a real life biological example.\nsimplified experiment setup:\nex vivo purified B cells undergo 3 washes in PBS (spin and resuspend), then they are incubated in vitro for 24 hrs and analyzed by flow cytometry using Acqua Zombie and PI for dead cell exclusion. \nExperiment 1: pipeting after washes using 1ml tip \nExperiment 2: pipeting after washes using 10ml pipette</p>\n\n<p>Cell survival as analyzed by flow cytometry: \nExperiment 1: 9.96%\nExperiment 2: 43.9%</p>\n"
}
] |
2,790 |
<p>When people try to explain evolution, they tell me that evolution is a cumulative result of mutations & natural section of the more superior individuals of a particular species. I think I'm fairly convinced with this explanation.</p>
<p>But when I think about it, all of them assume that there was an organism, however simple, that was capable of self replication & occasionally mutate. How did such an organism come into existence? Can anyone explain this?</p>
<p>An answer I found <a href="http://www.reddit.com/r/explainlikeimfive/comments/upb42/eli5_evolution_how_can_human_beings_pop_out_of/c4zdmf4">on Reddit</a> didn’t really convince me.</p>
|
[
{
"answer_id": 2806,
"pm_score": 5,
"text": "<p>Evolution or (as Darwin called it) \"descent with modification\" is a theory which explains the origin of the species NOT the origin of life. How the first life arose is <strong>completely irrelevant</strong> to the theory of evolution. What evolution does explain is how and why we have such variety of life on earth all descending from the same organism.</p>\n\n<p>What you're asking about is not a theory of \"evolution\" but rather a theory of \"abiogenesis.\" Although there are many interesting hypothesis for how abiogenesis happened (e.g. the RNA world, the \"metabolism first\" theory, etc.), the fact is we simply do not know yet how life first arose. What we do know is that life first arose between 3.5 and 3.9 billion years ago. That's a really long time ago compared to lots of other important events in natural history (even the Cambrian explosion where modern animal phyla evolved was only half a billion years ago), and so it shouldn't be surprising that it's a hard problem.</p>\n"
}
] |
[
{
"answer_id": 2793,
"pm_score": 3,
"text": "<blockquote>\n <p>They teach us in Physics that the entropy of an isolated system is always increasing or at least constant. Then how can an organism be born under these conditions?</p>\n</blockquote>\n\n<p>The sun sends energy to the Earth, allowing for a decrease in entropy on Earth at the expense of the sun's entropy.</p>\n\n<blockquote>\n <p>But when I think about it, all of them assume that there was an organism, however simple, that was capable of self replication & occasionally mutate. How did such an organism come into existence? Can anyone explain this?</p>\n</blockquote>\n\n<p>That organism you're talking about is just a molecule that copies itself. Exactly how it has come about is not clear to me but it's not hard to imagine the possibility. A vast planet with molecules flying all over being bathed in ultraviolet light and if any molecule anywhere acquires the characteristic of copying itself, it will start growing exponentially and quickly spread all over the world.</p>\n"
},
{
"answer_id": 2797,
"pm_score": 3,
"text": "<p>We don't know how self-replicating molecules first arose (and probably never will know exactly) but the Earth is large and had 500 million years (i.e. the prebiotic Earth timescale) or so to experiment in organic chemistry. The land-sea interface (such as tidal pools) are a good candidate site since these are areas where high concentrations of organic goodies can be found.</p>\n\n<p>In this context, one focus that researchers have been looking at is self-replicating molecules.</p>\n\n<p>For example, one lab in <a href=\"http://www2.mrc-lmb.cam.ac.uk/groups/ph1/pub.html\">Cambridge,UK</a> has come up with tC19Z.</p>\n\n<p>tC19Z is the name of a RNA enzyme that acts like a self-replicating molecule. It can copy chunks of RNA almost 50% as long as itself. It can also make copies of other RNA enzymes. This molecule is not \"alive\" itself, but clearly demonstrates how greater complexity can arise.</p>\n"
},
{
"answer_id": 2823,
"pm_score": 2,
"text": "<p>This is an extremely interesting and extremely fundamental question, indeed, and thus far, biologists have failed at coming up with a satisfying answer.</p>\n\n<p>We know that all the parts are there, we just don't know how they were arranged, or which ones go where.</p>\n\n<p>The question is, in essence, composed of three sub-questions:</p>\n\n<ol>\n<li>How did the fundamental building blocks of life come about?</li>\n<li>How did the first self-replicating molecules come about?</li>\n<li>How did cell membranes come about?</li>\n</ol>\n\n<p>The answer generally takes the form of \"On primordial Earth, a small selection of the billions of organic compounds generated when UV-light hits a mess of carbon dioxide, nitrogen and water where captured in a tide pool where concentration and foam led to random chance producing self-replicating molecules in proto-cells.\"</p>\n\n<p>This answer, while almost certainly true, is also incredibly dissatisfying, because all it tells us is what deductive logic has already taught us, almost intuitively.</p>\n\n<p>Incidentally, the fact that all of this happens with a million to one odds isn't a problem: The Earth is big, and the time frame for this happening is along the lines of hundreds of millions of years: Anything that might happen once per year by a million to one shot would likely happen hundreds of times in that timeframe.</p>\n\n<p><strong><em>In any case</em></strong>, when it comes to evolution, or Darwin's Theory of Evolution, or any other theory of evolution, this is all irrelevant.</p>\n\n<p>Evolution is something that happens in any sufficiently complex (open) system, assuming it has the capacity to change at all.</p>\n\n<p>It is most easily observed in living organisms, because they are at the right scale, and incredibly diverse, but it happens on all scales of the universe.</p>\n\n<p>In fact, the easiest way to explain how life first originated, is just to keep counting backwards when you reach the Last Common Ancestor (of All Life on Earth), and propose models for how this proto-bacterium could be even simpler, until you're left with CO₂, N₂ and H₂O, and other simple molecules.</p>\n\n<p>At that end of the spectrum it is well-understood that e.g. H₂O \"evolves\" from H₂ and O₂, because H₂O has a quality that makes it more \"fit\" than either of its components, chemical stability.</p>\n\n<p>Furthermore, H2 \"evolves\" from free hydrogen by a similar mechanism, and free hydrogen \"evolves\" from protons and electrons, because it has the property of being electrically neutral, which is also a desirable property.</p>\n\n<p>Of course, at the level of protons and electrons, things get a little muddy, and evolution kind of breaks down as a method for explaining how things come about.</p>\n\n<p><strong>Edit:</strong> For reference: <a href=\"http://en.wikipedia.org/wiki/Abiogenesis#Current_models\" rel=\"nofollow\">Current Models of Abiogenesis</a> on Wikipedia.</p>\n"
},
{
"answer_id": 2826,
"pm_score": 2,
"text": "<p>While many point to RNA, or a variant of it, as being the first molecule of \"life\" very few people know where it came from. Some suggest that it came from outer space because it's uncertain how the material for <a href=\"http://www.nature.com/scitable/definition/phosphate-backbone-273\" rel=\"nofollow\">sugar-phosphate backbones</a> could have developed on earth and that the perhaps these materials found their way here <a href=\"http://www.pnas.org/content/108/34/13995\" rel=\"nofollow\">via meteorites</a>. There are several hypotheses as to how an early earth environment may have promoted the properties of these molecules, but it's difficult to ascertain what exactly happened.</p>\n\n<p>Somewhere within that abiogenesis wikipedia article is the mention of the role of deep-sea vents. The deep-sea vents and the currents that surround them basically facilitated a PCR reaction. Some of the early emerging DNA, maybe with some RNA and free nucleotides floating around, could have leveraged such an environment for replication and by sheer number (and some chance) entered into symbiotic relationship with other molecules to form the first cellular structures.</p>\n"
},
{
"answer_id": 21722,
"pm_score": 0,
"text": "<p>I think that it started like this:</p>\n\n<p>First stage:</p>\n\n<p>Chemicals like Na, Cl, O₂, O₃, CO₂, CO, HCN, and H₂SO₄ react to form small molecules.</p>\n\n<p>Second Stage:</p>\n\n<p>Next those small molecules react to form macromolecules.</p>\n\n<p>Third Stage:</p>\n\n<p>DNA, being the most stable was first to replicate. A membrane eventually enveloped this and formed the nucleus</p>\n\n<p>Fourth Stage:</p>\n\n<p>Via Endosymbiosis it envelops mitochondria in an outer membrane</p>\n\n<p>Fifth Stage: </p>\n\n<p>Cell starts forming membrane and protein for all of its organelles. It is now a eukaryotic cell.</p>\n\n<p>This is the DNA world Hypothesis.</p>\n\n<p>Because DNA can be single, double, triple, or quadruple stranded in organisms(That would be ssDNA, dsDNA, tsDNA, and qsDNA respectively) it can do much more than just code for proteins or rRNA or tRNA. </p>\n\n<p>In the single stranded state it can act like an enzyme forming deoxyribozymes.</p>\n\n<p>In the triple and quadruple stranded states it can act inhibitory without needing another protein or methyl group.</p>\n"
},
{
"answer_id": 21723,
"pm_score": 2,
"text": "<p>If you are interested in this question, I highly recommend you look at the work of <a href=\"http://molbio.mgh.harvard.edu/szostakweb/\" rel=\"nofollow\">Jack Szostak</a> - Nobel Prize winner at Harvard who is currently doing some of the best work in this area. His work is grounded in good experiments that point to how abiogenesis <em>could</em>\n have happened. </p>\n"
}
] |
3,177 |
<p>We use electromagnetic communication everywhere these days. Cell phones, wifi, old-school radio transmissions, television, deep space communication, etc.</p>
<p>I'm curious about some of the possible reasons we have never seen biological systems having evolved to use electromagnetic, i.e. radio, for communication. The one obvious exception to this are organisms that generate their own light, i.e. bioluminescence. Cuttlefish are masters of this, and many other species as well.</p>
<p>It seems like bio-radio could have offered all kinds of evolutionary advantages for animals capable of using it.</p>
<p>Are their basic physical limits in chemistry, or excess energy requirements or something that would basically have made this impossible? Or was this perhaps just something that life never evolved to use, but would otherwise be possible in evolution?</p>
|
[
{
"answer_id": 3180,
"pm_score": 6,
"text": "<p>There is a very different mechanism for generation (and detection) of ultraviolet, visible and infrared light vs radio waves.</p>\n\n<p>For the first, it is possible to generate it using chemical reactions (that is, <a href=\"http://en.wikipedia.org/wiki/Chemiluminescence\">chemiluminescence</a>, <a href=\"http://en.wikipedia.org/wiki/Bioluminescence\">bioluminescence</a>) with a typical energy of order of 2 eV (<a href=\"http://en.wikipedia.org/wiki/Electronvolt\">electronovolts</a>). Also, it is easy to detect with similar means - coupling to a bond (e.g. using <a href=\"http://en.wikipedia.org/wiki/Opsin\">opsins</a>).</p>\n\n<p>For much longer electromagnetic waves, and much lower <a href=\"http://halas.rice.edu/conversions\">energies per photon</a>, such mechanism does not work. There are two reasons:</p>\n\n<ul>\n<li>typical energy levels for molecules (but it can be worked around),</li>\n<li>thermal noise has energies (0.025 eV) which are higher than radio wave photon energies (<0.001 eV) (it rules out both controlled creation and detection using molecules).</li>\n</ul>\n\n<p>In other words - radiation which is less energetic than thermal radiation (far infrared) is not suitable for communication using molecular mechanisms, as thermal noise jams transmission (making the sender firing at random and making the receiver being blind by noise way stronger than the signal). </p>\n\n<p>However, one can both transmit, and detect it, using wires. In principle it is possible; however, without good conductors (like metals, not - salt solutions) it is not an easy task (not impossible though).</p>\n"
}
] |
[
{
"answer_id": 3178,
"pm_score": 2,
"text": "<p>A quick comparison between light and sound vs. Radio</p>\n\n<ul>\n<li><a href=\"http://en.wikipedia.org/wiki/Light\" rel=\"nofollow noreferrer\">Light</a>: Wavelength 380 nm -740 nm</li>\n<li><a href=\"http://en.wikipedia.org/wiki/Sound\" rel=\"nofollow noreferrer\">Sound</a>: 17 mm - 17 m</li>\n<li><a href=\"http://en.wikipedia.org/wiki/Radio_frequency\" rel=\"nofollow noreferrer\">Radio</a>: 1mm - 10e5 km</li>\n</ul>\n\n<p><img src=\"https://i.stack.imgur.com/gSMxk.png\" alt=\"EM spectrum\"></p>\n\n<p>From the Planck relation, the energy of a wave is inversely proportional to the wavelength. As a result light is stronger than sound which is stronger than FM radio which is stronger than AM radio. Very likely, the energy density provided by radio is far too weak to have meaningful signal processing.</p>\n\n<p>However, there are some uses in the radio frequency. <a href=\"http://en.wikipedia.org/wiki/Animal_echolocation\" rel=\"nofollow noreferrer\">Bat echolocation</a> occurs at a frequency of 14,000 to 100,000 Hz which is well within the radio frequency. </p>\n"
},
{
"answer_id": 3239,
"pm_score": 3,
"text": "<p>Actually, electromagnetic communication is used by certain fish, the mormyrids and the gymnotids. Pulse modulated in the former and amplitude modulated in the latter.</p>\n\n<p>However, the frequencies used are not much greater than 1Khz, which is not what we ordinarily consider to be in the radio frequency spectrum.</p>\n\n<p>There is, too, another biological species in which the use of the full RF spectrum has evolved. Its activities even extend to the use of the UV and X-ray frequencies.</p>\n\n<p>That species is our own. I am not being flippant here. We must not fall into the trap of considering ourselves as apart from nature. Contrary to our usual intuitions, technologies have evolved autonomously within the collective imagination of our species.</p>\n\n<p>The broader evolutionary model which supports this contention is outlined, very informally, in \"The Goldilocks Effect: What Has Serendipity Ever Done For Us?\" , a free download in e-book formats from the \"Unusual Perspectives\" website. </p>\n"
},
{
"answer_id": 9790,
"pm_score": 3,
"text": "<p>Because the intermediate stages are not evolutionarily favoured. That's why.</p>\n\n<p>Sound and light perception are useful without any generative capability. An organism with a tiny amount of perception for either of these things has an advantage over those without; and an organism with a tiny amount more has an advantage over those with a tiny bit less. This advantage forms the basis for selection and thus improved sensory capabilities (balanced, of course, by the cost of those capabilities).</p>\n\n<p>Being able to perceive radio on the other hand provides no useful information about the world at low level perception so even if an organism was to randomly mutate so as to detect radiowaves* there would be no selection for this ability, and thus no mechanism to drive the evolution of advanced radio reception. Without the ability to perceive radiowaves there is no possibility of evolving the ability to generate radio signals in a controlled manner.</p>\n\n<p>*-In fact, since radiowaves generally interact very little with organic materials unlike heat, light and sound even this first step of random mutation is much less likely than for sense that have evolved.</p>\n"
},
{
"answer_id": 35956,
"pm_score": 2,
"text": "<p>I just found a research about possibility of organism with loop DNA (Mostly bacteria) could use there DNA as antenna to transmit and receive radio wave around 1kHz</p>\n\n<p><a href=\"http://www.wired.com/2011/04/bacterial-radio/\" rel=\"nofollow\">http://www.wired.com/2011/04/bacterial-radio/</a></p>\n\n<p>But as other said. Communication mostly evolve from sensory organ. So the radio wave has too much noise and could not give useful information about situation. They don't selectively evolve to the point that they could be used to communicate</p>\n\n<p>But the bacteria has inherently possibility from start. So they may actually do some communication</p>\n"
}
] |
3,304 |
<p>Layman here. So I have never really quite understood this facet of human evolution, (or any other for that matter), in that, I understand the evolutionary process, but I get lost on the 'border' cases. </p>
<p>For example, we, as humans, evolved from monkeys, (to use the colloquial term, I am not a biologist by any measure). </p>
<p>My question is, doesn't this mean that at some, discrete point, there had to have been a human, whose parents were not? If that is true, how does that work, in the sense that we now have species1 giving birth to species2. </p>
<p>If not, then how exactly does this border case work? The only other alternative I see, is that the borders are 'fuzzy', but then that necessarily means that the definition of a species is itself fuzzy, which I understand is not the case. </p>
<p>Thanks!</p>
|
[
{
"answer_id": 3305,
"pm_score": 6,
"text": "<p>Actually, your last paragraph is more the case than not.</p>\n\n<p><strong>There are currently three common definitions for delineating discrete species:</strong></p>\n\n<p>1) Phenotypically different from related species (looks or acts differently).</p>\n\n<p>2) Produces viable offspring in the wild.</p>\n\n<p>3) Some % of genetic difference.</p>\n\n<p><strong>There are strengths to all three:</strong></p>\n\n<p>1) Very easy to ascertain and measure.</p>\n\n<p>2) Most common conception of a species.</p>\n\n<p>3) Genes control the first two, so genetic divergence gets to the heart of the matter.</p>\n\n<p><strong>There are also weaknesses to all three:</strong></p>\n\n<p>1) Is notorious for mis-labeling and missing species.</p>\n\n<p>2) Some species which can mate and produce fertile offspring under enclosed conditions do not do so in the wild (Tigers and Lions, for instance).</p>\n\n<p>3) The <em>amount</em> of divergence has, thus far, been completely arbitrary. If there is a certain % or patterns of mutation required in the genome, science hasn't yet discovered it.</p>\n\n<p>The fuzzy definition of species, combined in the not-exactly-intuitive generational-type thinking required for understanding evolution, and the answer to your question is (at least to the best of my understanding) the following:</p>\n\n<p>Yes, at some point one of our ancestors gave birth to the first <em>Homo sapien</em> that was somehow genetically different from its parents. However, the magnitude of the difference is probably not as great as you might think. </p>\n\n<p>We've already observed our closest evolutionary cousins, the Bonobos, making basic tools through flint napping: <a href=\"http://www.newscientist.com/article/dn22197-bonobo-genius-makes-stone-tools-like-early-humans-did.html\">http://www.newscientist.com/article/dn22197-bonobo-genius-makes-stone-tools-like-early-humans-did.html</a></p>\n\n<p>It's also possible that disputes between male chimpanzees are mediated by an older female: <a href=\"http://www.cpradr.org/Resources/ALLCPRArticles/tabid/265/ID/121/Primates-and-Me-Web.aspx\">http://www.cpradr.org/Resources/ALLCPRArticles/tabid/265/ID/121/Primates-and-Me-Web.aspx</a></p>\n\n<p>And that both Chimpanzees and Capuchin monkeys can be taught the concept of currency (which, somewhat comedically, they then used for prostitution): <a href=\"http://www.nytimes.com/2005/06/05/magazine/05FREAK.html?ei=5090&en=af2d9755a2c32ba8&ex=1275624000&partner=rssuserland&emc=rss&adxnnlx=1118160068-1EGJuan4FJH1LooxHYd5/g&pagewanted=all\">http://www.nytimes.com/2005/06/05/magazine/05FREAK.html?ei=5090&en=af2d9755a2c32ba8&ex=1275624000&partner=rssuserland&emc=rss&adxnnlx=1118160068-1EGJuan4FJH1LooxHYd5/g&pagewanted=all</a></p>\n\n<p>Then there's the everlasting impact of Koko, the Silverback Gorilla who was taught - and perfectly capable of replying in - sign language: <a href=\"http://en.wikipedia.org/wiki/Koko_%28gorilla%29\">http://en.wikipedia.org/wiki/Koko_%28gorilla%29</a></p>\n\n<p>The idea that humans jumped onto the scene with unforeseen amounts of intelligence and capability probably isn't what happened. Obviously we are capable of constructing and using the most advanced tools on the planet, but this is after several thousand generations of innovation. The very first human might have been more intelligent (or at least had the capacity to be), but otherwise probably fit in pretty well with its parents and other relatives since the <em>vast majority</em> of what we learn comes from our parents and personal experience.</p>\n\n<p>Then over time the number of individuals with the capacity for higher modes of thinking increased as a result of the genetic inheritance of whatever mutation created the first human. The first human, to put it simply, was successfully able to pass on their mutation which gave them our unique traits, and their offspring were also successful - until you have an entire population of humans living amongst each other. Eventually our innovative capacity lead, step by step, to our dominant position on the planet.</p>\n\n<p>Even now humans are yet evolving. Lactose tolerance (the ability to consume dairy products after childhood) is a <em>very</em> new trait among humans (and unprecedented among all mammals) only a few hundred generations old (roughly 10,000 years) that evolved <strong>twice</strong> in separate populations of humans (North Africa and Northern Europe). Our jaws are getting progressively smaller (which is why some people have to remove their wisdom teeth to maintain a straight smile - and some people don't have wisdom teeth at all), some muscles are disappearing (the Palmaris Longus is one example - it's present in about 80% of humans), and other subtle changes are occurring. </p>\n\n<p>Just don't make the mistake of equating \"evolved\" with \"superior.\" Evolution is dictated by the ever-changing demands of the environments we find ourselves in, and what's beneficial today isn't guaranteed to be beneficial forever. </p>\n"
}
] |
[
{
"answer_id": 3306,
"pm_score": 5,
"text": "<blockquote>\n <p>but I get lost on the 'border' cases.</p>\n</blockquote>\n\n<p>Not surprisingly, since there are no borders, and this is probably the greatest misunderstanding: Evolution is gradual. It’s not generally possible to say where a complex feature (or a species) starts and another one ends. We <em>could</em> in theory say, for individual mutations on the genetic level, in which generation they first occurred, or when they became fixed in the population. But we cannot infer from these atomic changes where our ancestors started becoming humans. So the whole concept of “first human” is not biologically meaningful.</p>\n\n<p>The best analogy remains a gradient between two colours. Going from the left, where does blue end and red start?</p>\n\n<p><img src=\"https://i.stack.imgur.com/3ltqb.png\" alt=\"Colour gradient\"></p>\n\n<p>By the way, you spotted this very well by yourself:</p>\n\n<blockquote>\n <p>[if there is no first human] then that necessarily means that the definition of a species is itself fuzzy</p>\n</blockquote>\n\n<p>Exactly, that’s the case. For more details on definitions of species, refer to MCM’s answer. But it’s indeed crucial to note that the definition of species (or any other biological classification) is an ever-changing approximation which tries to fit a definitive yes/no answer onto a gradually changing scale.</p>\n"
},
{
"answer_id": 3311,
"pm_score": 1,
"text": "<p>While the definition of species certainly is fuzzy, the process of species generation is easily defined: <strong>migration</strong> of a population part leads to two <strong>geographically isolated gene pools</strong> which do not communicate genetic information. Both pools will, through <strong>genetic drift</strong> (mutations/inserts/deletions), develop away from each other to the point that, if they were to meet again, they could no longer produce offspring with each other. Voilà, a new species.</p>\n"
},
{
"answer_id": 3313,
"pm_score": 3,
"text": "<p>I'd just like to expand on Konrad and MCM's answers. If I understand you correctly, your main question is \"what were the 1st human's parents\". You cannot really get an answer to that because the question itself is wrong. </p>\n\n<p>The idea that evolution moves in discrete bounds, that is that <a href=\"https://en.wikipedia.org/wiki/Speciation\" rel=\"nofollow\">speciation</a> occurs suddenly, from one generation to the next (also known as <a href=\"https://en.wikipedia.org/wiki/Lamarckism\" rel=\"nofollow\">Lamarckian evolution</a>) has been abandoned years ago. That is simply not how evolution works (our modern knowledge of <a href=\"https://en.wikipedia.org/wiki/Epigenetics\" rel=\"nofollow\">epigenetics</a> notwithstanding). The color analogy given by Konrad is indeed a good one.</p>\n\n<p>So, there was never an individual 'proto human'. This is also the case for all other species. What you <em>do</em> get, usually, is that a change in a species' environment (e.g. temperature, atmospheric pH, the introduction of a new predator etc) causes a particular mutation, or set of mutations, to become advantageous.</p>\n\n<p>One has to remember that a <a href=\"https://en.wikipedia.org/wiki/Genome\" rel=\"nofollow\">genome</a> (an organism's genetic material, their DNA) is <em>not</em> stable. It is in fact extremely dynamic and constantly undergoing mutational changes. Most of these mutations are neutral, they do not affect the organism in any way. However, when an external change such as I mentioned before occurs, some of these mutations may become advantageous. </p>\n\n<p>Imagine a random mutation that causes an individual of a species to be more resistant to cold. If this occurs at the beginning of an ice age, that individual is more likely to reproduce, passing the mutation to its offspring. Over time, since the mutation-carriers are likelier to survive and reproduce, this mutation will spread across the population and become \"fixed\". </p>\n\n<p>At some point these changes accumulate past a certain <em>indefinable</em> point and we call a speciation event. This does not occur at the <em>individual</em> but at the <em>species</em> level. A good analogy here is the <a href=\"https://en.wikipedia.org/wiki/Sorites_paradox\" rel=\"nofollow\">sorites paradox</a>. How many stones does it take to make a pile?</p>\n\n<p>So, to sum up, <strong>humans did not evolve <em>from</em> monkeys</strong>. Humans <em>and</em> monkeys at some point shared a common ancestor. Then, over a long time period, successive changes caused the two species to diverge. That is not the same thing. The linear concept of evolution that has one species morphing into the next is one of the greatest misrepresentations of a scientific concept ever perpetrated by the media and inflicted upon the unsuspecting public. </p>\n"
},
{
"answer_id": 3314,
"pm_score": 3,
"text": "<p>There are a lot of good answers here, but let me try to streamline things a bit: @Konrad's analogy to the color spectrum is spot on - where does red begin in that spectrum? This is essentially your question - where in the continuum of generations does the <em>Homo sapiens</em> species begin?</p>\n\n<p>Just like our definition of color is imprecise (we usually can identify bright red and deep blue, but we cannot be sure about the shades in between), our definition of species is imprecise. We can identify a modern human and we could identify a far ancestor as such, but if we were presented with somebody from an intermediate generation, we could not confidently say if they are <em>Homo sapiens</em> or not.</p>\n\n<p>We could, arbitrarily, point to a particular individual and say it was the first human, but it would not have any scientific meaning.</p>\n"
},
{
"answer_id": 3323,
"pm_score": 4,
"text": "<blockquote>\n <p><a href=\"http://books.google.com.tr/books?id=rR9XPnaqvCMC&pg=PA308&lpg=PA308&dq=Ernst%20Mayr,%20distinguished%20elder%20statesman%20of%20twentieth-century%20evolution,%20has%20blamed%20the%20delusion%20of%20discontinuity%20%E2%80%94%20under%20its%20philosophical%20name%20of%20Essentialism%20%E2%80%94%20as%20the%20main%20reason%20why%20evolutionary%20understanding%20came%20so%20late%20in%20human%20history.&source=bl&ots=4QD7rcrxpk&sig=8AaXVIAvov9aDk4jKtIuSZTxQwk&hl=tr&redir_esc=y#v=onepage&q=Ernst%20Mayr,%20distinguished%20elder%20statesman%20of%20twentieth-century%20evolution,%20has%20blamed%20the%20delusion%20of%20discontinuity%20%E2%80%94%20under%20its%20philosophical%20name%20of%20Essentialism%20%E2%80%94%20as%20the%20main%20reason%20why%20evolutionary%20understanding%20came%20so%20late%20in%20human%20history.&f=false\" rel=\"nofollow noreferrer\">Ernst Mayr, distinguished elder statesman of twentieth-century\n evolution, has blamed the delusion of discontinuity — under its\n philosophical name of Essentialism — as the main reason why\n evolutionary understanding came so late in human history.</a> Plato, whose\n philosophy can be seen as the inspiration for Essentialism, believed\n that actual things are imperfect versions of an ideal archetype of\n their kind. Hanging somewhere in ideal space is an essential, perfect\n rabbit, which bears the same relation to a real rabbit as a\n mathematician’s perfect circle bears to a circle drawn in the dust. To\n this day many people are deeply imbued with the idea that sheep are\n sheep and goats are goats, and no species can ever give rise to\n another because to do so they’d have to change their ‘essence’.\n There is no such thing as essence.</p>\n</blockquote>\n\n<h2><img src=\"https://i.stack.imgur.com/OGqvi.jpg\" alt=\"enter image description here\"></h2>\n\n<blockquote>\n <p><a href=\"http://books.google.com.tr/books?id=rR9XPnaqvCMC&pg=PA310&lpg=PA310&dq=Actually%20it%20isn%E2%80%99t%20paradoxical%20to%20anybody%20but%20a%20dyed-in-the-wool%20essentialist.%20It%20is%20no%20more%20paradoxical%20than%20the%20statement%20that%20there%20is%20never%20a%20moment%20when%20a%20growing%20child%20ceases%20to%20be%20short%20and%20becomes%20tall.%20Or%20a%20kettle%20ceases%20to%20be%20cold%20and%20becomes%20hot.&source=bl&ots=4QD7rcrwlj&sig=bPXlGriqB6ne6cDjHt0eK31X66A&hl=tr&redir_esc=y#v=onepage&q=Actually%20it%20isn%E2%80%99t%20paradoxical%20to%20anybody%20but%20a%20dyed-in-the-wool%20essentialist.%20It%20is%20no%20more%20paradoxical%20than%20the%20statement%20that%20there%20is%20never%20a%20moment%20when%20a%20growing%20child%20ceases%20to%20be%20short%20and%20becomes%20tall.%20Or%20a%20kettle%20ceases%20to%20be%20cold%20and%20becomes%20hot.&f=false\" rel=\"nofollow noreferrer\">The barrier would not come suddenly.</a> There would never be a generation\n in which it made sense to say of an individual that he is Homo sapiens\n but his parents are Homo erectus. You can think of it as a paradox if\n you like, but there is no reason to think that any child was ever a\n member of a different species from its parents, even though the daisy\n chain of parents and children stretches back from humans to fish and\n beyond. <strong><em>Actually it isn’t paradoxical to anybody but a\n dyed-in-the-wool essentialist. It is no more paradoxical than the\n statement that there is never a moment when a growing child ceases to\n be short and becomes tall. Or a kettle ceases to be cold and becomes\n hot.</em></strong> The legal mind may find it necessary to impose a barrier\n between childhood and majority — the stroke of midnight on the\n eighteenth birthday, or whenever it is. But anyone can see that it is\n a (necessary for some purposes) fiction. If only more people could see\n that the same applies to when, say, a developing embryo becomes\n ‘human’.</p>\n</blockquote>\n\n<p><a href=\"http://t.co/RR0L23ld\">The Ancestor’s Tale</a> <a href=\"http://www.youtube.com/watch?v=j4ClZROoyNM&feature=player_embedded\" rel=\"nofollow noreferrer\">Richard Dawkins</a>, </p>\n"
},
{
"answer_id": 51958,
"pm_score": 2,
"text": "<p>The border is fuzzy.</p>\n\n<blockquote>\n <p>but then that necessarily means that the definition of a species is itself fuzzy, which I understand is not the case.</p>\n</blockquote>\n\n<p>The concept of species, <em>applied at one moment (or brief period) in time</em>, is (fairly) well-defined. It breaks down if you try to apply it over a stretch of millenia.</p>\n\n<p>The most commonly used definition of species is \"a population whose members are capable of interbreeding with each other\". (This was <a href=\"http://www.blackwellpublishing.com/ridley/a-z/biological_species_concept.asp\" rel=\"nofollow noreferrer\">Ernst Mayr's</a> definition.) So, take a group of humans and a group of chimpanzees. Humans can make babies with humans, and chimpanzees can make babies with chimpanzees. A human and a chimpanzee can't make a baby, even if they try. There's no fuzziness or ambiguity here. They're separate species.</p>\n\n<p>Yet we share a common ancestor. So some of our ancestors <em>could</em> mate with some of their ancestors. And the transition from that state of affairs to this one was fuzzy.</p>\n\n<p>(The sort of thing that might have happened is this. Once upon a time there was a population of chimp-ish creatures. Then, some of them ended up on the other side of a canyon and stayed there. Gradually, whether through genetic drift or local adaptation to slightly different conditions, they became sexually incompatible. This might have started off as simply behavioural - even if they met, they wouldn't find each other sexy - but eventually became more of a genomic, biochemical incompatibility, such that even if they did try to mate, either (earlier on) the baby would be sterile or (later on) nothing would come of it.)</p>\n\n<p><a href=\"https://i.stack.imgur.com/L8XxM.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/L8XxM.jpg\" alt=\"enter image description here\"></a></p>\n\n<p>Actually, there are indeed fuzzy cases where this species concept isn't perfect, even when applied contemporarily. A fun one is this picture. There's a horseshoe-shaped mountain range, with salamanders that live on it. Salamanders in the green bit can't mate with salamanders in the purple bit. But they can mate with salamanders in the yellow bit; and yellow can mate with red; and red can mate with magenta; and <em>magenta</em> can mate with purple. So are all these salamanders a \"population capable of interbreeding\", or not? And how many species are they?</p>\n\n<p>(There's a fun chapter about these salamanders in Richard Dawkins' <em>The Ancestor's Tale</em>, making the point about fuzziness.)</p>\n"
}
] |
3,315 |
<p><a href="http://en.wikipedia.org/wiki/Hijra_%28South_Asia%29" rel="nofollow">Hijra</a> are people who have a penis (not sure if sexually active) but look much like a female (perhaps for some feminine biological property). Wikipedia says they are <em>"physiological males who have feminine gender identity"</em></p>
<p>Also, I just came to know there are some more types of <a href="http://en.wikipedia.org/wiki/Third_gender" rel="nofollow">third gender</a> people.</p>
<p>Now, <strong>is there really any <em>BIOLOGICAL</em> third gender</strong> which cannot be categorized as male or female? Or its always possible to categorize them to male or female?</p>
|
[
{
"answer_id": 3317,
"pm_score": 5,
"text": "<p>When dealing with <em>humans</em>, there are only two <strong>Biological</strong> genders as defined by the presence or absence of the Y-Chromosome. If the Y-Chromosome is not present, or through some process gets totally deactivated, the human will appear and function as a Female.</p>\n\n<p>XX = Female</p>\n\n<p>XY = Male</p>\n\n<p>XXY = Male (Klinefelter's Syndrome)</p>\n\n<p>XYY = Male (Aneuploidy - Normal Functioning Males)</p>\n\n<p>XXX = Female (Aneuploidy - Normal Functioning Females)</p>\n\n<p>X = Female (Turner's Syndrome - Generally infertile, other issues)</p>\n\n<p>Y = Fatal (The Y-Chromosome is drastically smaller than the X-Chromosome, which contains many <em>necessary</em> genes)</p>\n\n<p>XXYY = Male</p>\n\n<p>...</p>\n\n<p>The list goes on, since there have been records of up to XXXXX.</p>\n\n<p>If there is a Y-Chromosome present, the human born will be male.</p>\n\n<p>However, that is not to say that a person cannot <strong>psychologically</strong> identify as something else. It's also worth noting that the majority of known species are asexual and do not have genders, and that those which do have genders do not always follow the same rules (Fruit Flies, for instance, use the <em>ratio</em> of genes to determine sex).</p>\n"
}
] |
[
{
"answer_id": 3318,
"pm_score": 0,
"text": "<p>As I read the Wikipedia article you reference, its useful to remember that conventional chromosomal definitions of gender, the genitals are soft tissue which has many recorded morphological abnormalities. <a href=\"http://en.wikipedia.org/wiki/Hermaphrodite#Humans\" rel=\"nofollow\">hermaphrodites</a> and a <a href=\"http://en.wikipedia.org/wiki/Intersex\" rel=\"nofollow\">spectrum of tissue shapes do occur</a> to the extent that the conventional gender identity is not acceptable. </p>\n\n<p>Physiological definition of gender, despite the chromosomes do need to be medically and socially addressed. I am not sure that all these 'intersex' people really should be grouped into a single 'third sex', but some way of recognizing their essential human rights should be out there in my opinion. </p>\n"
},
{
"answer_id": 3337,
"pm_score": 4,
"text": "<p>I think you might be confusing <em>sex</em> and <em>gender</em>. The terms are often used interchangeably, but strictly speaking, they have different biological meanings. <a href=\"http://en.wikipedia.org/wiki/Sex\">Sex</a> refers to the biological categorization based on genetics, reproductive organs, or similar things, whereas <a href=\"http://en.wikipedia.org/wiki/Gender\">gender</a> is based on social identity.</p>\n\n<p>For humans, there are only two sex chromosomes, X and Y, and they determine the male and female sexes. But there are many situations that don't fall under the XX/XY categorization, and people with these conditions are usually referred to as <a href=\"http://en.wikipedia.org/wiki/Intersex\">intersex</a>. These can include conditions such as congenital adrenal hyperplasia, androgen insensitivity syndrome, and 5-alpha-reductase deficiency. So in short, there is no biological third <em>sex</em>, but that doesn't mean you can always categorize a person as biologically male or female.</p>\n\n<p>As you quoted, the hijira are usually physiologically male but have a different <em>gender</em> identity.</p>\n"
},
{
"answer_id": 14452,
"pm_score": 0,
"text": "<p>Adding to @MCM answer, there are also chromosomal crossover that might happen between non homologous. You can have some of the genes of Y chromosome going to X chromosome or elsewhere, for instance, further expanding the possibilities for different sexualities...</p>\n"
},
{
"answer_id": 38575,
"pm_score": -1,
"text": "<p>There is an actual third gender. That is true hermaphroditism. Some humans are true hermaphrodites. The most common cause of this? 2 eggs fusing, 1 male and 1 female before they start differentiation.</p>\n\n<p>These have both male and female characteristics and so they can't be classified as either male or female.</p>\n\n<p>Here is my source:</p>\n\n<p><a href=\"https://en.wikipedia.org/wiki/True_hermaphroditism\" rel=\"nofollow\">https://en.wikipedia.org/wiki/True_hermaphroditism</a></p>\n"
}
] |
3,365 |
<p>I have an AP Bio class where I have to name 3 properties of water and I chose adhesion and cohesion for one of them. I'm having trouble finding out how exactly trees use adhesion and cohesion to move water. There is a lot of different answers out there on the net. How do trees use adhesion and cohesion to move water against gravity?</p>
|
[
{
"answer_id": 3378,
"pm_score": 4,
"text": "<p>In high school, we did an experiment that showed this.</p>\n\n<p>Basically, if you take a glass of water, and let it sit out, perhaps in front of an open window, it will eventually lose water due to evaporation. It may take a few days/weeks to really see a large difference, but the level will go down. But, if you take a few flexible straws, put them in so the bendy part is submerged, the water level will drop much more quickly. (I'm not exactly sure if the bendy straw part is really that important here. Logically, I don't think it is, but I haven't done the experiment so I can't really say.)</p>\n\n<p>The reason the straws cause evaporation to happen more quickly is because as wind blows across the top of the straws, it pulls some of the water with it. And because, as the last person said, of cohesion and adhesion, the column of water is pulled up with it and thus it evaporates faster.</p>\n\n<p>Similarly, these fluid mechanics are why toilets and siphoning work. When you siphon, you create a low pressure area inside the tube, like you are sucking out of a straw. Because of this low pressure, liquid is pulled into the tube. If you fill the tube with liquid, and turn the tube down toward the ground so the liquid starts coming out the end, the force of the liquid coming out of the tube creates low pressure in the tube again, thus causing more liquid to be sucked up.</p>\n\n<p>This is very similar to how trees work. In the stomata, or the pores in the leaves that allow the leaves to \"breathe,\" wind helps to pull the water out of the pores. But because of the decrease in pressure cause by the liquid being sucked out of the pore, water gets pulled up the tubes in the tree (xylem).</p>\n"
}
] |
[
{
"answer_id": 3367,
"pm_score": 3,
"text": "<p>The mechanism is called \"capillary action\". It requires a tube of a small diameter and happens because of the adhesion of water to the walls and the cohesion within the water (=surface tension).</p>\n"
},
{
"answer_id": 60862,
"pm_score": 0,
"text": "<p>I don't buy this explanation. Trees don't have leaves in early spring and water comes up the tree with no problem. Also, if water was put under enough pressure to get sucked up a hundred feet, it would have so much heat that it would become steam. It's why buildings that are super high need pumps every so often to get it to go up. </p>\n\n<p>I have a theory. In a tree you have different parts of the trunk. Heart wood, sap wood, cambium layer, and bark. I think because the heart wood and bark aren't taking up water, they aren't expanding like the sap wood is. The cambium layer is very slippery and let's the tension between the bark and sapwood to slip past each other. I think the expanding sapwood eventually gets squeezed and osmosis does the rest.</p>\n"
},
{
"answer_id": 68208,
"pm_score": 0,
"text": "<p>Trees don’t use either adhesion or cohesion to move water against gravity.\nIt is impossible to “suck” above 10.3 m, which is equal to our atmospheric pressure.\nAir Pressure is pushing up the xylem Micro-tubes - which have a lower pressure / vacuum at the top (created be evaporation from the leaf).\nThis “siphon effect” is powered by Air Pressure, pushing up a closed tube.</p>\n"
},
{
"answer_id": 78768,
"pm_score": 0,
"text": "<p>It has to do with heat transfer and Newton's Law of thermodynamics. Matter that is heated will always travel to a cooler location. The roots are like a sponge, soaking up water from the ground. The water moving through the capillaries causes friction = heat, These heated water molecules collide with carbon atoms and form CO2, which is expelled trough the leaves in summer, but is negligible in winter. </p>\n"
},
{
"answer_id": 80733,
"pm_score": 0,
"text": "<p>I somehow discovered that in some trees with thin bark, I could place my ear on the bark and hear the movement of the water in the tree. It was not a continuous flow, but with hesitations like spurts or pauses. I thought there might be a valve system to keep the water from coming back down. But by saying it was pulled up by evaporation from the leaves, I can't explain the pauses.</p>\n"
}
] |
3,427 |
<p>I've recently seen the term <em>synthetic biology</em> being used to describe research involving genetic modification of organisms. What is the difference between <em>synthetic biology</em> and <em>genetic engineering</em>?</p>
<p>Is it just a new term for the same thing, or is it something different? Does one of the two terms encompass the other?</p>
|
[
{
"answer_id": 3434,
"pm_score": 4,
"text": "<p>My understanding is that synthetic biology is genetic engineering 2.0. The difference is in the approach. Whereas genetic engineering projects are usually ad hoc, synthetic biology aims to apply proper engineering principles such as standardisation, modularisation, and reusability. Synthetic biologists create and use libraries of standard parts that are characterised, so they can be easily reused in projects. A part could be a gene, a terminator, a promoter, etc. </p>\n\n<p>Synthetic biology also has greater ambitions. The focus is on creating whole systems/circuits of genetic regulation. This means there is a need for computational modelling and understanding of how biological systems work. In this aspect synthetic biology is a sister of systems biology a bit like synthetic chemistry (engineering) is a sister of chemistry (science).</p>\n\n<p>You could of course argue that it's just a marketing ploy to invent a new name for something that is just the next step in genetic engineering, but the differences in approach are quite large and a new name signifies it.</p>\n\n<p>With regards to synthesised vs. PCRed DNA: It doesn't really matter which you use in synthetic biology. However, cheap synthesis is one of the technologies that enable easier synthetic biology. The idea for the future is that you will be able to synthesise whole plasmids and chromosomes instead of having to \"cut and paste\" DNA. When that happens physical parts repositories will be obsolete, but they will remain crucial <em>in silico</em>. Cheap synthesis is nice, but doesn't make or brake synthetic biology.</p>\n"
}
] |
[
{
"answer_id": 3428,
"pm_score": 2,
"text": "<p>In genetics engineering we use and manipulate natural genetic elements but in synthetic biology we make new gene elements and network.</p>\n"
},
{
"answer_id": 3429,
"pm_score": 3,
"text": "<p>It seems to me that the difference is mainly semantic, although the aims of synthetic biology are undoubtedly more ambitious than those of genetic engineering in, say, the 80s and 90s.</p>\n\n<p>The Wikipedia page on <a href=\"https://en.wikipedia.org/wiki/Genetic_engineering\">genetic engineering</a> has this definition of the difference: </p>\n\n<blockquote>\n <p>Synthetic biology is an emerging discipline that takes genetic engineering a step further by introducing artificially synthesized genetic material from raw materials into an organism.</p>\n</blockquote>\n\n<p>I must say that for me this doesn't really stand up to close scrutiny. To give just just one example from my own experience - for a long time now yeast geneticists have used PCR to make DNA for targetted gene disruption. This seems to me to fit the definition in the quote: the primers were made chemically and the PCR product was made in vitro using dNTPs as raw materials. (Admittedly the template DNA would be normally produced in vivo.) But I don't think we ever thought that we were doing synthetic biology.</p>\n\n<p>Perhaps the term <em>synthetic biology</em> was intended to herald a new approach that would be more fundable?</p>\n\n<p>I look forward to reading the responses to this rather cynical answer :)</p>\n"
},
{
"answer_id": 3431,
"pm_score": 3,
"text": "<p>They seem to be practically the same, with the exception of the goals. <em>Genetic Engineering</em> is the direct modification of the genes of an organism which results in capabilities being added or taken away. <em>Synthetic Biology</em> aims to modify the behaviors of an organism or integrate the behaviors of multiple organisms into a singular whole.</p>\n\n<p>As is explained in <a href=\"http://dx.doi.org/10.1038/msb4100073\" rel=\"nofollow\"> <strong>Andrianantoandro E, Basu S, Karig DK, Weiss R</strong>. 2006. Synthetic biology: new engineering rules for an emerging discipline. Molecular systems biology 2: 2006.0028</a>:</p>\n\n<blockquote>\n <p>One useful analogy to conceptualize both the goal and methods of synthetic biology is the computer engineering hierarchy (<a href=\"http://www.nature.com/msb/journal/v2/n1/fig_tab/msb4100073_F1.html\" rel=\"nofollow\">Figure 1</a>). Within the hierarchy, every constituent part is embedded in a more complex system that provides its context. Design of new behavior occurs with the top of the hierarchy in mind but is implemented bottom-up. At the bottom of the hierarchy are DNA, RNA, proteins, and metabolites (including lipids and carbohydrates, amino acids, and nucleotides), analogous to the physical layer of transistors, capacitors, and resistors in computer engineering. The next layer, the device layer, comprises biochemical reactions that regulate the flow of information and manipulate physical processes, equivalent to engineered logic gates that perform computations in a computer. At the module layer, the synthetic biologist uses a diverse library of biological devices to assemble complex pathways that function like integrated circuits. <strong>The connection of these modules to each other and their integration into host cells allows the synthetic biologist to extend or modify the behavior of cells in a programmatic fashion.</strong> </p>\n</blockquote>\n"
},
{
"answer_id": 3490,
"pm_score": 2,
"text": "<p>In general:</p>\n\n<p>genetic engineering = cutting and pasting existing DNA extracted from organisms</p>\n\n<p>synthetic biology = chemically synthesizing DNA from scratch, which is used to create new genes and constructs from scratch. The synthetic sequences may not exist or may exist in nature.</p>\n"
},
{
"answer_id": 81482,
"pm_score": 0,
"text": "<p>I am not a big fan of definitions and terminology in molecular biology, because biology is not physics, and things that we might describe and define change, as does our understanding of them. However, as this question has surfaced again after a number of years, it might be worthwhile giving a more recent example of synthetic biology, rather than just defining it. That way the reader can get an idea of what it is about.</p>\n\n<p>I would say that:</p>\n\n<blockquote>\n <p>Synthetic biology is a particular type of genetic engineering.</p>\n</blockquote>\n\n<p><strong>Definitions</strong></p>\n\n<p>A reasonable definition of <strong>genetic engineering</strong> is given by <a href=\"https://www.britannica.com/science/genetic-engineering\" rel=\"nofollow noreferrer\">Encyclopedia Britannica</a>:</p>\n\n<blockquote>\n <p>The artificial manipulation, modification, and recombination of DNA or\n other nucleic acid molecules in order to modify an organism or\n population of organisms.</p>\n</blockquote>\n\n<p>So this could include making a single base change to inactivate a gene or introducing and expressing the gene for human insulin in, say, yeast.</p>\n\n<p>The definitions of <strong>synthetic biology</strong> are more contorted, e.g. that from the <a href=\"http://www.synbioproject.org/topics/synbio101/definition/\" rel=\"nofollow noreferrer\">Royal Society</a></p>\n\n<blockquote>\n <p>Synthetic biology is an emerging area of research that can broadly be\n described as the design and construction of novel artificial\n biological pathways, organisms or devices, or the redesign of existing\n natural biological systems.</p>\n</blockquote>\n\n<p><strong>Example</strong></p>\n\n<p>So why is the expression of insulin in yeast not considered synthetic biology? Basically because it lacks the complexity of a completely novel system. Consider the following <a href=\"https://cosmosmagazine.com/biology/life-2-0-inside-the-synthetic-biology-revolution\" rel=\"nofollow noreferrer\">description</a> of an <strong>arsenic biosensor</strong> designed to test for arsenic in drinking water:</p>\n\n<blockquote>\n <p>“Chris French at Edinburgh University led a team that turned the E.\n coli bacterium into an arsenic sensor by rewiring two genes. One gene\n senses arsenic and activates genes to pump it out of the cell; the\n other allows the bacteria to digest the sugar lactose, producing\n lactic acid. The rewiring involves putting the gene for digesting\n lactose under the control of the arsenic sensor. When arsenic is\n detected, the lactose-digesting gene switches on. The lactic acid it\n produces makes the water more acidic, which can be detected using a\n cheap pH indicator: if the reading is blue, the water is safe; yellow\n means it is dangerous.”</p>\n</blockquote>\n\n<p>So they have engineered a completely new system with two different genes, which have been modified and their regulation co-ordinated (“rewired” in the article) in an original manner. And there is a tendency to embody some of the complexity into modules that can be reused by others allowing even more complex and sophisticated systems to be constructed.</p>\n\n<p>You could say that the difference from insulin expression in yeast is only a matter of degree, but here the devil is really in the detail.</p>\n"
}
] |
5,007 |
<p>I would like to know if evolution is continuing to happen in modern humans, assuming things like existence of the nuclear family structure, fidelity to one partner, etc. It seems to me the answer would be NO because evolution depends on differential reproductive rates, but in the modern world, all male humans have roughly 2.5 (or whatever the number) kids. Add in the process of culturally modified selection pressure, and it seems to me that even an "unfit" male would end up having a couple of offspring. The fittest male (or female) is no better off than his or her contemporaries because of this "leveling" effect. </p>
<p>However, the impression I get from the popular science media is that scientists think evolution is continuing to happen. I would like to know what the actual scientific consensus is, and why. Thanks. </p>
|
[
{
"answer_id": 5008,
"pm_score": 6,
"text": "<p>It is certainly not true that \"all male humans have roughly 2.5 (or whatever the number) kids\". First of all, male and female humans have <em>exactly</em> the same reproductive rate. For obvious reasons, every time a male has offspring, a female must have had also. Last I checked neither male nor female humans are capable of <a href=\"https://en.wikipedia.org/wiki/Parthenogenesis\" rel=\"nofollow\">parthenogenesis</a> (certain popular religious beliefs notwithstanding).</p>\n\n<p>Second, let's assume that the 2.5 number is correct. That would be the <em>average</em> number of children per couple. That does not mean that all couples will have 2.5, or even that <em>most</em> couples will have 2.5. It just means that the <em>average</em> will be 2.5. If, for example you have one couple with 6 children, one with 2 and two with 1, the average will be (6+2+1+1)/(1+1+2)= 2.5. </p>\n\n<p>On to the main point. What does selection mean? In its simplest form, that the individual most likely to survive (the famous \"fittest\") is also most likely to reproduce. This is a very simple concept, the longer you live the higher your chances of managing to have offspring. If you die two weeks after birth it is going to be hard to manage to reproduce yourself. This has not changed. </p>\n\n<p>So, what does \"fitness\" mean? It can mean many things. If you are a warm blooded creature at the beginning of an ice age for example, it could mean being better at regulating your temperature than your peers. If you are a 21st century human, it could mean being funnier on twitter than your peers. The two are not fundamentally different. They can both be selected for or against. As long as one mate is chosen over another, selection is happening and the \"fittest\" (in each particular context) is most often selected. </p>\n\n<blockquote>\n <p>Add in the process of culturally modified selection pressure, and it\n seems to me that even an \"unfit\" male would end up having a couple of\n offspring. The fittest male (or female) is no better off than his or\n her contemporaries because of this \"leveling\" effect.</p>\n</blockquote>\n\n<p>\"Culturally modified selection pressure\", as you call it, is still selection pressure. Cultural factors can change what it means to be \"the fittest\" but there is no objective gold standard of \"fitness\". While it may be true that in modern human society, different characteristics are selected for than was the case with early <em>Homo sapiens</em>, this does not mean that \"evolution is not occurring\". On the contrary, it is occurring but perhaps it is moving in a new direction. In fact, this is essentially a circular argument. By definition, \"fittest\" means most likely to survive and reproduce. It does not mean strongest or fastest or prettiest. It just means whoever is better at reproducing. If that happens to be those individuals who are best at square dancing, then it is they who are the fittest.</p>\n\n<p>Take the example of a modern human with diabetes. Medicine allows diabetics to lead fully productive and largely normal lives. So, perhaps diabetes is no longer a selective criterion. This does not mean that the diabetic cannot be selected for or against based on their fitness on other scales. </p>\n\n<p>Whatever the selective pressure, whatever it may be that defines a \"good mate\", if selection is present then so is evolution. The only way to remove a species from the process of selection would be to have <em>all</em> (or none) individuals of each and every generation reproducing at the same rate. This is clearly not the case with humans. Surely not everyone around you has, or will have, children? There you go, selection!</p>\n\n<hr>\n\n<p>UPDATE:</p>\n\n<p>In answer to your comment, yes indeed, in order for a selective pressure to make itself felt and affect phenotype (at the species level), it needs to be constant across several generations. However, even the absence of selective pressure affects evolution. As others have mentioned below, active selection is not the only mechanism of evolution. </p>\n\n<p>Your main question however seems to be the following: If modern society (medicine etc) allows individuals that would not survive in the wild to reproduce, how does that affect evolution? The main points in my answer, and all others here, are:</p>\n\n<ol>\n<li><p>Even if we accept that modern humans have removed themselves from the purely \"biological fitness\"-based selection pressure (an assumption I am not at all sure is true), and assuming that this removal is constant enough over many generations (again unclear), even if all this is true, evolution is most certainly still occurring. It may even be faster since genotypes that would not survive in the wild persist in the gene pool, thereby increasing its diversity.</p></li>\n<li><p>As you point out in your comment below, for such social pressure to make itself felt, it needs to be constant across many generations. We are probably not there yet. </p></li>\n<li><p>Most importantly, as I said above, <strong>there is no such thing as an absolute biological fitness</strong>. When the ecosystem changes, so does the definition of fitness. Modern humanity's ecosystem, our habitat, is intimately connected with our culture and society. If an individual is better at reproducing in that context, then that individual <em>is</em> more fit. </p></li>\n</ol>\n"
}
] |
[
{
"answer_id": 5058,
"pm_score": 2,
"text": "<p>Darwin used the term “<em>descent with modification</em>” to describe evolution. That means <strong>a change between generations</strong> in the characteristics, or traits, of a population. It is a process which occurs by four processes - mutation, migration, drift, and selection. The conditions for evolution are <em>i)</em> a population must be able to reproduce, resulting in a descendant population, <em>ii)</em> offspring must tend to resemble their parents and this occurs because traits are determined by heritable information, e.g. DNA, and <em>iii)</em> that heritable information must have the potential to change from one generation to the next. <strong>It does not require selection</strong>.</p>\n\n<p><a href=\"https://i.stack.imgur.com/IZsJ4.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/IZsJ4.jpg\" alt=\"enter image description here\"></a></p>\n\n<p><a href=\"http://www.huli.group.shef.ac.uk/Milot.pdf\" rel=\"nofollow noreferrer\">Here is a paper about evolution and adaptation in humans:</a></p>\n\n<blockquote>\n <p>\"Despite popular misconceptions, natural selection does operate in\n modern human populations. New studies even show that changes\n associated with modernization are deeply reshaping selection pressures\n and, perhaps, bits of our biological nature.\"</p>\n</blockquote>\n\n<p><strong>Selection is still occurring in humans too</strong>, <a href=\"https://biology.stackexchange.com/questions/42050/if-evolution-is-not-about-improvement-why-is-there-so-much-improvement/42063#42063\">leading to further adaptation (a <em>subprocess</em> of evolution)</a> (e.g. <a href=\"http://www.pnas.org/content/109/21/8044.abstract\" rel=\"nofollow noreferrer\">here</a> and <a href=\"http://www.nature.com/nrg/journal/v11/n9/full/nrg2831.html\" rel=\"nofollow noreferrer\">here</a>). Many people naively think and suggest that selection has been halted in humans, the fact is, it hasn't. <strong>We still have variance in reproductive success based upon the genes individuals possess</strong>, e.g. some people die from genetic diseases before reproduction.</p>\n\n<hr>\n\n<p>Here are some illustrations describing the <strong>mechanisms of evolution</strong>. Note that drift and selection both cause variance in reproductive success among individuals in a population, for drift the variance is <em>independent</em> of the genes, while for selection it is a tendency for the carriers of one allele to have higher reproductive output than another.</p>\n\n<p><strong>Mutation:</strong>\n<a href=\"https://i.stack.imgur.com/a3bvT.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/a3bvT.jpg\" alt=\"enter image description here\"></a></p>\n\n<hr>\n\n<p><strong>Migration:</strong>\n<a href=\"https://i.stack.imgur.com/431yn.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/431yn.jpg\" alt=\"enter image description here\"></a></p>\n\n<hr>\n\n<p><strong>Drift:</strong>\n<a href=\"https://i.stack.imgur.com/BSffA.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/BSffA.jpg\" alt=\"enter image description here\"></a></p>\n\n<hr>\n\n<p><strong>Selection:</strong>\n<a href=\"https://i.stack.imgur.com/6XRIp.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/6XRIp.jpg\" alt=\"enter image description here\"></a></p>\n"
},
{
"answer_id": 5069,
"pm_score": 3,
"text": "<p>Evolution is defined as the change in the allele frequency of a population through time. In other words a change in the genetic diversity of the population through time. This change can be the result of 4 processes, known as the mechanisms of evolution:</p>\n\n<p>1) gene flow - this is the movement of individuals into or out of the population.</p>\n\n<p>2) genetic drift - this is the removal of individuals due to random events (such as accidents).</p>\n\n<p>3) mutation - this is the spontaneous change in the DNA, which instantly increases genetic diversity.</p>\n\n<p>4) selection (natural, sexual or artificial) - this is the increase in the frequency of alleles (traits) that confer a fitness advantage (i.e., those with a given trait will leave more offspring). Most adaptive changes in gene frequency are the result of selection.</p>\n\n<p>Even if one presumes that your analysis is correct and natural selection is no longer operating on modern humans (although this is suspect, as is pointed out by other answers), evolution would still be occurring due to mechanisms 1 - 3. If we go further and consider the Earth's human population as a whole (eliminating gene flow as a mechanism) you would still have evolution via genetic drift and mutation. </p>\n\n<p>In other words, yes, evolution is not only possible but inevitable in modern human populations.</p>\n"
},
{
"answer_id": 5073,
"pm_score": 3,
"text": "<p>In the US, different races have <a href=\"http://blogs.discovermagazine.com/gnxp/2010/09/which-american-racial-group-has-the-lowest-fertility/\" rel=\"nofollow\">significantly different birth rates</a>. Obviously race has a genetic component, though I'm guessing that the racial differences are mostly due to cultural and economic reasons. Still in this sense, the US population is evolving: alleles associated with some populations (African Americans, Hispanics) are becoming more common, while those associated to other populations (white non-hispanic, etc) are becoming less common. So the US is definitely evolving to become \"less white\". Note that this is true even though the overall birth rate reported in the study is not much above the minimal replacement rate of 2.0.</p>\n\n<p>Another example: <a href=\"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2723861/\" rel=\"nofollow\">religiosity is associated with increased fertility</a>, and there is some evidence that <a href=\"http://marginalrevolution.com/marginalrevolution/2011/02/genetic-factors-and-the-religious-life.html\" rel=\"nofollow\">religiosity has a genetic component</a>. In that sense, the population may be evolving to be more religious over time.</p>\n\n<p>Similarly, there are <a href=\"http://en.wikipedia.org/wiki/Genetics_of_obesity\" rel=\"nofollow\">genetic factors to obesity</a>, which has a <a href=\"http://www.sciencedaily.com/releases/2007/03/070307075723.htm\" rel=\"nofollow\">negative effect on fertility</a>. These genes may even have been actively selected for in the past (the thrifty genome hypothesis), but are probably being selected against now.</p>\n\n<p>We are currently undergoing one of the biggest shifts in human fertility in the history of our species: in the past century, we've developed technologies which allow people to more carefully choose when to become pregnant (condoms, abortions, hormone birth control). Any genetic factor which has an impact on use of birth control could lead to evolutionary changes: this could range anywhere from ethnicity associated with economic or religious status (poverty, Catholicism), impulse control, etc.</p>\n\n<p>This is all somewhat speculative (except for the first example), but it's certainly possible for evolution to occur in modern human society, and it likely is occurring.</p>\n"
},
{
"answer_id": 5182,
"pm_score": 1,
"text": "<p>Evolution is possible for the same reasons it has always been possible (and I'll let the other answers' details comment on the mechanics, as they have done already...</p>\n\n<p>I would like to offer a *slightly more philosophical point of view on the term, however. I think that we have arrived at a point in our evolution where our prefrontal cortex is impeding our biologically driven urges, somewhat (which would have us evolving in similar ways to all the creatures less aware of the consequence of their actions).</p>\n\n<p>I think it's impossible to say to what extent our evolution will now be driven by conscious choices we make about what traits we value vs. the traits that our biology drives us towards. Certainly innate biological drivers are incredibly powerful, but as is evidenced by our desire to promote our intellect, and our progressive urge to help even the sickly and mentally challenged to get the most out of life (up to and including procreating), rather than to evaluate our potential partners purely based on physical traits and our brute strength, these purely biological imperatives are governing our reproductive choices less and less.</p>\n\n<p>There is also much (reasonable) speculation as to what our new found understanding of genetics will allow us to artificially do to ourselves in the near future. </p>\n\n<p>I think it's important to consider both these factors when speculating about how we're evolving, but I think it's not even slightly controversial to suggest that we're definitely evolving in a different way now than we were 500k years ago. </p>\n"
},
{
"answer_id": 25887,
"pm_score": 2,
"text": "<p>Modern humans are continuing to evolve. Let me give you an example.</p>\n\n<p>Before cattle were domesticated over 99% of all adults were lactose-INtolerant (i.e., they did not produce the enzyme needed to break down lactose (lactase) and could not digest it, i.e. got diarrhoea if they drank milk). All infants produce this enzyme, but in lactose-intolerant people the gene that codes the enzyme responsible for breaking down lactose becomes suppressed after the age of 1 or so. Before domestication of cattle, lactose-intolerant people were by far the majority in any human population. Why? Because if you never consume milk, constantly producing an unneeded enzyme is a huge waste of protein, especially in conditions of limited food supply. With the domestication of cattle, people who could utilize lactose suddenly had a huge advantage - they had another source of protein and calcium. They quickly became bigger and stronger than people who could not consume dairy products in adulthood. Thus, people in Europe and Africa (where cattle were domesticated) quickly became lactose-tolerant, unlike people in Asia, where to this day most people are lactose-intolerant. The evolutionary pressure at that time was huge - people in Europe and Africa went from mostly lactose-intolerant to mostly lactose-tolerant in 10 000 years or so. Interestingly enough, in this respect cats evolved in parallel to humans and now cats in Europe are predominantly lactose-tolerant, whereas cats in Asia are mostly lactose-intolerant. </p>\n\n<p>Of course, this is not the only change that has occurred within the last 10 000 years and it surely is not the last one that will take place. It is just an illustrative (and hopefully interesting) example of evolution and natural selection in modern humans. In what direction humans will evolve in the future is very speculative.</p>\n\n<p>As requested, a couple of references: <a href=\"http://evolution.berkeley.edu/evolibrary/news/070401_lactose\" rel=\"nofollow\">http://evolution.berkeley.edu/evolibrary/news/070401_lactose</a></p>\n\n<p><a href=\"http://www.smithsonianmag.com/arts-culture/lactose-tolerance-and-human-evolution-56187902/?no-ist\" rel=\"nofollow\">http://www.smithsonianmag.com/arts-culture/lactose-tolerance-and-human-evolution-56187902/?no-ist</a></p>\n"
}
] |
5,148 |
<p>If a hermaphrodite animal (like slug, snail, etc) finds a partner they can mate immediately.</p>
<p>If another animal with "normal" reproduction (lets say a mouse) finds a partner they can only mate if they are opposite genders.</p>
<p>So it seems logical that the hermaphrodite way of reproduction is more successful than the "normal" way.</p>
<p>But it is not, as far as I know all higher developed species are using, the standard way of reproduction (male and female).</p>
<p>Why? What are the disadvantages of hermaphroditism?</p>
|
[
{
"answer_id": 5150,
"pm_score": 6,
"text": "<p>Firstly I'll clarify that you are talking about <em>simultaneous</em> hermaphrodites rather than <em>sequential</em> hermaphrodites (1st one sex, then the other e.g. the limpet Patella vulgata).</p>\n\n<p>It is perhaps easiest to address the question by countering it and asking why dioecy (2 sex systems/2 gonochoric types e.g. male and female) is better? As you have pointed out there are obvious advantages to being a hermaphroditic species such as more chance of mating - more likely to provide an advantage at very low population densities where interactions are infrequent.</p>\n\n<p>There are two key disadvantages of hermaphroditism which I will briefly cover but have been discussed in <a href=\"http://www.sciencedirect.com/science/article/pii/0022519377903630\" rel=\"noreferrer\">this paper</a> and probably other costs. </p>\n\n<p>The first is energy costs. Maintaining the capacity to produce male and female gametes will be more costly than maintaining one. This gives the hermaphrodite a fitness disadvantage because energy is rarely an infinite resource. Therefore at higher population densities, when mating opportunities are not rare, the gonochoric individuals will have a higher fitness because they have more energy. Monogamy is also analogous to rare encounters but true monogamy is rare (1 partner for life).</p>\n\n<p>The second disadvantage of hermaphroditism is self fertilisation. This will cause an increase in homozygosity and lead to inbreeding depression (reduced fitness).</p>\n\n<p>So you are right to some extent...</p>\n\n<blockquote>\n <p>the hermaphrodite way of reproduction is more successful than the\n \"normal\" way.</p>\n</blockquote>\n\n<p>...but the conditions which give rise to an hermaphroditic advantage are restricting. Overall, the above costs, combined with the obvious complexity of evolving the ability to produce male and female gametes, the ability to both fertilise and be fertilised, pregnancy and birth, and mating systems, mean that it is often more beneficial to be a dioecious species. Thus dioecy evolves.</p>\n\n<hr>\n\n<p><strong>EDIT: Question Raised by @Single_Digit</strong></p>\n\n<blockquote>\n <p>I have been pondering this question for a while and I get what RG255\n is saying. I'm just not sure I entirely buy it. Take earthworms, for\n example. They are simultaneous true hermaphrodites (as far as I\n understand). The anatomy doesn't have to be that complex*. They simply\n have two genital openings (one for eggs and one for sperm) and they\n line up in a \"69\" (excuse the vulgarity) position. This should, in\n theory, minimize the inbreeding depression. However, it doesn't\n eliminate the maintenance of two sets of reproductive systems. But\n most organisms are not internally fertilized mammals with wildly\n complicated systems of internalized embryonic care. Most species lay a\n pile of eggs that a male squirts sperm on or squirt eggs while the\n male squirt sperm and then they hope for the best.</p>\n \n <p>I would think the advantages of simultaneous parenting (after all,\n many MANY species' males don't provide much in the way of child care)\n and its fitness advantage would vastly outweigh the burden of a second\n set of reproductive organs.</p>\n \n <p>With that said, I don't have a better explanation, but I find the\n question a very interesting one. The linked article is pay-walled,\n aside from the abstract, but I still disagree with some of its tenets.\n To me true hermaphroditism should be very common (I realize it isn't)\n in species that don't need two parents to raise offspring, but do\n benefit from some (as in one parent's) parental care. I recognize that\n it would do little to help species that merely dump gametes and leave\n because specialization of one reproductive system would likely do the\n job better and both genders equally contribute under that type of\n system.</p>\n \n <p>So, RG255 convince me! Clearly there are good reasons, since gender\n (or asexual repr) is the norm, but I need more/better evidence.</p>\n \n <ul>\n <li><ul>\n <li>Yes I realize they would need separate internal anatomies for each type of gamete, but still...</li>\n </ul></li>\n </ul>\n</blockquote>\n\n<p><strong>My response:</strong></p>\n\n<blockquote>\n <p>You have presented one example of hermaphroditism and used that as\n evidence that all species should be hermaphrodites. Earthworms are\n small slow creatures living in soil, I don't imagine they have high\n rates of encounter, and therefore low rates of encountering the\n opposite sex, therefore hermaphroditism would be favoured as discussed\n above. </p>\n \n <p>Further, you say most species are external fertilisers (do you\n have a reference for this?) and therefore it is not costly be a\n hermaphrodite. I don't see your logic there, the cost is not\n necessarily to do with the cost of bearing child, producing &\n maintaining the gonads and gametes is also a costly process. I would\n argue that this is extremely complex. This is not just on a\n morphological level but also physiological: in non-hermaphroditic\n species the sexes have very different, and often, conflicting gene\n expression and hormone production patterns. Hermaphrodites would not\n be able to optimize to the fulfilling both the male and female roles.</p>\n \n <p>Finally, you pointed out that the worms do not inbreed. Inbreeding\n avoidance does not have to be the cause of the hermaphroditism\n persisting, if the environment/other factors favour hermaphroditism. I\n never said that both were simultaneously necessary. </p>\n \n <p>I hope this\n clarifies it for you, if not please expand as to why, I am on here\n because I want to help people understand biology properly!</p>\n</blockquote>\n\n<p><strong>Further response from @single_digit:</strong></p>\n\n<blockquote>\n <p>Well fair enough about my external fertilizers comment. I don't have a\n reference, but I was thinking all multicellular life and I'd have to\n imagine that when you factor in plants, that external fertilization is\n relatively the norm (as is hermaphrodism (dioecy) for the plants). As\n to earthworms, I disagree about your description of them. Their\n densities are actually pretty high, so I'd wager they encounter each\n other frequently, so I'm not sure where that leaves them in terms of\n pressures for hermaphroditism. Your point on the physiologic/hormonal\n issues of maintaining the systems is one I haven't previously\n considered. I honestly don't have any clue as to how daunting (or\n simple) that is, but I'd imagine that the sophistication of the\n systems would play a pretty key role. Makes me wonder how much this\n has been researched in true hermaprhodites. I suppose the main thing I\n keep coming back to is the overwhelming disadvantage gender has in\n terms of potential to create offspring. Males in many (most?) species\n essentially act as little more than sperm donors, thus half the\n individuals have effectively zero fitness. That just seems like an\n overwhelming advantage for hermaphrodites.</p>\n</blockquote>\n\n<p><strong>My Response</strong></p>\n\n<blockquote>\n <p>Why do you consider half of the individuals to have zero fitness?\n Fitness is widely accepted as the number of offspring a parent\n produces because this is directly related to number of copies of their\n genes passed to the next generation. Sperm donor type males achieve\n increased fitness by mating as do females - with out the male they\n would never be fertilized. The key disadvantage of dioecy is the\n halved (assuming equal sex ratio) frequency of potential encounters\n that could lead to mating. The general disadvantages of\n hermaphroditism are inbreeding depression and high cost & complexity.</p>\n</blockquote>\n\n<p><strong>Single_digit:</strong></p>\n\n<blockquote>\n <p>Zero fitness isn't exactly correct, but if we look at parental care as\n conveying a survival advantage for K selected species, and huge\n numbers of offspring conveying an advantage for r-selected species\n (obviously the type of env affects this) does a deadbeat dad really\n optimize for either of these? Passing on genes is fine, but if\n offspring survival is low, does it matter? Does it simply boil down to\n the maintenance of two repr systems plus decreased fitness from\n inbreeding vs the increased reproductive success from extra child\n care? Or is there more?</p>\n</blockquote>\n\n<p><strong>My response:</strong></p>\n\n<blockquote>\n <p>r/K selection theory has generally been disregarded in the\n evolutionary biology community due to the substantial evidence against\n it so it is unhelpful to think of selection in this way. As long as\n the 2 sexes strategy is more successful at passing on genes than a\n hermaphroditic strategy it will (should) prevail. Dioecy will be more\n successful if the hermaphroditism introduces to much cost through\n production and maintenance of sexual organs/gamete and inbreeding\n whilst not attaining substantial gains from higher potential mating\n frequency.</p>\n</blockquote>\n\n<p><strong>@Single_Digit</strong></p>\n\n<blockquote>\n <p>Interesting about r/K selection. I hadn't heard that. Do you have any\n links? I'd be curious to learn more there. I incorrectly earlier made\n a comment about dioecy where I meant monecy. But this seems to beg the\n question, why is monecy/hermaphroditism so much more prevalent in\n plants? Obviously there are different survival pressures, but I'd\n think the same basic principles would apply as in animals, but the\n condition seems to be far more common than in animals.</p>\n</blockquote>\n\n<p><strong>My Response</strong></p>\n\n<blockquote>\n <p>I seem to remeber there being a reason in plants, don't\n have time to look it up right now. The work about r/K selection was\n Reznick/Stearns/Charlesworth. Reznicks is the most recent and more\n overview type paper - best place to start:\n <a href=\"http://www2.hawaii.edu/~taylor/z652/Reznicketal.pdf\" rel=\"noreferrer\">http://www2.hawaii.edu/~taylor/z652/Reznicketal.pdf</a></p>\n</blockquote>\n"
}
] |
[
{
"answer_id": 5347,
"pm_score": 1,
"text": "<p>I have been pondering this question for a while and I get what RG255 is saying. I'm just not sure I entirely buy it. Take earthworms, for example. They are simultaneous true hermaphrodites (as far as I understand). The anatomy doesn't have to be <em>that</em> complex*. They simply have two genital openings (one for eggs and one for sperm) and they line up in a \"69\" (excuse the vulgarity) position. This should, in theory, minimize the inbreeding depression. \nHowever, it doesn't eliminate the maintenance of two sets of reproductive systems. But most organisms are not internally fertilized mammals with wildly complicated systems of internalized embryonic care. Most species lay a pile of eggs that a male squirts sperm on or squirt eggs while the male squirt sperm and then they hope for the best.</p>\n\n<p>I would think the advantages of simultaneous parenting (after all, many MANY species' males don't provide much in the way of child care) and its fitness advantage would vastly outweigh the burden of a second set of reproductive organs. </p>\n\n<p>With that said, I don't have a better explanation, but I find the question a very interesting one. The linked article is pay-walled, aside from the abstract, but I still disagree with <em>some</em> of its tenets. To me true hermaphroditism should be very common (I realize it isn't) in species that don't need two parents to raise offspring, but <strong>do</strong> benefit from some (as in one parent's) parental care. I recognize that it would do little to help species that merely dump gametes and leave because specialization of one reproductive system would likely do the job better and both genders equally contribute under that type of system.</p>\n\n<p>So, RG255 convince me! Clearly there are good reasons, since gender (or asexual repr) is the norm, but I need more/better evidence.</p>\n\n<p>* - Yes I realize they would need separate internal anatomies for each type of gamete, but still...</p>\n\n<hr>\n\n<p>Well fair enough about my external fertilizers comment. I don't have a reference, but I was thinking all multicellular life and I'd have to imagine that when you factor in plants, that external fertilization is relatively the norm (as is hermaphrodism (dioecy) for the plants).\nAs to earthworms, I disagree about your description of them. Their densities are actually <a href=\"http://www.sciencedirect.com/science/article/pii/S0038071707001757\" rel=\"nofollow\">pretty high</a>, so I'd wager they encounter each other frequently, so I'm not sure where that leaves them in terms of pressures for hermaphroditism. </p>\n\n<p>Your point on the physiologic/hormonal issues of maintaining the systems is one I haven't previously considered. I honestly don't have any clue as to how daunting (or simple) that is, but I'd imagine that the sophistication of the systems would play a pretty key role. Makes me wonder how much this has been researched in true hermaprhodites. I suppose the main thing I keep coming back to is the overwhelming disadvantage gender has in terms of potential to create offspring. Males in many (most?) species essentially act as little more than sperm donors, thus half the individuals have effectively zero fitness. That just seems like an overwhelming advantage for hermaphrodites. </p>\n"
},
{
"answer_id": 8861,
"pm_score": 0,
"text": "<p>This is a bit expressed in an unclear way but I think it solves the problem.</p>\n\n<p>I think the reason is simply that if you have all the hermaphrodites being difficult about their mates they will evolve fast because the best mates will mate more and the worst won't mate a lot. But if the hermaphrodite individual is hard to get, it also won't be motivated to pursue sex and it will be hard for the 'best' individuals to mate more cause they will be too hard to get. So the requirement to impress while also being hard to get are contradictory in non differentiated individuals. In most animals, the difference in libido of the female versus that of the male can solve this paradox. One has to show they have good genetic material (the male) and the other just have to be hard to get. This is pretty shitty for females, but nature often is. I think the fitness of this difference almost disappears in monogamous species where both have an advantage if they are hard to get. So we can hope hermaphroditism is not an advantage only for an intermediary stage of evolution but can become one again in higher species. This would alleviate some of the sexual conflict.</p>\n"
},
{
"answer_id": 16098,
"pm_score": 2,
"text": "<p>I'm not at a biologist, but I have a pet theory I'd like to throw into the ring: hermaphroditism tends to be unstable in a similar way to strong sex skews. Imagine species A where 90% of offspring are female; at moderate population density, the 10% male population will be more than sufficient to maintain the females, and having 90% of the population able to breed will out-compete another species with a 50/50 distribution. However, a mutation which tends to produce more males will tend to become more common, because the males of species A reproduce much more often than the females. Eventually, this stabilizes at roughly equal frequencies for the sexes.</p>\n\n<p>Back to the hermaphroditic species C, imagine that a mutation led to a variant which had a flawed female reproductive system, meaning it could not lay as many eggs when fertilized, but it had some other advantage which made it better at mating: perhaps by diverting energy from the female systems, it was slightly larger and stronger and could intimidate others, or perhaps it put this energy into a stronger immune system. Eventually, the population evolving in this direction could lose its ability to lay eggs or birth young entirely, and instead focus entirely on being better at finding mates to impregnate.</p>\n\n<p>Looking at it from the other side, if some individuals de-prioritize that side of things and instead concentrate on being the best egg-layers and care-providers possible, that could be a stronger evolutionary position than trying to be equally good at both roles. Eventually, this split would produce recognizably male and female subgroups.</p>\n\n<p>If this idea has already been proposed and either taken seriously or shot down, I'd appreciate any pointers to further reading.</p>\n"
},
{
"answer_id": 57892,
"pm_score": 1,
"text": "<p>It's actually quite simple if you consider the following two points:\n1.Males only have to mate with TWO MORE individuals in each reproductive cycle to outcompete a hermaphrodite.\n2.mobility is important and this gives male-only animals a big advantage.</p>\n\n<p>I can't see anyone clearing expressing this already but apologies if someone has.\nSimple animals generally produce a lot of eggs to pass on their genes to as many offspring as possible. However this slows them down, when looking for a mate, in spending time laying their eggs, and in expended energy producing the eggs.\nIn such a hermaphroditic population, eventually a male will randomly evolve that doesn't bother to produce eggs. Providing that this gives it an advantage over its hermaphroditic counterparts, such that it can mate with at least two more egg-laying individuals in the time taken for the hermaphroditic version to produce and lay its eggs, then this male-only version will produce more offspring sharing its genes than the hermaphrodite would. This means that more of the next generation will also be male only. </p>\n\n<p>This ensures that males always exist (at least at some percentage of the population), as chances are they will mate with many more individuals than their slower hermaphroditic competitors and pass on their genes more successfully. Simple.</p>\n\n<p>(This is probably also the reason that most plants are hermaphroditic, as mobility is not a factor.)</p>\n"
},
{
"answer_id": 80154,
"pm_score": 0,
"text": "<p>The non-hermaphroditic sex systems I'm most familiar with arise from hermaphrodite populations. Suppose a male-only mutant arises, it can cheat the hermaphrodite system by putting its reproductive energy into the \"cheap\" sperm and fertilising many eggs, instead of sharing the energy burden of expensive eggs and cheap sperm. the male-only out-competes the hermaphrodites and so over generations this male-only trait spreads. the male + hermaphrodite population has an excess of males, selecting for any female-only mutant to do well. Suppose a mutant female-only arises. She Put all her energy into egg production, so there are more and/oor better eggs. A female-only outc-ompetes a hermaphodite if there is an EXCESS OF MALES. A female-only does less well than a hermaphrodite if there is a male/female balance</p>\n\n<p>So, in hermaphrodite species, we see avenues to the formation of a male-only and female-only subpopulation</p>\n"
},
{
"answer_id": 100788,
"pm_score": -1,
"text": "<p>The female & male organs compete against each other. A stud hermaphrodite has little incentive to have female organs. A human stud who can have 1000s of kids would be slowed down considerably if he\\it had to spend 9 months\\year being pregnant & raising infants & it's costly to maintain female organs.</p>\n"
}
] |
5,445 |
<p>From the moment we learn to communicate, we always get told, whether by our parents, or our teachers, or by anyone else, to avoid the cold, or to put a jacket on to avoid catching a cold, to dry our hair before we go outside, because we'll get sick otherwise, so on and so forth. I also was diagnosed with a pneumonia last year, while in Switzerland under chilly conditions ($-20^◦\text{C}$). This made me wonder, why does the cold make us sick? It doesn't seem logical to me that a viral infection like the common cold, or a viral/bacterial infection such as a pneumonia is more prevalent when it's colder outside. I always figured it was because our bodies are less 'effective' under cold temperatures, but this seems lacking to me. Can anyone explain? </p>
|
[
{
"answer_id": 5511,
"pm_score": 5,
"text": "<p>it does not, really. unless we're talking about things like frostbite or severe hypothermia.</p>\n<p>it's a myth that it does.\nthe virus is more stable in colder air, however.</p>\n<p>see more here:</p>\n<p><a href=\"http://www.nytimes.com/2007/12/05/health/research/05flu.html\" rel=\"noreferrer\">Study Shows Why the Flu Likes Winter</a></p>\n<p><a href=\"http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.0030151\" rel=\"noreferrer\">Influenza Virus Transmission Is Dependent on Relative Humidity and Temperature</a></p>\n<blockquote>\n<p>Innate responses proved to be comparable between animals housed at 5 °C and 20 °C, suggesting that cold temperature (5 °C) does not impair the innate immune response in this system.</p>\n</blockquote>\n"
}
] |
[
{
"answer_id": 5498,
"pm_score": -1,
"text": "<p>Most likely the energy to stay warm is not being used to fight infection. Also the virus is likely designed to operate with your respiratory system at a colder temperature more effective that the immune system is at that cooler temperature.</p>\n"
},
{
"answer_id": 5519,
"pm_score": 3,
"text": "<p>Cold weather makes your body use more energy for keeping warm and less energy for other activities. This is made at various levels: 1) modifications of the diameter of arteries changes the blood supply in specific regions\n2) In the electron transport chain, that is a metabolic pathway involved in producing energy after glycolis and Krebs cycle there is a disjunction between the electron transport chain and the oxidative phosphorylation caused by the production of thermogenin. This causes a minor production of ATP (energy available for metabolic processes) and dissipation of energy as heat.\nMoreover enzymes need a specific environment to work (ph and temperature). A cold weather can decrease the temperature of the body and reduce enzyme activity. When you are sick your body can use fever to stimulate enzymes and power immunitary system activity.\nMoreover cold weather causes a reduction of the movements of the cilia of the trachea, so dust and bacteria can enter into the respiratory system more easily. These are just a few examples. There may be others. I'm available for further discussion. </p>\n"
},
{
"answer_id": 6985,
"pm_score": 2,
"text": "<p>I think this site best answers the question:</p>\n\n<p><a href=\"http://dumbscientist.com/archives/cold-weather-can-make-you-sick\" rel=\"nofollow\">Cold Weather Can Make You Sick</a></p>\n\n<p>Here is a part:</p>\n\n<p>\"Professor Eccles explained this effect by saying that our bodies restrict blood flow to the extremities when we get cold to help conserve body heat for the torso and brain, which really need to be warm. Cutting off the blood flow reduces the supply of white blood cells which are the immune system’s primary weapon against germs.</p>\n\n<p>While his explanation makes sense, there may be a more general effect at work. The human body is a machine that accepts fuel in the form of food, and uses that fuel’s energy to keep us warm and to power our immune systems, muscles and brains. However, in frigid conditions our bodies have probably evolved to say “who cares if I might get sick a week later when I’m going to die of hypothermia in half an hour?”\"</p>\n"
},
{
"answer_id": 71362,
"pm_score": 2,
"text": "<p>From what I understand, the current top answer states that it is a myth that us being cold or warm has little to do with the likelihood to get sick. </p>\n\n<p>This cannot possibly be the compete answer, without even needing any additional science. Simply go outside, at times of equal temperature and humidity, with or without adequate clothing.</p>\n\n<p>Are you getting sick more easily being warm or freezing your butt off?</p>\n\n<p>That's an experiment anyone can do and has inadvertently done at some time. I have VERY strong data that your own body temperature has a HUGE effect on your likelihood to get sick, so the virus alone cannot be the complete answer. </p>\n\n<p>Constricted blood flow during times of cold might be a factor in this. There is data on this. </p>\n\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pubmed/6131011\" rel=\"nofollow noreferrer\">https://www.ncbi.nlm.nih.gov/pubmed/6131011</a></p>\n\n<p>But there are also studies that do confirm that the virus itself is adapted to cold. </p>\n\n<p><a href=\"http://www.pnas.org/content/112/3/827.full\" rel=\"nofollow noreferrer\">http://www.pnas.org/content/112/3/827.full</a></p>\n\n<p>The evolution of this virus might have been reciprocal actually. Other cells seem to divide better at higher temperatures. The interaction between animals, being more susceptible, due to their bodies conserving heat in winter, might have caused these particular pathogens to also adapt in reverse and to do better in colder weather.</p>\n\n<p>The complete answer whether it is our bodies or the cold temperature is probably \"both\".</p>\n"
}
] |
5,524 |
<p>Imagine humans were to colonize a distant planet and it was a single one-way trip. How many people would they need to bring?</p>
<p>Obviously 2 is the minimum, but that would result in a lot of inbreeding.</p>
<p>So what number is the minimum number of people you can have in an isolated community and still maintain a healthy diversity?</p>
|
[
{
"answer_id": 5526,
"pm_score": 6,
"text": "<p>Actually it is a very important question for laboratory animals (and, I imagine, endangered species) and was calculated to be 25 couples.</p>\n\n<p>With any number of animals (including humans), there is always some inbreeding happening, but you can reduce it with the number of breeding pairs and careful pairing. When you get to 25 pairs (50 animals) and have complete control over pairing, you can sustain the genetic diversity practically infinitely (especially if you take into account spontaneous mutations).</p>\n\n<p>Of course, such control over who can have children with who (plus whether one is at all allowed to procreate and what will be the sex of their children!) would be questionable morally, so in case of populating a distant planet, we would need a larger group, to provide for sexual preferences, fertility problems etc.</p>\n\n<p><a href=\"http://isogenic.info/html/outbred_stocks.html#definition\">Some information on laboratory outbred stocks.</a></p>\n"
}
] |
[
{
"answer_id": 15686,
"pm_score": -1,
"text": "<p>Inbreeding isn't negative at all, so one couple would suffice for colonization.</p>\n\n<p>Inbreeding fixes recessive traits and the ones displaying unwanted traits can be culled. Actually, inbreeding is one of the most potent weapons of evolution, it speeds things up greatly. We went through a major bottleneck event ourselves and lived to tell the tale.</p>\n\n<p>The exact number of individuals needed for a healthy species that will survive X number of generations depends on the species though. To maintain healthy genetic diversity and establish enough different alleles to allow for sustainability of the species. I don't remember the exact number but I think for humans it was something between 1000 or 10000, and if you get below that number the species will likely go extinct by natural causes.</p>\n\n<p>Of course, everything is completely different when you have full control over who mates with who. But still, in the above example of 1 couple, they can successfully start a seemingly healthy population, but due to low genetic diversity they - as a species - won't be able to respond to, say, increased radiation, changes in atmosphere, a virus, bacteria, shortage of food, etc. That's why 1 couple is basically enough, but to ensure longetivity of the species 25 couples is far from enough.</p>\n"
},
{
"answer_id": 53811,
"pm_score": -1,
"text": "<p>I'm not an expert, but after reading more about it I would say between 500 - 1500 couples without trying to control the pairing.</p>\n<p>I don't know where Dan Horvat took these assertion:</p>\n<blockquote>\n<p>To maintain healthy genetic diversity and establish enough different\nalleles to allow for sustainability of the species. I don't remember\nthe exact number but I think for humans it was something between 1000\nor 10000, and if you get below that number the species will likely go\nextinct by natural causes.</p>\n</blockquote>\n<p>but it seems to be supported by the evidence of past bottlenecks in human population, like the <a href=\"https://en.wikipedia.org/wiki/Toba_catastrophe_theory#Genetic_bottleneck_theory\" rel=\"nofollow noreferrer\">Toba Cathastrofe Theory</a>. The human population is supposed to had a maximum of 3,000–10,000 surviving individuals. I am very optimistic and take the minimum: 1500 couples. It left to match that amount with Dan's source.</p>\n<p>The exact answer would come by the designer of the life and DNA. ;-) That info seems to have been leaked by the creator's son in a conference. Thomas has taken <a href=\"http://gnosis.org/naghamm/gthlamb.html\" rel=\"nofollow noreferrer\">note</a> from his words:</p>\n<blockquote>\n<p>I shall choose you, one out of a thousand, and two out of ten\nthousand, and they shall stand as a single one.</p>\n</blockquote>\n<p>It seems to me that it is talking about genetic diversity, and the minimal proportions are those: 1/1000. That's why I take 500 couples as minimun.</p>\n<p>By the way, in the previuos versicle it seems to says that that selection would be in the moment when the human race has finally ended evolving to the intended social and morphological status (very rare indeed):</p>\n<blockquote>\n<p>When you make the two one, and when you make the inside like the\noutside and the outside like the inside, and the above like the below,\nand when you make the male and the female one and the same, so that\nthe male not be male nor the female female; and when you fashion eyes\nin the place of an eye, and a hand in place of a hand, and a foot in\nplace of a foot, and a likeness in place of a likeness; then will you\nenter the kingdom.</p>\n</blockquote>\n<p>Going back to science, it seems that not to much effort should be made to control the pairing, because we seem to have a subconcient attraction for those individuals of the other sex that present better <a href=\"https://en.wikipedia.org/wiki/Major_histocompatibility_complex_and_sexual_selection\" rel=\"nofollow noreferrer\">histocompatibility</a> with us. In the case of humans given by odor and appeareance (mostly simetry).</p>\n<p>Also the genetic diversity is supposed to be reached faster, if the environment is more aggresive. Normally a big mutation and adaptation happen after hostile and persistent environment over near 40 generations, something observed with the <a href=\"https://en.wikipedia.org/wiki/Peppered_moth_evolution\" rel=\"nofollow noreferrer\">Peppered moth evolution</a></p>\n<p>So I suppose that if you use well cared laboratory animals, the number can be 25 couples. But if you use a natural hostile enviroment the genetic diversity could be reached sooner.</p>\n<p>It might be that if you build a nice human space station in another planet, maybe you need 25 couples, but if you let them nude with no technology and fig leaves you need fewer couples in order the species to survive more adapted (Although you might got many failed attempts)</p>\n<p>Another point to consider, is how valuable are those animals for genetic studies?, how much is the study affected by the captivy of their population?, resembles their growing places the natural environment?, how hostile are these environment? resembles this environment the natural population dynamics ? how many generations ago their ancestors had a natural environment ?</p>\n<p>Laboratory animals might have less genetic diversity and might need more couples.</p>\n"
},
{
"answer_id": 69559,
"pm_score": -1,
"text": "<p>I think the issue of epigenetics throws this answer into debate once again. This reminds me of my biggest issue with the book <em>The Transhumanist Wager</em>, which was centered around a very Libertarian tenant of \"worth\". </p>\n\n<p>Without knowledge of the way in which every aspect of human genetics (including epigenetics) works, how can we possibly establish the \"worth\" of a given set of base allele, and thus determine minimum viable population? If such a bottleneck were forced (through disaster or \"choice\") would such a resultant population still be considered \"human\" by today's standards?</p>\n\n<p>I would say that Humanity must still be defined by more than the sum of our current knowledge of genetics.</p>\n\n<p>I believe these questions are something that are very often missing from the <em>debate</em> around The Singularity [establishing an artificial intelligence beyond the intelligence of humanity]. Most argue that such an event would be the end of humanity, but I disagree; as any intelligence created by humanity would not be so stupid as to destroy the diversity of intelligence that essentially established its baseline. In this line of thinking, personally I believe it would be more along the lines of the ideas presented in the movie <em>Her</em>, in which such Intelligence(s) would establish a way to remove themselves from direct human control, but ultimately observe/compare/contrast humanity as \"wild stock\" useful for error-correction, and a seperate line of modeling.</p>\n"
},
{
"answer_id": 76671,
"pm_score": -1,
"text": "<p>You only need a single female. The space ship could carry a database of genetic material in the form of frozen sperm and eggs. The first female would impregnate herself to breed and raise as many daughters as she can, using as much genetic variety as possible. The daughters would do the same once they can.</p>\n"
}
] |
5,588 |
<p>Mammals, reptiles, arachnids, insects, etc are all as far as I am aware symmetrical in appearance.</p>
<p>Take a human for instance, make a line from the top of our head right down the middle. However, internally it is not the same. Our organs <em>excluding</em> the kidneys, lungs, reproductive organs, etc are not symmetrically placed in our body.</p>
<ul>
<li>Why do we not have an even number of each organ so it can be placed symmetrically?</li>
<li>If we have a single organ why is it not placed in the middle like the brain or bladder is for instance?</li>
<li>Is there some evolutionary advantage that led to this setup?</li>
</ul>
|
[
{
"answer_id": 5601,
"pm_score": 6,
"text": "<p>First, I think it worthwhile considering 'Why would internal symmetry be beneficial?' Developmental simplicity jumps to mind immediately. You can also consider relationship to external organs; the stomach and esophagus are lined up with the mouth which is symmetrical about the sagittal plane. Or maybe even balance; the lungs are large organs and if put to one side would likely cause locomotive issues. (Perhaps this is even an interesting topic for another question.)</p>\n\n<p>That said, I feel, at it's core the evolutionary advantage which led to the lack of ubiquitous internal symmetry is <strong>space</strong>. Simply put, there is only so much room inside an organism and every little counts. Thus, if there isn't a need for a particular organ to be mirrored about a plane then there <em>is</em> a benefit in putting elsewhere: utilization of space.</p>\n\n<p>I think a fantastic example of this is the human digestive tract. The key factor in the shape of the intestines is utilization of space, which directly affects the point at which is connects to the stomach, itself contributing to the asymmetrical shape of the stomach. One could envision other configurations, sure, and nature has. However, this configuration works quite well and the extraordinary use of limited space seems to outweigh all benefits of symmetry.</p>\n\n<p>To directly respond to your questions above:</p>\n\n<ul>\n<li><p><strong>Question:</strong> Why do we not have an even number of each organ so it can be placed symmetrically?\n<strong>Response:</strong> Each organ addresses (or addressed) a need of the organism. Addressing that need with multiple organs working in concert has benefits and consequences, as does addressing the need with a single organ alone. These benefits and consequences are balanced throughout the evolution of an organism.</p></li>\n<li><p><strong>Question:</strong> If we have a single organ why is it not placed in the middle like the brain or bladder is for instance?\n<strong>Response:</strong> <em>I feel</em> space. Again, there are benefits to symmetry but there are many other factors at play. Some of which, it seems, are more important than symmetry at times.</p></li>\n<li><p><strong>Question:</strong> Is there some evolutionary advantage that led to this setup?\n<strong>Response:</strong> I hope this has been addressed - I don't claim to have 'answered' anything, this is a question for discussion.</p></li>\n</ul>\n\n<p><strong>Other fuel for discussion:</strong></p>\n\n<p>In thinking through this question I found myself able to rationalize why internal symmetry isn't necessary. However, I'd be interested in seeing opinions on why, then, external symmetry is so prevalent.</p>\n"
}
] |
[
{
"answer_id": 5760,
"pm_score": 3,
"text": "<p>Building on the answer given by Sean Connolly above, it would be very easy to imagine evolutionary scenarios where organs are more likely to develop asymmetrically than symmetrically.</p>\n\n<p>For instance, imagine an organism that has a simple digestive system that consists only of a single undifferentiated intestine that runs directly from mouth to anus in a straight line, as in primitive annelids. Let's say that there is also only one enzyme present to break down the food particles, and that this is present throughout the intestine. </p>\n\n<p>Now, perhaps for space issues, or for reasons that are entirely unrelated to internal organs, the intestine itself becomes asymmetrical. This could be because a longer intestine is needed to dissolve and take up more of the food, but the organism cannot become longer (for instance, it might live in dead coral reefs, and the size of the hollows cannot be controlled by the organism itself, so there is an external limitation to how long the organism can become). One way to solve this would be to fold the intestine, which can make it asymmetrical.</p>\n\n<p>Now, because food particles that enter the mouth are exposed to the single enzyme throughout the intestine, the gut fluid will be less and less nutritious the farther posterior it gets along the gut. Possibly, more anterior parts of the intestine will become specialized in breaking down and absorbing more frequent kinds of food, while more posterior parts will become specialized in less common foodstuffs. This could lead to differentiation of secretory organs along the intestine, and if this is already bent because of external selection pressures, it is not impossible that a given secretory organ will develop asymmetrically simply because the intestine at the point where the enzymes secreted by this organ are to be used is not near the mid-line of the body. </p>\n\n<p>For instance, if we needed to absorb substance X from our food, but substance X only became abundant in the gut fluid at a distance from the mouth that corresponds to a place when our intestine is located on the left side of the body, it is not unreasonable that development of this excretory organ would develop on the left side of the body. This could then be self-reinforcing, as a more ready access to substance X may mean that this substance becomes more important for us, and the secretory organ may become larger and more dominant, and eventually we have a large organ that exists only on the left side of the body, without ever having existed in a symmetrical form.</p>\n\n<p>This is, of course, pure speculation, and I know of no example of this, but it is one that is not at odds with evolution in general, and could certainly be plausible. The same could occur if differentiation of enzyme secretion organs occur in a symmetrical gut, which later becomes asymmetrical and the whole secretory organ becomes displaced to one side. Retaining a symmetrical pair of secretory organs on each side of the body, but having the enzymes work on food only asymmetrically would imply that one of the secretory organs had a very long duct and the other had a very short one. It is reasonable to assume that over evolutionary time, the one with the long duct would become less important and may disappear.</p>\n\n<p>A similar reasoning could be applied to the blood circulation system and any organs relevant to that.</p>\n\n<hr>\n\n<p>There are many examples of external asymmetry throughout the animal kingdom. Many decapods, for instance, have asymmetrical claws that are used for different purposes (feeding in lobsters, for instance). Several genera of bird lice (e.g. <em>Struthiolipeurus, Bizarrifrons</em>) have asymmetrical heads, which probably have something to do with how they attach to their hosts' feathers. I believe that many groups of sessile invertebrates have anal openings displaced to one side, but that may be caused by internal asymmetry or because it is less efficient to have our anus situated so that feces is filtered into your mouth again. </p>\n"
},
{
"answer_id": 43836,
"pm_score": 1,
"text": "<p>I would like to add an answer here to explain how the internal asymmetry of animal organs might be consistent with their external symmetry.\nHere's my argument:</p>\n\n<p>1) In the case of vertebrates the important internal organs are protected by the animal's skeleton. </p>\n\n<p>2) The internal organs are soft matter and so their physics is very different from how they would behave if they were nearly rigid bodies.</p>\n\n<p>3) Internal asymmetry isn't a big issue because the mass distribution is approximately symmetrical in a bilateral sense.</p>\n\n<p>To make this concrete I mean:</p>\n\n<p>a) If you should try slicing a vertebrate down the middle you will notice that the left and right sides of a vertebrate have approximately the same weight</p>\n\n<p>b) The left and right sides of the vertebrate's head have approximately the same weight...etc. </p>\n"
},
{
"answer_id": 72677,
"pm_score": 0,
"text": "<p>Imagine that the intestine is a long, symmetric, flexible tube, about 20 feet long. Now imagine what the tube would look like if it were packed into a 5-gallon bucket. It would be literally, mathematically, impossible to pack it in symmetrically. In physics we call that \"spontaneously broken symmetry\". It would take a lot of genetic instruction to pack a long intestine into a small volume even approximately symmetrically. Of course this doesn't explain all the asymmetry you're wondering about, but does explain some of it.</p>\n"
},
{
"answer_id": 82872,
"pm_score": 2,
"text": "<p><strong>You change one thing and you have to change everything else to compensate.</strong> </p>\n\n<p>Lets look at what organs are not symmetric in tetrapods, the heart and the digestive system, everything else is symmetric. Note these are symmetric in more basal vertebrates like fish.</p>\n\n<p>the heart starts symmetrical in vertebrates but that changes when animals evolve independent circulatory systems, that is flow of blood to the lungs that is separated from the flow to the body, allowing for differential blood pressure. that evolved by having one side of the heart supply the lungs and the other supply the body, since they have vastly different blood pressures it would make sense the sides of the heart creating that blood pressure would also be different. this change in shape forces some asymmetry on the lungs that have to share space with the heart.</p>\n\n<p><a href=\"https://i.stack.imgur.com/gfxZH.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/gfxZH.jpg\" alt=\"enter image description here\"></a></p>\n\n<p>The digestive system is even easier, again it starts as a straight tube, but two major changes occur. first a longer digestive track allows you to extract more nutrients, and making a human (or nearly any animal) long enough to hold a straight digestive track of the same length would be incredibly wasteful. For scale the human digestive tract is about 10 meters long. </p>\n\n<p>The other change is the development of the stomach (which not all vertebrates have). having a portion of the digestive system dedicated to storage and soaking is useful by allowing animals to eat larger quantities when situations allow without having to hurry it through the digestive system and lose most of the benefits. And again the only good way to enlarge a section of a straight tube without elongating the body is to have it turn and be offset, this forces many other organs out of place (liver and spleen) which attach along the digestive tract's length. Note in many fish this is all still symmetrical, but this changes when they evolve away from a tall thin cross section into a more rounded cross section which is favored in shallow water and eventually life on land. Once that happens you can't simply stack everything up along the mid-line without wasting a lot of space. </p>\n\n<p><a href=\"https://i.stack.imgur.com/neyxY.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/neyxY.jpg\" alt=\"enter image description here\"></a></p>\n\n<p>you can see how changes to the digestive track might evolve in many different lineages that change the shape of the body like crabs or molluscs. which are the other groups with asymmetric internal organs. Note these other two groups are often externally asymmetric as well. Snails in particular because they changed a long straight shell into a compact coiled shell, which forces asymmetry on many systems. </p>\n"
}
] |
6,827 |
<p>Why did humans/animals evolve to become self-aware of their own thoughts. That is, why don't humans act and compute like a machine, or walking zombie. In my mind, such creatures would still be as smart and equally capable of surviving, the only difference being they don't experience the phenomenon of self-awareness. (To understand my question think: unconsciously sleep walking)</p>
|
[
{
"answer_id": 6831,
"pm_score": 4,
"text": "<p>There have been many proposals over the years as to why human consciousness has emerged and how, or even what it is. </p>\n\n<p>Most of us will not be surprised to know that there is no consensus about an answer here. Its hard to draw a trend from a single example. </p>\n\n<p>Here is a little survey of the one's I've heard. </p>\n\n<ol>\n<li><p>We are intelligent because we have opposable thumbs and can use tools, which evolved our brains. This is an old one - maybe as old as Darwin's time. I think its mostly ignored now because so many animals - including pandas and other non primates have opposable thumbs or use tools or both. (monkeys and chimps use tools, and recently crows have also been observed to use tools.)</p></li>\n<li><p>brain size. We do have a large brain to body size ratio. There are other animals with similar ratios and they don't have internets. </p></li>\n<li><p>We are 'self-aware'. That is to say we recognize ourselves as an individual. <a href=\"http://psycnet.apa.org/journals/amp/32/5/329/\" rel=\"noreferrer\">It was proven that other primates can recognize themselves</a> in mirrors (putting a red dot on their forehead. when they see their reflection, they touch their own forehead). So that's not exclusive either. its not a bad idea, but so far it doesn't seem to make the </p></li>\n<li><p>'We ate something' I once read a discussion of <a href=\"https://www.greenpassion.org/index.php?/topic/20997-humans-primates-psychedelics/\" rel=\"noreferrer\">how humans might have ingested psychotropic plants or fungi</a>. As you can see, this was 2010. Its not the worst idea, but its hard to prove. Lots of experiments on cats since the '60s have not produced cat's who care to tell us if they are intelligent. Maybe they are just too smart in the first place. </p></li>\n</ol>\n\n<p>These theories, from when I was a student are so discounted now, you can't find too much record of anymore since they were pre-internet and also they seem so unlikely now. </p>\n\n<p>More modern theories have locked onto <a href=\"http://en.wikipedia.org/wiki/Evolution_of_human_intelligence#Models\" rel=\"noreferrer\">social configurations of human societies which drive intelligent adaptations</a>. This is stemming from observations that human evolution (the rate at which genetic variants are retained in the gene pool) <a href=\"http://www.ncbi.nlm.nih.gov/pmc/articles/pmc2410101/\" rel=\"noreferrer\">are accelerating since humans have become social</a>. </p>\n\n<p>These new theories while standing on some amazing evidence are still feeling around in the dark - stuff about how social interactions have created a preference for intelligence-like traits. There is probably something to that - once intelligence gets a toehold it is a clear advantage. But how did it show up only once and why us? I think that's the hard part that science has, for the moment, given a rest. </p>\n"
}
] |
[
{
"answer_id": 13624,
"pm_score": 2,
"text": "<p>I don't think you can ever ask or answer for that matter WHY questions in biology. The only answer there is: because it works. Asking why questions implies that there was a reason, and reason cannot exist alone by itself. Reason is held by someone or something. And reason is something that doesn't exist, it is something we created and use for our own purposes and we cannot attribute it to anything else having one. Now, if you asked \"how?\", that's an answer biology was created for.</p>\n\n<p>There could have been many outcomes to everything in biology but this is the one that appeared and works. This doesn't mean that it is some sort of theoretical or practically optimum, but the law of this universe is survive long enough to improve if needed.</p>\n\n<p>I know that this is an opinion, but it's as close to the answer that you can get. If someone gives an answer to the WHY question, you could never prove it, or you could find evidence for all the possible reasons. And we can't also tap into the reasons of the universe because our intellect and modes of expression are way lower than the universe has.</p>\n"
},
{
"answer_id": 56455,
"pm_score": -1,
"text": "<p>Animals are not self aware, sentience is the quality of placing yourself in time and space, and the capability of introspection. We humans know we exist, we know we live in a universe, we ponder what's the meaning of life, where we came from and how we came to exist, where we go after we die, animals don't, they act by instinct and have different levels of intelligence, their behavior is written in their DNA code, but they aren't self-aware, this is the basic trait that separates us from animals.</p>\n\n<p>Concerning how we became self-aware, that will depend on your beliefs (another trait of our advanced intelligence), but those who believe in evolution pretty much agree that we developed sentience because our brains developed much further than that of any other species, our advanced cortex and cognitive system gave us this ability. Different religions also have different accounts to our origin and history, in the proto-Indo-European cosmology for example, we are descendant of aliens, called pleiadians or nordic aliens, they came to earth through a portal in the sun, and brought their seed to our planet and gave origin to us, all our knowledge and manifestation of our humanity, like science, art... come from them.</p>\n"
},
{
"answer_id": 56466,
"pm_score": 2,
"text": "<blockquote>\n <p>Why did humans/animals evolve to become self-aware of their own\n thoughts.</p>\n</blockquote>\n\n<p>Answer is pretty simple. Most mammals are self aware... it is just a matter of degree. It is a lot more advance in humans, but it is there in animals. like pride of Lioness hunting... setting up an ambush together... which means a lion can predict what zebra will do in a situation. And what other lioness will do. </p>\n\n<p>And why have it? The answer is simple... being aware of you own thought, is basically being able to prediction the thoughts of others. And this is pretty useful.</p>\n\n<p>We have the example of lioness pride ambush hunting. It requires a degree of self awareness in order to communicate and in heat of the chase predict what the other members of your pride will do and what will the prey animal will do.</p>\n\n<p>Being alpha (wolf, lion, chimp, elephant, hyena, meerkats) is great. There are many biological benefit (first to eat, drink and have babies). However for a there to be an alpha, there must first be a group to be alpha over. And when there is a group, there is a beta, and while beta might not be able to beat you individually, beta might team up with delta..to remove you.</p>\n\n<p>So as you can see, living in groups quickly leads to complications. And if you can understand others, you can use others to benefit yourself. Much selection pressure there for to evolve consciousness. </p>\n"
},
{
"answer_id": 57856,
"pm_score": 1,
"text": "<p>Probably density of cortical columns. I tested this on a mouse recently, it was aware I was trying to help it and actually walked calmly into the jar.\nReleased it but did wonder if it will make an appearance again one day.</p>\n\n<p>Perhaps in this case, neural nets are not complicated enough unless the connectivity threshold is in a critical range. This is apparently why we are one of only three intelligent species on this planet, sharing this with dolphins and African Grey parrots.\nFour if you count octopi.</p>\n\n<p>I speculated a while back based on my knowledge that connectivity modulators like psilocin, xenon and other compounds could be used to trace the actual neural connections responsible. This has been linked to Orch-OR and other QC like phenomena, also allowing for strong AI to be developed by synchronizing classical processors with a quantum link using entangled photons.</p>\n"
},
{
"answer_id": 84872,
"pm_score": 1,
"text": "<p>Natural selection doesn't select for the type of consciousness. It selects for brains that work for its purposes. The brain I think is like a Conway's game of life. It theoretically can pull off all kinds of tasks, and that can be explained just by the laws of physics acting on the brain.</p>\n<p>The question of how the brain creates consciousness is an entirely different question maybe a philosophical one. I have aspergers. I sometimes do some abstract thinking. I sometimes sort of feeling like I'm conceiving of an object with properties that most intuitive theories prove cannot exist. They would say it's just my brain inventing the sentence "This object has those properties" and they're probably right. However, I sometimes actually have a small bit of feel for thinking in one and would feel like I'm conceiving of a real object which is distinct from its formalization which people would see if they looked at an image of my brain. I think we then decide to define consciousness according to the way the brain is in that kind of way.</p>\n"
}
] |
6,915 |
<p>Obviously, the temperature of water does not affect its chemical composition. At least not in the ranges we are likely to drink it in. Yet it is clearly far more pleasant and refreshing to drink cool water than it is to drink tepid or warm water.</p>
<p>Is there actually any difference to the organism or is this just a matter of perception? Is cool water somehow more efficient at rehydrating a cell? In any case, surely by the time water reaches individual cells it will have warmed up to body temperature. </p>
<p>So, what, if any, is the difference between drinking cool and warm water in terms of its effect on the human (or other animal) body?</p>
<p>Extra bonus for explaining why the <em>taste</em> of water changes when it is cold.</p>
|
[
{
"answer_id": 30657,
"pm_score": 5,
"text": "<p><strong>Short answer</strong>: Cold is pleasant only when your are not already freezing and cold might satiate thirst better because it acts as enhancer of the \"water intake flow meter\".</p>\n\n<hr>\n\n<p><strong>Is cold water more tasty than warm water?</strong> No, it is actually the reverse as detailed in my footnote.</p>\n\n<p>Cold is pleasant when your body is over-heating and definitely not if you live naked in the North Pole. Over-heating means sweating which means you loose water and therefore feel thirsty faster. Yet drinking cold water will not rehydrate the body more than warm water and drinking water has only a very small impact on the body temperature. So why do we like it?</p>\n\n<p>A study was actually conducted on the subject and answers most of your questions. <a href=\"http://www.sciencedirect.com/science/article/pii/S0195666313003930#\" rel=\"noreferrer\">Here the reference</a>. </p>\n\n<p><strong>The temperature of the body will indeed not change</strong>.</p>\n\n<blockquote>\n <p>cold stimuli applied to the mouth\n (internal surface of the body) do not appear to impact on body\n temperature and are not reported to cause any reflex shivering\n or skin vasoconstriction that influence body temperature.</p>\n</blockquote>\n\n<p>As you pointed out, the temperature of the ingested water will <strong>not affect the overall hydration of the body</strong> as cells are rehydrated mostly via the blood stream and the blood temperature will not be affected. Someone could argue that, at identical volumes, cold water (above 4C) contains more molecules (i.e. is denser) than warm water but this difference is likely very slim.</p>\n\n<p>In this paper they also define \"thirst\".</p>\n\n<blockquote>\n <p>Thirst is a homeostatic mechanism that regulates blood osmolarity\n by initiating water intake when blood osmolarity increases</p>\n</blockquote>\n\n<p>The problem is that it takes some time before the water reaches the blood stream, and therefore you need a feedback mechanism that tells you to stop drinking independently of the blood's osmolarity. This is where cold might play a role.</p>\n\n<blockquote>\n <p>The cold stimulus to the mouth from ingestion of water may act\n as a satiety signal to meter water intake and prevent excessive\n ingestion of water</p>\n</blockquote>\n\n<p>The picture would then be the following\n<img src=\"https://i.stack.imgur.com/BgAON.png\" alt=\"enter image description here\"></p>\n\n<p>In essence, a cold sensation is pleasant in warm weather, both on the skin and in the mouth, and it apparently helps in reducing thirst by being some kind of an enhancer of the \"water intake flow meter\".</p>\n\n<hr>\n\n<p><strong>Footnote</strong></p>\n\n<p>Reading the comments I just want to clarify some points.</p>\n\n<p>The 5 basic tastes (sweet, salty, bitter, sour and umami) are very distinct from taste sensations (pungency, smoothness, cooling to name a few). The main difference is that taste and \"sensation\" signals use completely different paths to reach the brain - namely, the facial and glossopharyngeal nerves for the former and the trigeminal nerve for the latter.</p>\n\n<p>Is the temperature affecting basic taste perceptions? The answer is <a href=\"http://www.nature.com/nature/journal/v438/n7070/full/nature04248.html\" rel=\"noreferrer\">yes</a>. How this happens is quite simple if you understand the fundamental concepts of molecular taste perception. Essentially the temperature affects the response of the receptor TRPM5 which is the main player in depolarizing taste receptor cells in the papillae. To put it simply, higher temperatures provoke a greater perception for taste, and this is not only in term of perceived taste but really modifies the amplitude of the response at the molecular level. As an example this is why ice cream does not taste sweet when frozen but only after it melted in the mouth or on the tongue.</p>\n"
}
] |
[
{
"answer_id": 6922,
"pm_score": 3,
"text": "<p>I think it's because we are more often thirsty in a warm/hot/dry environment.<br>\nSince almost all of us have a house with a household furnace creating that warm/dry environment. </p>\n\n<p>Thus cold water would be more refreshing since it also cools us off a bit.<br>\nI doubt that people that are on a north-pole expedition would still prefer that cold drink over a warm one. </p>\n\n<p>This link contains a lot of information on this topic:<br>\n<a href=\"http://chestofbooks.com/health/nutrition/Dietetics-4/Temperature-And-Digestion.html\" rel=\"nofollow\">http://chestofbooks.com/health/nutrition/Dietetics-4/Temperature-And-Digestion.html</a></p>\n"
},
{
"answer_id": 16363,
"pm_score": 2,
"text": "<p>Here's an armchair evolutionary explanation. In nature, running water tends to be cold whereas tepid water tends to be lukewarm. And for reasons having nothing to do with temperature, running water tends to contain less harmful bacteria. Therefore, our ancestors who preferred to drink cold water over lukewarm had an evolutionary advantage over those who preferred the opposite. </p>\n"
},
{
"answer_id": 30634,
"pm_score": 2,
"text": "<p>In addition to cultural preferences and psychological factors, there may be some evolutionary basis in this.</p>\n\n<p>Cooking food is a relatively new development and unique to the <em>Homo spp.</em> line. It makes sense that the tongue/mouth may be more sensitive to cooler temperatures than warm temperatures, given the amount of actual exposure it is given to sunlight and/or objects (across all species).</p>\n\n<p>This is perhaps supported by the concentration of various receptor channels, TRPV1-4, TRPA1 and TRPM8, which are each sensitive/activated across various temperature ranges. TRPV3 operates through a range close to body temp. and has been associated with taste perception. One could hypothesise that in the mouth there is a greater concentration of cold-sensitive channels (such as TRPA1 and TRPM8) than warm ones, thus cold is perceived more readily and the addition of 'taste' channels (TPRV3) may contribute to the preference for cool water over say luke warm/room temp. water. This thinking falls down when we think of the amount of hot food we eat and can of course taste, in addition to the many studies conducted on taste perception, however this entire answer is very rudimentary.</p>\n\n<p>I haven't found literature detailing the relative proportions of said channels, however, this makes for an interesting read: <a href=\"http://www.mnf.uni-greifswald.de/fileadmin/Zoologisches_Museum/Hildebrandt/Dokumente/schepers10.pdf\" rel=\"nofollow\">http://www.mnf.uni-greifswald.de/fileadmin/Zoologisches_Museum/Hildebrandt/Dokumente/schepers10.pdf</a></p>\n"
},
{
"answer_id": 30660,
"pm_score": 0,
"text": "<p>The organism as a thermodynamic machine does need a coolant. The more difference in temperature the more efficiently thermal machine can use energy. Also in all processes in organism it is produced excessive thermal energy, which should be removed.</p>\n\n<p>Thus colder water and air are pleasant.</p>\n"
}
] |
7,492 |
<p>I've been to local zoo the other day and one lizard caught my attention: its pupils are circular, which, I thought, is not usual for reptiles. Turns out it is, but now I can't find any explanation on why some animals have one kind of pupil and others have the other. Lizards can have both, and so can snakes. The only difference I have found is that circular pupil can't shrink quite as much as a cat's-eye pupil, but that hardly explains why circular pupil even evolved in the first place as I don't see any advantage to it. </p>
<p>Ideas?</p>
<p>P. S. Fish only have circular pupils so that shape is older, right?..</p>
|
[
{
"answer_id": 7514,
"pm_score": 5,
"text": "<p>Circular pupils are <em>always</em> functionally superior to vertical pupils; a slit does not correctly focus light from all directions whereas a circular pupil does. If you observe cats when they're hunting at dawn and dusk*, they have big, circular pupils; it's only when they're in bright light that the pupil shrinks to a slit. So why have vertical pupils at all? Because, as you mention they're capable of letting a more controlled range of light into the eye.</p>\n\n<p>Thus vertical slits let you be active in a wider range of light conditions at the cost of poorer vision in bright light; whilst circular pupils continue to function well in brighter light but at the cost of not allowing such a large range of control over the amount of light entering the eye.</p>\n\n<p>It is then easy to see why you get both kinds of pupil: circular pupils are favoured by animals that are typically active in bright light and need good vision under these circumstances; vertical pupils are favoured by animals that are primarily active in low light but need some ability to see in bright light.</p>\n\n<p>*- it's often stated that cats are nocturnal, this is untrue; cats are <em>crepuscular</em> - that is they are most active at dawn and dusk.</p>\n"
}
] |
[
{
"answer_id": 7500,
"pm_score": 2,
"text": "<p>Your mention of cats hinted that vertical pupils have to do with night vision, and <a href=\"http://www.newscientist.com/article/mg16422167.600-the-last-word.html\" rel=\"nofollow\">indeed they do.</a></p>\n\n<p>The retinas of cats and other nocturnal animals are very sensitive to even the tiniest amount of light. This can make their eyes hurt when exposed to bright sunlight. So their pupils have to shrink as much as possible in the sunlight, and, as you pointed out, vertical pupils can shrink more than circular ones. </p>\n\n<p>EDIT: People pointed out in the comments that cats have vertical eye pupils only in bright sunlight. In low-light conditions, the pupils expand to a circle. </p>\n"
},
{
"answer_id": 17485,
"pm_score": 2,
"text": "<p>In bright light, a cat can also squint, thus approximating a circle with a square-like aperture. So a vertical pupil is not that much of a liability to focusing. The same cannot be said of a horizontal pupil (unless the eyelids are vertical). Additionally, a vertical pupil might optimize detection of horizontal movement, which is likely an advantage in hunting prey on the savannah.</p>\n"
},
{
"answer_id": 33013,
"pm_score": -1,
"text": "<p>I see one possible advantage to round pupils. A slit pupil gives higher visual acuity vertically than horizontally because of diffraction and when a slit pupil is very nearly shut, there's high diffraction in the horizontal direction giving poor horizontal visual acuity. A round pupil on the other hand gives a creature the highest visual acuity in all directions for a given area of pupil. A smaller pupil is better for reducing chromatic aberration but chromatic aberration can be pretty much neglected because for any creature with evolutionary pressure for sharp vision in all directions, good accomodation will ensure at least one wavelength of light focuses onto the retina forming a sharp image because the sun emits a continuous range of wavelengths.</p>\n"
},
{
"answer_id": 41990,
"pm_score": 2,
"text": "<p>There was a study published <strike>this</strike> last year (2015) that suggests that the pupil style of an animal is related to its strategy for predation. This means that land animal pupils evolved as adaptations to the niche that they filled. </p>\n\n<p>The study distinguishes between herbivorous, active, and ambush foraging behaviors. Ambush predators tend towards vertical pupils, where as active predators (those that chase down and kill their prey) tend more towards circular. The pupils of herbivorous foragers tended to be mostly horizontally-elongated as is the case with goats. Eyes also tend to be forward set in predatory animals and more at the side of the head in prey animals.</p>\n\n<p>In <a href=\"http://advances.sciencemag.org/content/1/7/e1500391.full\" rel=\"nofollow noreferrer\">Why do animal eyes have pupils of different shapes?</a> Banks, et. al. Science Advances<br>\n07 Aug 2015: Vol. 1, no. 7, e1500391 DOI: 10.1126/sciadv.1500391 It is suggested that</p>\n\n<blockquote>\n <p>Abstract<br>There is a striking correlation between terrestrial species’ pupil shape and ecological niche (that is, foraging mode and time of day they are active). Species with vertically elongated pupils are very likely to be ambush predators and active day and night. Species with horizontally elongated pupils are very likely to be prey and to have laterally placed eyes. Vertically elongated pupils create astigmatic depth of field such that images of vertical contours nearer or farther than the distance to which the eye is focused are sharp, whereas images of horizontal contours at different distances are blurred. This is advantageous for ambush predators to use stereopsis to estimate distances of vertical contours and defocus blur to estimate distances of horizontal contours. Horizontally elongated pupils create sharp images of horizontal contours ahead and behind, creating a horizontally panoramic view that facilitates detection of predators from various directions and forward locomotion across uneven terrain.</p>\n</blockquote>\n\n<p><a href=\"https://i.stack.imgur.com/vY9gk.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/vY9gk.jpg\" alt=\"enter image description here\"></a><br>\n<sup>Figure 1. <a href=\"http://advances.sciencemag.org/content/1/7/e1500391.full\" rel=\"nofollow noreferrer\">Why do animal eyes have pupils of different shapes?</a> Banks, et. al. Science Advances<br>\n07 Aug 2015: Vol. 1, no. 7, e1500391 DOI: 10.1126/sciadv.1500391</sup></p>\n"
}
] |
7,847 |
<p>According to Wikipedia, muscle cramps are caused by the inability of myosin fibers to break free from the actin filaments during contraction, resulting in a prolonged contraction.</p>
<p>A lack of ATP would obviously produce cramping, as myosin requires ATP to become free from actin.</p>
<p>However, I have heard that potassium and sodium are useful for treating cramps and that their deficiencies can lead to cramping.</p>
<p>So, how does a deficiency in sodium or potassium result in the inability of myosin fibers to break free from the actin filaments during contraction?</p>
|
[
{
"answer_id": 7859,
"pm_score": 4,
"text": "<p>The quick and simple answer:</p>\n\n<p>Cramps of a hypokalemic origin are much more common than those of a hyponatremic origin because the Na-K pump is more effective at moving potassium in comparison to sodium.\nAt the onset of a muscle contraction, the presence of calcium triggers the opening of the Na-K channels in the membrane. Potassium is a calcium inhibitor, so as the potassium flows out of the cell, it eventually reduces the presence of calcium. This causes the closure of the Na-K channel (negative feedback mechanism). In a hypokalemic state, the lack of sufficient K doesn't inhibit the calcium channel, and in turn doesn't properly terminate the muscle contraction at the cellular level. </p>\n\n<p>The continued presence of calcium, which has a lot to do with nerve impulses, means that the nerves keep firing, and in some cases such as a 'charlie horse', these impulses fire fast and continuously. The body at this point is reaching a small local state of metabolic acidosis resulting from the extremely high oxygen consumption, increasing levels of CO₂ (the acidosis component) and reducing blood partial oxygen levels. Since the oxygen is no longer as abundant as it was, it inhibits the bodies ability to locally produce the ribose and phosphate necessary for ATP. Less ATP = more myosin that can't be disconnected from actin = continued muscle cramp.</p>\n"
}
] |
[
{
"answer_id": 11302,
"pm_score": 2,
"text": "<p>Muscle contraction occurs when the brain tells the body to move. The brain then starts an action potential down the motor neurons, until it reaches the terminal bouton. At the terminal bouton, it releases the neurotransmitter, acetylcholine, which travels through the myoneural junction and into the myoneural cleft. ACH binds to the receptor, which causes an action potential in both directions along the cell membrane. \n The action potential repels the potassium, which travels down the cell membrane until it falls into a transverse tubule. K+ continues to fall into a transverse tubule and accumulates, which increases voltage (-70 to -50 mV). The voltage change causes the calcium gates to open and to diffuse the calcium. \n Calcium then binds to troponin, which in turn binds to tropomyosin and pulls it, exposing the g-actin binding site that allows myosin and actin to bind. The myosin head changes shape (called power or working stroke) and pulls the actin towards the M line, and the muscle contracts. Similar to a tug of war, the myosin heads (your hands) pull on the actin (the rope) to contract a muscle. Like team members in a tug of war, the myosin heads alternate between pulling and holding on to the actin; the only way that myosin will release actin is to add ATP, which forces the two apart and thus relaxes the muscle (as mentioned above).</p>\n\n<p>Now, a lack of potassium, sodium, or calcium would prevent the muscle from contracting but won't relieve a muscle cramp. The common advice of eating a banana actually does help relieve cramps but not because of the potassium. Bananas also have sugar and fat, which are converted into ATP.</p>\n\n<p>Muscle cramps are primarily caused by a lack of ATP in the body. ATP forces the myosin to release the actin; thus, the muscle relaxes and the cramp is relieved.</p>\n\n<p>Another cause could be the lack of magnesium, which helps the ATPase sodium/potassium pump, which, in turn, returns the voltage to resting potential and relaxes the muscle.</p>\n"
},
{
"answer_id": 15162,
"pm_score": 1,
"text": "<p>None of these answers makes sense, and there some minor errors in them. I know that action potentials may continue to fire down the axon. One reason may be because acetylcholinesterase is not coming to the rescue and cleaning up all the acetylcholine in the synaptic cleft. But that usually happens if there are drugs involved. So, in terms of natural muscle cramps, it really does not make any sense whatsoever. </p>\n\n<p>A really good reason is mainly because of a lack of potassium. The function of potassium inside the muscle cell is to repolarize the membrane. However, if there is not enough potassium, the time it takes for it to repolarize is very slow. On the other hand, sodium is used to depolarize the membrane. As a result, since there is an unequal distribution of sodium to potassium, less potassium flows out the membrane while more sodium flows into the membrane, causing it to depolarize faster than it repolarizes. Since the inside of the cell is becoming more positive with the help of sodium, and since the outside of the cell is becoming negative with the help of potassium, the inside of the cell is pulling back the potassium. But, again, there is an unequal distribution of potassium compared to sodium, so it will never achieve that electrochemical equilubrium (resting membrane potential). Since electrochemical equilibrium can not be achieved, sodium is flowing inside the membrane, causing it to depolarize across the membrane and to form an unfused tentanus at a rapid rate.</p>\n\n<p>The rate in which this is happening is so fast that it won't let the myosin head detach from actin for a long period, so it is continuously making the sacromere shorter, causing a pain receptor to travel toward the CNS. This is my hypothesis. </p>\n"
},
{
"answer_id": 15163,
"pm_score": 0,
"text": "<p>One of the things that I would like to point out is that ATP detached the myosin head but does not control the powerstroke! If there are no more ATP being produce, then rigor mortis results. You will just be really tense/sore because the myosin head is not being released, and it's staying contracted (perhaps a fused tentanus), but it does not make the sacromere shorter if ATP are no longer able to be produced. And if there are no more ATP being produce, it can't be hydrolyzed into ADP and inorganic phosphate (Pi). \nThat would help to create the cross bridge. In addition, inorganic phosphate, not ATP, is the essential compound when you want the power stroke to happen. </p>\n"
},
{
"answer_id": 39171,
"pm_score": 1,
"text": "<p>One possible reason why low sodium levels induce cramps may lie in the cation selectivity of the nicotinic acetylcholine receptor (nAChR), which is an ion channel. When ACh binds to the receptor site on the nAChR protein, the protein changes shape to open a pore formed by the protein in the cell membrane. This pore allows the influx of both sodium and calcium ions, which induce depolarisation (a positive shift in the membrane voltage) to trigger the voltage-dependent ion channels responsible for action potentials.\nA reduction in sodium ions would mean more calcium is able to enter the cell through the nAChR. The calcium ion carries greater charge as it is formed by the loss of two electrons from its outer shell, while the sodium ion is formed by the loss of one electron. This means that, each time the nAChR channel opens, the cell undergoes greater depolarisation. The muscle response is harder and faster to the same neural stimulus, which results in a depletion of energy stores.</p>\n"
},
{
"answer_id": 67800,
"pm_score": 0,
"text": "<p>A quote from Flex Pharma:</p>\n\n<blockquote>\n <p>Most muscle cramps are not caused by dehydration, lactic acid,\n electrolyte imbalance, or muscle tightness. That is why popular\n remedies like sports drinks, bananas, magnesium tablets, and\n stretching are usually ineffective. New research has shown that cramps\n and spasms do not originate in the muscle itself, but are caused\n instead by a neural mechanism: excessive firing of the motor neurons\n in the spinal cord that control muscle contraction.</p>\n</blockquote>\n\n<hr>\n\n<p>Activation of transient receptor potential (TRP; TRPV1 and TRPA1) ion channels reduces muscle cramps.</p>\n\n<hr>\n\n<p><a href=\"http://www.flex-pharma.com/scientific-presentations.php\" rel=\"nofollow noreferrer\">http://www.flex-pharma.com/scientific-presentations.php</a></p>\n"
}
] |
7,854 |
<p>A plasmid is a small DNA molecule that is physically separate from, and can replicate independently of, chromosomal DNA within a cell. </p>
<p>In general, in eukaryotes, episomes are closed circular DNA molecules that are replicated in the nucleus. Viruses are the most common examples of this, such as herpesviruses, adenoviruses, and polyomaviruses. Episomes in eukaryotes behave similarly to plasmids in prokaryotes in that the DNA is stably maintained and replicated with the host cell. </p>
<p><a href="http://en.wikipedia.org/wiki/Plasmid" rel="nofollow">Source is wikipedia.</a> </p>
|
[
{
"answer_id": 7859,
"pm_score": 4,
"text": "<p>The quick and simple answer:</p>\n\n<p>Cramps of a hypokalemic origin are much more common than those of a hyponatremic origin because the Na-K pump is more effective at moving potassium in comparison to sodium.\nAt the onset of a muscle contraction, the presence of calcium triggers the opening of the Na-K channels in the membrane. Potassium is a calcium inhibitor, so as the potassium flows out of the cell, it eventually reduces the presence of calcium. This causes the closure of the Na-K channel (negative feedback mechanism). In a hypokalemic state, the lack of sufficient K doesn't inhibit the calcium channel, and in turn doesn't properly terminate the muscle contraction at the cellular level. </p>\n\n<p>The continued presence of calcium, which has a lot to do with nerve impulses, means that the nerves keep firing, and in some cases such as a 'charlie horse', these impulses fire fast and continuously. The body at this point is reaching a small local state of metabolic acidosis resulting from the extremely high oxygen consumption, increasing levels of CO₂ (the acidosis component) and reducing blood partial oxygen levels. Since the oxygen is no longer as abundant as it was, it inhibits the bodies ability to locally produce the ribose and phosphate necessary for ATP. Less ATP = more myosin that can't be disconnected from actin = continued muscle cramp.</p>\n"
}
] |
[
{
"answer_id": 11302,
"pm_score": 2,
"text": "<p>Muscle contraction occurs when the brain tells the body to move. The brain then starts an action potential down the motor neurons, until it reaches the terminal bouton. At the terminal bouton, it releases the neurotransmitter, acetylcholine, which travels through the myoneural junction and into the myoneural cleft. ACH binds to the receptor, which causes an action potential in both directions along the cell membrane. \n The action potential repels the potassium, which travels down the cell membrane until it falls into a transverse tubule. K+ continues to fall into a transverse tubule and accumulates, which increases voltage (-70 to -50 mV). The voltage change causes the calcium gates to open and to diffuse the calcium. \n Calcium then binds to troponin, which in turn binds to tropomyosin and pulls it, exposing the g-actin binding site that allows myosin and actin to bind. The myosin head changes shape (called power or working stroke) and pulls the actin towards the M line, and the muscle contracts. Similar to a tug of war, the myosin heads (your hands) pull on the actin (the rope) to contract a muscle. Like team members in a tug of war, the myosin heads alternate between pulling and holding on to the actin; the only way that myosin will release actin is to add ATP, which forces the two apart and thus relaxes the muscle (as mentioned above).</p>\n\n<p>Now, a lack of potassium, sodium, or calcium would prevent the muscle from contracting but won't relieve a muscle cramp. The common advice of eating a banana actually does help relieve cramps but not because of the potassium. Bananas also have sugar and fat, which are converted into ATP.</p>\n\n<p>Muscle cramps are primarily caused by a lack of ATP in the body. ATP forces the myosin to release the actin; thus, the muscle relaxes and the cramp is relieved.</p>\n\n<p>Another cause could be the lack of magnesium, which helps the ATPase sodium/potassium pump, which, in turn, returns the voltage to resting potential and relaxes the muscle.</p>\n"
},
{
"answer_id": 15162,
"pm_score": 1,
"text": "<p>None of these answers makes sense, and there some minor errors in them. I know that action potentials may continue to fire down the axon. One reason may be because acetylcholinesterase is not coming to the rescue and cleaning up all the acetylcholine in the synaptic cleft. But that usually happens if there are drugs involved. So, in terms of natural muscle cramps, it really does not make any sense whatsoever. </p>\n\n<p>A really good reason is mainly because of a lack of potassium. The function of potassium inside the muscle cell is to repolarize the membrane. However, if there is not enough potassium, the time it takes for it to repolarize is very slow. On the other hand, sodium is used to depolarize the membrane. As a result, since there is an unequal distribution of sodium to potassium, less potassium flows out the membrane while more sodium flows into the membrane, causing it to depolarize faster than it repolarizes. Since the inside of the cell is becoming more positive with the help of sodium, and since the outside of the cell is becoming negative with the help of potassium, the inside of the cell is pulling back the potassium. But, again, there is an unequal distribution of potassium compared to sodium, so it will never achieve that electrochemical equilubrium (resting membrane potential). Since electrochemical equilibrium can not be achieved, sodium is flowing inside the membrane, causing it to depolarize across the membrane and to form an unfused tentanus at a rapid rate.</p>\n\n<p>The rate in which this is happening is so fast that it won't let the myosin head detach from actin for a long period, so it is continuously making the sacromere shorter, causing a pain receptor to travel toward the CNS. This is my hypothesis. </p>\n"
},
{
"answer_id": 15163,
"pm_score": 0,
"text": "<p>One of the things that I would like to point out is that ATP detached the myosin head but does not control the powerstroke! If there are no more ATP being produce, then rigor mortis results. You will just be really tense/sore because the myosin head is not being released, and it's staying contracted (perhaps a fused tentanus), but it does not make the sacromere shorter if ATP are no longer able to be produced. And if there are no more ATP being produce, it can't be hydrolyzed into ADP and inorganic phosphate (Pi). \nThat would help to create the cross bridge. In addition, inorganic phosphate, not ATP, is the essential compound when you want the power stroke to happen. </p>\n"
},
{
"answer_id": 39171,
"pm_score": 1,
"text": "<p>One possible reason why low sodium levels induce cramps may lie in the cation selectivity of the nicotinic acetylcholine receptor (nAChR), which is an ion channel. When ACh binds to the receptor site on the nAChR protein, the protein changes shape to open a pore formed by the protein in the cell membrane. This pore allows the influx of both sodium and calcium ions, which induce depolarisation (a positive shift in the membrane voltage) to trigger the voltage-dependent ion channels responsible for action potentials.\nA reduction in sodium ions would mean more calcium is able to enter the cell through the nAChR. The calcium ion carries greater charge as it is formed by the loss of two electrons from its outer shell, while the sodium ion is formed by the loss of one electron. This means that, each time the nAChR channel opens, the cell undergoes greater depolarisation. The muscle response is harder and faster to the same neural stimulus, which results in a depletion of energy stores.</p>\n"
},
{
"answer_id": 67800,
"pm_score": 0,
"text": "<p>A quote from Flex Pharma:</p>\n\n<blockquote>\n <p>Most muscle cramps are not caused by dehydration, lactic acid,\n electrolyte imbalance, or muscle tightness. That is why popular\n remedies like sports drinks, bananas, magnesium tablets, and\n stretching are usually ineffective. New research has shown that cramps\n and spasms do not originate in the muscle itself, but are caused\n instead by a neural mechanism: excessive firing of the motor neurons\n in the spinal cord that control muscle contraction.</p>\n</blockquote>\n\n<hr>\n\n<p>Activation of transient receptor potential (TRP; TRPV1 and TRPA1) ion channels reduces muscle cramps.</p>\n\n<hr>\n\n<p><a href=\"http://www.flex-pharma.com/scientific-presentations.php\" rel=\"nofollow noreferrer\">http://www.flex-pharma.com/scientific-presentations.php</a></p>\n"
}
] |
7,932 |
<p>In physics, "almost everything is already discovered, and all that remains is to fill a few unimportant holes." (See <a href="http://en.wikipedia.org/wiki/Philipp_von_Jolly" rel="noreferrer">Jolly</a>.) Therefore, on Physics SE, people are veering off into different directions: <em>biology</em>, for example.</p>
<p>Thus, it happens that <a href="https://physics.stackexchange.com/q/61174/17609">a question about bicycles</a> generates some discussion about evolution in biology and animals with wheels.</p>
<p>Three explanations are offered for the apparent lack of wheely animals (also on <a href="https://en.wikipedia.org/wiki/Rotating_locomotion_in_living_systems#Biological_barriers_to_wheeled_organisms" rel="noreferrer">Wikipedia</a>, where, by the way, most Physics SE questions are answered perfectly).</p>
<ol>
<li><p>Evolutionary constraints: "[A] complex structure or system will not evolve if its incomplete form provides no benefit to an organism."</p></li>
<li><p>Developmental and anatomical constraints.</p></li>
<li><p>Wheels have significant disadvantages (e.g., when not on roads).</p></li>
</ol>
<p>Now, I suggest that all three can be "solved".</p>
<ol>
<li><p>With time.</p></li>
<li><p>With a symbiotic relationship between a wheel-like animal and a "driver"-like animal, although this gets awfully close to a <a href="https://www.youtube.com/watch?v=R8XAlSp838Y" rel="noreferrer">"driver"-animal</a> to jump onto an actual (man-made) wheel. (So, perhaps, you can suggest a better loophole around this constraint.)</p></li>
<li><p>Roads are presumably not the only ecological niche where animals with wheels could thrive. I'm thinking of frozen lakes, although there skates would be better than wheels.</p></li>
</ol>
<p><strong>What, therefore, is <em>the</em> explanation for there not being any wheeled animals?
Please consider, in your answer, the counterfactual: What assumption of yours would be falsified once a wheely animal <em>is</em> discovered?</strong></p>
|
[
{
"answer_id": 7937,
"pm_score": 7,
"text": "<p>Wheels are possible on the molecular level — bacterial flagella are rotating cores inside a molecular motor, but wheels larger than the flagellum have not really been found.</p>\n<p><img src=\"https://i.stack.imgur.com/1YlbP.jpg\" alt=\"enter image description here\" /></p>\n<p>A single animal with a wheel is an improbable* development that would require a single animal have two separable parts (axle/wheel and body).</p>\n<p>[*read as: <em>pretty much impossible</em>]</p>\n<p>It's hard to imagine how such a thing could evolve. A wheel and axle would need to be made of living tissue, otherwise it would be vulnerable to wear and tear. Wheels also have problems going over uneven terrain, which is really all terrain animals live in. It's difficult to imagine what sort of selection conditions would be strong enough to push animals away from legs.</p>\n<p>If you include driver-vehicle symbionts where the 'car' and 'wheel' are actually two animals, then they <em>have</em> evolved. Parasites can have all sorts of symbiotic control over their victims including as means of transport. The Jewel Wasp is one which is the most suggestive of what you may be thinking. The wasp stings its victim (a cockroach) in the thorax to immobilize the animal and then again just behind its head. After this, the wasp can ride the beetle, steering it by holding its antennae back to its nest where the roach is immobilized to feed the wasp larvae there.</p>\n<p><a href=\"http://www.the-scientist.com/?articles.view/articleNo/31536/title/Animal-Mind-Control/\" rel=\"nofollow noreferrer\">(see section "Pet cockaroaches" in this reference.)</a></p>\n<p>As to the three schools of thought you added to the question, I would probably rather say there were two strong arguments against. The first is whether there is an evolutionary path to wheels (argument 1 in your question), which I doubt. Given even a large amount of evolutionary time you will not see a naked human being able to fly on their own power. Too many structural characteristics of the body plan have been made to all be reversed so that wings or other means of aerial conveyance will show up. The same can be said for wheels when the body plans have fins/legs/and wings already.</p>\n<p>Argument 3, which I also tend to agree with, is perhaps more convincing. By the time a pair of animals makes a symbiotic relationship to do this, or a single macroscopic animal evolves wheels, they will literally develop legs and walk away. When life came onto the land this happened, and since then it's happened several times. It's sort of like saying that the random movement of water molecules might line up to run a stream uphill. There's just such a strong path downwards, that the statistical chances of you seeing it happen are nil.</p>\n<p>This is a hypothetical case, but arguing this in a convincing way I think you would need to lay out: a) an environment whose conditions created enough of a selective advantage for wheels to evolve over legs or other similar adaptations we already see. Perhaps based on the energy efficiency of wheels; b) some sort of physiological model for the wheels that convey a reasonable lifestyle for the wheel.</p>\n<p>There are lots of questions that would need to be satisfied in our thought experiment. Here are some: "the symbiotic wheel would be spinning constantly; if it died the driver creature would be completely defenseless"; "if the ground were bumpy, all these wheeled animals would get eaten"; "the wheel symbiont — how would it eat while its spinning all the time? Only fed by the driver? Even symbionts such as barnacles or lampreys on the flanks of sharks still have their own ability to feed."</p>\n<p>For many similar questions the same sort of discussion ensues where there are many disadvantages which outweigh advantages for animals. e.g. "why are all the flying animals and fish and plants even more similar to airplanes than helicopters?"</p>\n<p>Sorry if I seem negative, but way back in grad school I actually did go over some of these angles.</p>\n<hr />\n<p><strong>UPDATE: <a href=\"http://www.popularmechanics.com/science/environment/the-first-gear-discovered-in-nature-15916433\" rel=\"nofollow noreferrer\">First Gear found in a Living Creature</a>.</strong>\nA <a href=\"http://www.sciencemag.org/content/341/6151/1254.full\" rel=\"nofollow noreferrer\">European plant-hopper insect with one of the largest accelerations known in biology has been found to have gears</a>! (There's a movie on the article page.\n)</p>\n<p>The little bug has gears in its exoskeleton that synchronize its two jumping legs. Once again selection surprises.</p>\n<blockquote>\n<p>The gears themselves are an oddity. With gear teeth shaped like cresting waves, they look nothing like what you'd find in your car or in a fancy watch. There could be two reasons for this. Through a mathematical oddity, there is a limitless number of ways to design intermeshing gears. So, either nature evolved one solution at random, or, as Gregory Sutton, coauthor of the paper and insect researcher at the University of Bristol, suspects, the shape of the <em>issus</em>'s gear is particularly apt for the job it does. It's built for "high precision and speed in one direction," he says.</p>\n</blockquote>\n<p>The gears do not rotate 360 degrees, but appear on the surface of two joints to synchronize them as they wind up like a circular spring. The gear itself is not living tissue, so the bug solves the problem of regenerating the gear by growing a new set when it molts (i.e. gears that continually regenerate and heal are still unknown). It also does not keep its gears throughout its lifecycle. So the arguments here still stand; the exception still supports the rule.</p>\n<p>Additional Note: In his book "<a href=\"https://en.wikipedia.org/wiki/The_God_Delusion\" rel=\"nofollow noreferrer\">the God Delusion</a>" (Chapter 4 somewhere) Richard Dawkins muses that the flagellar motor is the only example of a freely rotating axle that he knows of, and that a wheeled animal might be a true example of 'irreducibly complexity' in biology... but the fact that there is no such example is probably to the point.</p>\n"
}
] |
[
{
"answer_id": 7938,
"pm_score": 4,
"text": "<p>Shigeta's molecular answer is spot on. However, at the large scale level I think the key problem with a biological wheel needs to be spelled out clearly: how does an organism with separate parts maintain these parts? Let's suppose that an organism evolves a fully rotational joint, how do they then provide nutrients to the tissue on the other side? If they don't provide nutrients how does self-repair in this tissue continue without nutrients?</p>\n\n<p>Mind you, I'm not sure that the biological problems with a wheel are the real answer. I'm not sure how a wheel evolves. What's the functional intermediate? How does a semi-connected wheel out-perform a limb? Remember than evolution is canalised by what has gone before.</p>\n"
},
{
"answer_id": 7941,
"pm_score": 4,
"text": "<p>In your question, you mention frozen lakes and rightly say that skates would be far easier than wheels, but you could have used salt flats as an example.</p>\n\n<p>I think the reason there are no actual wheels is a mixture of ontogenetic and phylogentic barriers, maintenance (nutrition), lubrication and control (nerve connections). There would have to be severe and sustained evolutionary incentives to go from something simple, cheap and extant (legs) to something way more difficult and complex.</p>\n\n<p>However, there are several species of plants and animals that use rolling as a form of locomotion. Tumbleweeds are a good example of plants, and for animals, there are <a href=\"https://www.youtube.com/watch?v=bzAF7WuXhKA\">spiders</a>, <a href=\"https://www.youtube.com/watch?v=HmLS2WXZQxU\">caterpillars and salamanders</a>.</p>\n\n<p>It only takes a small evolutionary development to take something like this from a passive motion (rolling down hill to escape predators) to active (perhaps creating waves of flexion to roll like... ahem, caterpillar tracks).</p>\n"
},
{
"answer_id": 30947,
"pm_score": 3,
"text": "<p>There's a basic philosophical problem with asking why there aren't such-and-such. We could as easily ask why there are no six-limbed vertebrates, or creatures that use hydrogen to fly like balloons. It's not (necessarily) that they're mechanically or biologically impossible, it's just that evolution started down another pathway first, and (by changing the nature of the \"adjacent possible\") that closed off the paths that led to such creatures.</p>\n"
},
{
"answer_id": 108310,
"pm_score": -1,
"text": "<p>Probablity of evolution of wheel legs, helicopters birds and propellor fish and also depends on:</p>\n<ol>\n<li><p>The strength of the advantage gained (wheels are inefficient in 99% of biological habitats, forests, praries, wheras salt flats have adverse conditions)</p>\n</li>\n<li><p>The ease of development of intermediate forms: Small wheels and half weels have little to no efficiency.</p>\n</li>\n</ol>\n"
}
] |
9,172 |
<p>I made an answer on the Scifi.SE that can be read <a href="https://scifi.stackexchange.com/questions/37780/how-did-they-clone-other-breeds-of-dinosaur-other-than-the-one-in-the-blood-of-t/37806#37806">here</a>. It is about how the characters in the story Jurassic Park might have gotten DNA for all the species shown.</p>
<p>In my answer, I said this:</p>
<blockquote>
<p>Apes and Humans, for example, share over 99% of their genes. That means the difference between our species is less than 1% of our genes. In fact, all life on Earth shares about 50% of it's genes.</p>
</blockquote>
<p>but in the original posting (before someone edited it) I chose to use the word DNA instead of genes.</p>
<p>He left this comment in the section to explain the edit:</p>
<blockquote>
<p>Sorry, I'm a biologist, I can't help it. Humans and apes share 99% similarity in the coding sequences of their DNA, the ~5% that codes for genes, not on all the DNA. I simplified this to genes for the answer.</p>
</blockquote>
<p>I have a basic high school understanding of DNA and genes, so I'm afraid I fail to see the difference between using "DNA" or using "genes" in my statement. I understand that genes are specific sequences of DNA that are used by the cell in some way. I understand that DNA is more generic, including all of the strands, whether they are used or not, whether they seem to code for something or not.</p>
<p>So is it wrong then to say that apes and humans share 99% of their DNA or is it equally correct to say "genes"?</p>
|
[
{
"answer_id": 9174,
"pm_score": 6,
"text": "<p>So, a quick molecular biology lesson. </p>\n\n<ul>\n<li><strong>Proteins</strong> are the things that make up a good percentage of our cells (which make up a good percentage of <em>us</em>), and are the things that do the work of the cells - many are catalysts and are known as \"enzymes\". </li>\n<li><p>Proteins are encoded by <strong>genes</strong> - while the statement that one gene\ncodes for one protein is not quite correct (one gene can code for\ndifferent variations of the same basic protein), it's a good way to\nthink about things in this context.</p></li>\n<li><p>Genes are made up of <strong>DNA</strong>, a polymeric molecule that constitutes our chromosomes, the informational portion of which resides four “letters” (chemical bases).</p></li>\n<li><p>However, now we get to the key part — although <em>all genes are made of DNA,\nnot all the DNA of chromosomes makes up genes</em>. In fact, as @terdon mentioned in a comment, only about 5% (or less) of the 4 billion letters in the total DNA — the <strong>genome</strong> — constitute genes - those sequences that<br>\ndirectly code for protein. </p></li>\n<li><p>The function of the rest of the genome is not entirely clear. Some is regulatory, some may be structural, and may be “junk DNA”. However it’s stuck around for millions of years, so it we assume it must have some purpose. This non-coding DNA differs between species to a greater extent than the genes themselves do, so perhaps it somehow contributes to the differences between organisms.</p></li>\n</ul>\n\n<hr>\n\n<p>From <a href=\"https://biology.stackexchange.com/users/1757/androidpenguin\">AndroidPenguin</a></p>\n\n<p>Here are the links to a paper about the function of \"junk\" DNA from 2013. </p>\n\n<ol>\n<li><p><a href=\"http://www.nytimes.com/2012/09/06/science/far-from-junk-dna-dark-matter-proves-crucial-to-health.html?pagewanted=all\" rel=\"nofollow noreferrer\">Summary in NY Times</a></p></li>\n<li><p><a href=\"http://www.nature.com/nature/journal/v489/n7414/full/489045a.html\" rel=\"nofollow noreferrer\">Abstract in Nature</a></p></li>\n<li><p><a href=\"http://www.nature.com/encode/#/threads\" rel=\"nofollow noreferrer\">ENCODE threads on nature.com</a></p></li>\n</ol>\n"
}
] |
[
{
"answer_id": 9173,
"pm_score": 3,
"text": "<p>Just to clarify definitions, your <a href=\"http://en.wikipedia.org/wiki/Genome\" rel=\"noreferrer\">genome</a> is made up of sequences of DNA. DNA is constructed pairs of four nucleic acids, or nucleotides (A,G,T,C). That DNA has many <a href=\"http://en.wikipedia.org/wiki/Locus_%28genetics%29\" rel=\"noreferrer\">loci</a> within it, each codes for a gene. Loci are given gene names such as SHH (sonic hedgehog) which is part of a discipline called <a href=\"http://en.wikipedia.org/wiki/Gene_nomenclature\" rel=\"noreferrer\">gene nomenclature</a>. Humans have two versions of each gene, one from each parent. These genes, such as SHH, have different variants called <a href=\"http://en.wikipedia.org/wiki/Allele\" rel=\"noreferrer\">alleles</a>. This is where you may have heard the terms homozygote and heterozygote, when a person has two copies of the same allele or two different ones respectively. You may remember talking about <a href=\"http://circuitsurfersdotcom.files.wordpress.com/2011/08/sickle-cell.jpg\" rel=\"noreferrer\">sickle cell anemia in high school.</a></p>\n<blockquote>\n<p>So is it wrong then to say that apes and humans share 99% of their DNA or is it equally correct to say "genes"?</p>\n</blockquote>\n<p>Well the similarity between humans and chimps in terms of known DNA sequence is about 98.8%, there is fairly low sequence divergence, so in my opinion you are right to say that they share 99% of their DNA. This means that in 100 nucleotides there is roughly one difference e.g. (showing 90 bases, made using random sample of four letters in R):</p>\n<blockquote>\n<p><strong>Human DNA strand:</strong></p>\n<p>atgactgtagcccatga <strong>t</strong>\ngtaaacgtaccaagcctcctcggctgtcccgaaatagatacgcctggtagacgtattaatagtgagtaa...cgt</p>\n<p><strong>Chimpanzee:</strong></p>\n<p>atgactgtagcccatga <strong>c</strong> gtaaacgtaccaagcctcctcggctgtcccgaaatagatacgcctggtagacgtattaatagtgagtaa...cgt</p>\n</blockquote>\n<p>Having said that, given that there is <a href=\"http://www.genome.gov/11006943\" rel=\"noreferrer\">>3,000,000,000 base pairs in the human genome</a> (the sequence of 4 nucleotides that make up the DNA) that equates to ~36,000,000 different base pairs (bnetween humans and chimps) which likely equates to a large difference. Sometimes even a single nucleotide polymorphism (SNP, pronounced snip), a change in just one base pair, can bring about quantifiable changes:</p>\n<blockquote>\n<p>a single base mutation in the APOE (apolipoprotein E) gene is\nassociated with a higher risk for Alzheimer disease.</p>\n</blockquote>\n<p>Here is a little <a href=\"http://www.amnh.org/exhibitions/past-exhibitions/human-origins/understanding-our-past/dna-comparing-humans-and-chimps\" rel=\"noreferrer\">reading on the humans vs chimp</a>. You may also wish to see this similar post on <a href=\"https://biology.stackexchange.com/questions/1981/how-many-genes-do-we-share-with-our-mother\">biology SE</a>.</p>\n<p>But the editor of your original post is right... only the Euchromatic region has been sequenced.</p>\n<blockquote>\n<p>"Humans and apes share 99% similarity in the <strong>coding sequences</strong> of their DNA"</p>\n</blockquote>\n<p>The euchromatic region is often thought of as the protein coding part of the DNA, and makes up <a href=\"http://www.nature.com/nature/journal/v431/n7011/full/nature03001.html\" rel=\"noreferrer\">92% of the genome</a> (I think this is perhaps 92% of genes, but only a small part of the physical DNA).</p>\n<p>The rest, the heterochromatin, contains non-sequenced information and could harbour some of the DNA variation between the two species. Some work has suggested that the heterochromatin, previously labelled as Junk DNA, actually has some effect on traits. For example in <em>Drosophila</em> there has been studies which show <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/18174442\" rel=\"noreferrer\">effects of the Y chromosome</a> on traits despite the Y chromosome being mainly heterochromatic.</p>\n<hr />\n<p>Further: I think a common source of confusion comes from the use of the word gene. It is often used interchangeably to mean either <strong><a href=\"http://en.wikipedia.org/wiki/Allele\" rel=\"noreferrer\">Allele</a></strong> or <strong><a href=\"http://en.wikipedia.org/wiki/Locus_%28genetics%29\" rel=\"noreferrer\">Genetic Locus</a></strong>. When someone says that humans and apes share 99% of their genes they mean they share 99% of their genetic loci. When someone says that a person shares 50% of their genes with a parent they mean that they share half of their alleles with that parent (it is only roughly half due to recombination and mutation). An individual has all (barring genetic defects <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/18157829\" rel=\"noreferrer\">such as deletions</a>) the same loci as their parent.</p>\n"
},
{
"answer_id": 9226,
"pm_score": 4,
"text": "<p>Since it was my edit of your question that started all this, I may as well weigh in. I will give a <strong>simplified</strong> version of genes and gene transcription, there are various details that make the process much more complicated than what I will describe but they are not relevant to the basic question here.</p>\n\n<p>First of all, as others have mentioned, genes are specific sequences of DNA. A gene's job is to \"code for\" a protein (first big simplification). However, not <em>all</em> of the gene codes for protein, only those parts of it called <a href=\"http://en.wikipedia.org/wiki/Exon\" rel=\"noreferrer\">exons</a> (image modified slightly from <a href=\"http://err.bio.nyu.edu/courses/index.php/Griffin\" rel=\"noreferrer\">here</a>):</p>\n\n<p><img src=\"https://i.stack.imgur.com/MZRny.png\" alt=\"enter image description here\"></p>\n\n<p>The take home message from the image above is that the red bits (the <a href=\"http://en.wikipedia.org/wiki/Intron\" rel=\"noreferrer\">introns</a>) are removed and do not affect the final protein product. So, only <em>part</em> of the gene codes for the protein. Introns tend to be far less conserved between different species than exons. </p>\n\n<p>Not only does the entire gene not code for protein but most of the genome does not contain genes. In fact, in humans, genes represent ~5% of the total DNA and <em>exons</em> represent ~2%. </p>\n\n<p>Another confounding factor are the sequences called <em><a href=\"https://en.wikipedia.org/wiki/Repeated_sequence_%28DNA%29\" rel=\"noreferrer\">repetitive elements</a></em>. These are various types of usually shortish sequences that exist in many copies in genomes, In the human genome ~41% <a href=\"http://www.ncbi.nlm.nih.gov.gate1.inist.fr/pubmed/8994846\" rel=\"noreferrer\">consists of repetitive elements</a> of various types, and ~10% represents copies of a single such element (Alu), that's twice as many as genes. Such repetitive elements are usually not considered when calculating whole genome similarity rates. </p>\n\n<p>In terms of their <em>entire</em> genome, human and chimp are very very similar. However, the exact percentages vary (I've seen estimates from ~85 to ~90something) depending on the way the sequences are studied. To be on the safe side, you should say that they share 99% similarity <em>at the gene level</em> and leave it at that.</p>\n"
},
{
"answer_id": 51384,
"pm_score": 3,
"text": "<p>Most of the answers here focus on the difference between the concepts of 'DNA' and 'genes' very well. However, the sequence identity between humans and chimpanzees is not covered as rigorously and remains unclear from what has been answered. Therefore, I will elaborate on that, so that the first part of the question is also covered.</p>\n\n<p>Humans and chimpanzees differ approximately every 100 nucleotides in their total DNA sequence. This is does not mean that 98.5% of the genes are shared. It means that humans have about 98.5% (more precisely about 98.8%, <a href=\"http://www.nature.com/nature/journal/v437/n7055/full/nature04072.html\" rel=\"noreferrer\">The Chimpanzee Sequencing and Analysis Consortium, 2005</a>) sequence identity with chimpanzees, disregarding <a href=\"https://en.wikipedia.org/wiki/Indel\" rel=\"noreferrer\">indels</a>. They treated indels and nucleotide differences separately and \"calculate[d] the g<strong>enome-wide nucleotide divergence between human and chimpanzee to be 1.23%</strong>\" which includes intergenic regions and introns - so obviously also <strong>non-genic regions</strong>. Sequence identity <em>at the gene level</em> is presumably way bigger.</p>\n\n<p><a href=\"http://www.nature.com/nature/journal/v437/n7055/full/nature04072.html\" rel=\"noreferrer\">The Chimpanzee Sequencing and Analysis Consortium</a> also gives information how this divergence is structured. The main part (about 85% of the 30 - 35 Mio. different nucleotides) comes from <strong>fixed differences</strong>: a fixed difference is a position in the haploid genome in which <strong>every human</strong> has, say, a G and <strong>every chimpanzee</strong> has a T. Accordingly, the site is different between the two species for <strong>every individual</strong> of the respective species. The smaller part (about 15%) comes from sites that are either variable (<a href=\"https://en.wikipedia.org/wiki/Single-nucleotide_polymorphism\" rel=\"noreferrer\">SNP</a>) in humans or variable in chimpanzees, or in both (there is even a small number of very old variants, i.e. <strong>shared alleles</strong> between humans and chimpanzees, e.g. see <a href=\"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4559023/\" rel=\"noreferrer\">Azevedo et al., 2015</a>). Note that the estimates get better the more individuals of the respective species are sequenced and compared. </p>\n"
},
{
"answer_id": 60202,
"pm_score": 1,
"text": "<p>I just read a article that says even the 99% stat is not technically correct. To get to that number they had to ignore 25% of the human DNA and I think 18% of the chimp DNA. I am also assuming the stat was only including the coded DNA. Because if the what they used to refer to as junk DNA is not the same, then the 99% stat from 2005 starts to look less and less accurate and bit misleading.\n<a href=\"https://futurism.com/watch-do-we-really-share-99-our-dna-chimps/\" rel=\"nofollow noreferrer\">https://futurism.com/watch-do-we-really-share-99-our-dna-chimps/</a></p>\n"
},
{
"answer_id": 68170,
"pm_score": 0,
"text": "<p>Humans and chimpanzees differ approximately every 100 nucleotides in their total DNA sequence.This is does not mean that 98.5% of the genes are shared.It means that human have about 98.5% (more precisely about 98.8%,The Chimpanzee Sequence and Analysis Consortium,2005) sequence identity with chimpanzees,disregarding indels.They treated indels and nucleotide differences separately and \"calculate[d] the genome-wide nucleotide divergence between \nhuman and chimpanzee to be 1.23%\" which includes intergenic regions and introns-so obviously also non-genic regions.Sequence identity at the gene level is presumably way bigger.</p>\n"
}
] |
9,419 |
<p>Reading this question, <a href="https://biology.stackexchange.com/questions/7932/why-are-there-no-wheeled-animals">Why are there no wheeled animals?</a>, I wondered why <strong>no organisms seem to make use of the tensile and other strengths of metal</strong>, as we do in metal tools and constructions. I am obviously not talking about the microscopic uses of metal, as in human blood etc.</p>
<p>Why are there no plants with metal thorns? No trees with "reinforced" wood? No metal-plated sloths? No beetles with metal-tipped drills? Or are there?</p>
<p>I can think of some <strong>potential factors</strong> why there are none (or few), but I do not know whether they are true:</p>
<ol>
<li>Is metal too <strong>scarce</strong> near the surface?</li>
<li>Are there certain chemical properties that make metal <strong>hard to extract and accumulate in larger quantities</strong>?</li>
<li>Is metal <strong>too heavy</strong> to carry around, even in a thin layer or mesh or tip?</li>
<li>Can metal of high (tensile etc.) strength only be forged under <strong>temperatures too high</strong> to sustain inside (or touching) organic tissue, and is <strong>crystallised metal too weak</strong>?</li>
<li>Are functionally comparable organic materials like horn, bone, wood, etc. in fact <strong>better at their tasks than metal</strong>, and do we humans only use metal because we are not good enough at using e.g. horn to make armour or chitin to make drills?</li>
</ol>
<p>As a predator, I would like to eat a lot of vertebrates and save up the metal from their blood to reinforce my fangs...</p>
<hr />
<p>A bonus question: are there any organisms that use the high <strong>electric conductivity</strong> of metal? Animals depend upon electric signals for their nervous system, but I do not think nerves contain much metal. The same applies to the few animals that use electricity as a weapon.</p>
|
[
{
"answer_id": 9420,
"pm_score": 7,
"text": "<p>There are some cases, as hinted at by the comments. But these are relatively small amount of metal.</p>\n<p>It's not that there is no metal available. Iron in particular <a href=\"https://www.livescience.com/29263-iron.html\" rel=\"nofollow noreferrer\">is the fourth most common element in the earth's crust</a> and soil that has a reddish color has iron in it. There are several reasons you don't see iron exoskeletons on animals all the time. Firstly, fully reduced (oxidation state 0) metal has a high energetic cost to create in reduced form.</p>\n<p>Iron is the <a href=\"http://en.wikipedia.org/wiki/Abundance_of_elements_in_Earth%27s_crust\" rel=\"nofollow noreferrer\">second most common metal after aluminum on the earth's crust</a> but it's almost entirely present in oxidized states - that's to say: as rust. Most biological iron functions in the +2/+3 oxidation state, which is more similar to rust than metal. <a href=\"http://rcsb.org/pdb/101/motm.do?momID=82&evtc=Suggest&evta=Moleculeof%20the%20Month&evtl=OtherOptions\" rel=\"nofollow noreferrer\">Cytochromes</a> and <a href=\"http://rcsb.org/pdb/101/motm.do?momID=41\" rel=\"nofollow noreferrer\">haemoglobin</a> are examples of how iron is more valuable as a chemically active biological agent than a structural agent, using oxidized iron ions as they do. <a href=\"http://www.siliconfareast.com/ox_potential.htm\" rel=\"nofollow noreferrer\">Aluminium, the most common metal on Earth, has relatively little biological activity - one might assume because its redox costs are even higher than iron</a>.</p>\n<p>If there are some reasons why reduced biometal doesn't show up very often, inability of biological systems to deposit reduced (metallic) metals is <em>not</em> one of them. Bone and <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/17950376\" rel=\"nofollow noreferrer\">shell</a> are examples of biomineralization where the proteins depositing the calcium carbonate or other oxides in the material are structured by the proteins to be stronger than they would be as a simple crystal. There are cases of admittedly small pieces of reduced metal being produced by biological systems. The <a href=\"http://en.wikipedia.org/wiki/Magnetotactic_bacteria#Magnetosomes\" rel=\"nofollow noreferrer\">Magnetosomes</a> in magnetotactic bacteria are mentioned, but there are also cases of <a href=\"http://www.nature.com/nature/journal/v495/n7440_supp/full/495S12a.html\" rel=\"nofollow noreferrer\">reduced gold being accumulated by microorganisms</a>.</p>\n<p>I would say that while iron skeletons might seem to be an advantage, they are electrochemically unstable - oxygen and water will tend to oxidize (rust) them quickly and the organism would have to spend a lot of energy keeping it in working form. Electrical conductivity sounds useful, but the nervous system favors exquisite levels of control over bulk current flow, even in cases like electric eels, <a href=\"http://www.pnas.org/content/70/9/2473.full.pdf\" rel=\"nofollow noreferrer\">whose current is produced by gradients from acetylcholine</a>.</p>\n<p>What's more, it is a fact that biological materials actually perform as well as or better than metal when they need to. Spider silk has a greater tensile strength than steel (along the direction of the thread). Mollusk shells are models for tank armor - they are remarkably resistant to puncture and breakage. The time it would take for metalized structures to evolve biologically might be too long - by the time the metalized version of an organ or skeleton got started, the bones, shells and fibers we know probably have a big lead and selective advantage.</p>\n"
}
] |
[
{
"answer_id": 9426,
"pm_score": 5,
"text": "<p>A few minor points to add to shigeta's excellent answer:</p>\n\n<p>Biological enzymes don't work well on metals. Some often incorporate metals (see <a href=\"https://en.wikipedia.org/wiki/Chelation\">chelation</a>) but elemental atoms aren't easy to process. For one, a large molecule would be identical everywhere, so cleavage, for example, would be indiscriminate and just leave a bunch of tiny tiny atoms.</p>\n\n<p>More to the point, once an organism incorporates metal there certainly isn't a lot it can do about that. A lot of shell-based organisms swap out their shells because of the inflexibility of those designs, and metal would be no different. It's difficult to grow when you're encased in a self-made iron maiden.</p>\n"
},
{
"answer_id": 9442,
"pm_score": 4,
"text": "<p>There are good reasons why tissues/structures with a very high metal content might cause problems (I defer to the other answers here).</p>\n\n<p>However, I am aware of one other example: some <a href=\"http://researchrepository.murdoch.edu.au/1728/1/radula_synthesis.pdf\">molluscs</a> incorporate high concentrations of iron into the points of the radula (basically a ribbon of teeth, used for grazing). This is especially important for grazing molluscs, as they essentially make a living by scraping a thin layer of microalgae directly off the rock surface.</p>\n"
},
{
"answer_id": 30253,
"pm_score": 4,
"text": "<p>Well there is the common Bloodworm (Glycera dibranchiata)which people use for fishing bait. The animals are unique in that they contain a lot of copper without being poisoned. Their jaws are unusually strong since they too contain the metal in the form of a copper-based chloride biomineral, known as atacamite.</p>\n\n<p><a href=\"http://www.sciencemag.org/content/298/5592/389.long\">http://www.sciencemag.org/content/298/5592/389.long</a></p>\n\n<p>And unlike the clamworm (Nereis limbata), whose jaws contain the metal zinc, the copper in the mineral in the jaws of Glycera is actually present in its crystalline form.</p>\n\n<p><a href=\"http://www.pnas.org/cgi/pmidlookup?view=long&pmid=12886017\">http://www.pnas.org/cgi/pmidlookup?view=long&pmid=12886017</a></p>\n\n<p>It is theorized that this copper is used as a catalyst for its poisonous bite.</p>\n\n<p>(I got this from Wikipedia)</p>\n"
},
{
"answer_id": 35254,
"pm_score": 4,
"text": "<p>Looks like some parasitoid wasps have zinc coated barbs on their ovipositors which may function to help them bore through wood and lay their eggs.</p>\n\n<p>Here's the blog entry about it on <a href=\"http://www.iflscience.com/plants-and-animals/these-wasps-have-zinc-tipped-drill-bits\">IFL Science</a>, and the original article:</p>\n\n<blockquote>\n <p>parasitoid ovipositor specimens had a weight percentage of zinc of 7.19±3.8% (N=42) in the tip regions, which was significantly higher (P<0.05) than that in pollinator and parasitoid remote regions (<1%; N=10).</p>\n</blockquote>\n\n<p><a href=\"http://jeb.biologists.org/content/217/11/1946.full\">Kundanati and Gundiah (2014) Biomechanics of substrate boring by fig wasps. <em>J Exp Bio</em> 217: 1946-1954</a></p>\n"
},
{
"answer_id": 44205,
"pm_score": 4,
"text": "<p><a href=\"https://en.m.wikipedia.org/wiki/Scaly-foot_gastropod\">https://en.m.wikipedia.org/wiki/Scaly-foot_gastropod</a></p>\n\n<p>Gastropod that incorporates greigite, pyrite, and graphite on it's shell and foot.</p>\n\n<p>Due to the large quantities of these compounds in dissolved form surround the hydrothermal vents.</p>\n\n<p>Speculation for purpose: the shell is extremely resilient, the metal does improve this greatly. Though whether evolution deemed this adaptation necessary because of an abundance of strong predators, or as a means of detoxification of the injested compounds, is unclear.</p>\n\n<p>The three populations of these snails have varied compositions, one which even being magnetic, due to the different compounds produced by the vents.</p>\n\n<p>Appologies, here is non wiki <a href=\"http://www.esa.org/esablog/research/iron-plated-snail/\">http://www.esa.org/esablog/research/iron-plated-snail/</a></p>\n"
},
{
"answer_id": 55182,
"pm_score": 3,
"text": "<p>Have you ever looked up the scaly foot gastropod? It uses iron as a form of body armor. Literally scale armor on It's foot. <img src=\"https://i.stack.imgur.com/r3R96.jpg\" alt=\"enter image description here\"></p>\n"
},
{
"answer_id": 56122,
"pm_score": 3,
"text": "<p>Though not in metallic (0) stage; an Iron ore called \"<a href=\"https://en.wikipedia.org/wiki/Bog_iron\" rel=\"noreferrer\">Bog-Iron</a>\" is formed via microbial process. </p>\n\n<hr>\n\n<blockquote>\n <p>Fig-1: <strong><em>Bog iron</em></strong><br>\n <a href=\"https://i.stack.imgur.com/p5Uto.jpg\" rel=\"noreferrer\"><img src=\"https://i.stack.imgur.com/p5Uto.jpg\" alt=\"Bog Iron\"></a><br>\n (<a href=\"https://commons.wikimedia.org/wiki/File:Hands-on-bog-iron.jpg\" rel=\"noreferrer\">Wikimedia</a>)</p>\n</blockquote>\n\n<hr>\n\n<p>It is formed inside <a href=\"https://en.wikipedia.org/wiki/Bog\" rel=\"noreferrer\">bogs</a> and <a href=\"https://en.wikipedia.org/wiki/Swamp\" rel=\"noreferrer\">swamps</a>, classically in <a href=\"https://en.wikipedia.org/wiki/Sphagnum\" rel=\"noreferrer\"><em>Sphagnum</em></a>-<a href=\"https://en.wikipedia.org/wiki/Moss\" rel=\"noreferrer\">moss</a>-<a href=\"https://en.wikipedia.org/wiki/Bog\" rel=\"noreferrer\">bogs</a>. It is also found in <a href=\"https://en.wikipedia.org/wiki/Peat#Characteristics_and_uses\" rel=\"noreferrer\">peat</a>.</p>\n\n<hr>\n\n<blockquote>\n <p>Fig-2: <strong><em>a bog</em></strong><br>\n <a href=\"https://i.stack.imgur.com/iAcq7.jpg\" rel=\"noreferrer\"><img src=\"https://i.stack.imgur.com/iAcq7.jpg\" alt=\"A bog\"></a><br>\n (<a href=\"https://en.wikipedia.org/wiki/Bog\" rel=\"noreferrer\">Wikipedia</a>) , (<a href=\"https://commons.wikimedia.org/wiki/File:Koitj%C3%A4rve_raba_05-2015.jpg\" rel=\"noreferrer\">Wikimedia</a>) </p>\n</blockquote>\n\n<hr>\n\n<blockquote>\n <p>Fig-3: <em>Sphagnum</em> sp, common bog moss of temperate and cold regions. \n <a href=\"https://i.stack.imgur.com/9eyTS.jpg\" rel=\"noreferrer\"><img src=\"https://i.stack.imgur.com/9eyTS.jpg\" alt=\"*Sphagnum* sp\"></a><br>\n (<a href=\"https://commons.wikimedia.org/wiki/File:Sphagnum.flexuosum.jpg\" rel=\"noreferrer\">Wikimedia</a>) </p>\n</blockquote>\n\n<hr>\n\n<p>When Fe(2) or ferrous ion, the more soluble form, obtained in the groundwater of bog region from some mineral-source such as <a href=\"https://en.wikipedia.org/wiki/Spring_(hydrology)\" rel=\"noreferrer\">spring</a>, the <a href=\"https://en.wikipedia.org/wiki/Anaerobic_organism\" rel=\"noreferrer\">anaerobic</a> <a href=\"https://en.wikipedia.org/wiki/Iron-oxidizing_bacteria\" rel=\"noreferrer\">iron oxidizing bacteria</a>, such as <em>Gallionella</em> and <a href=\"https://en.wikipedia.org/wiki/Leptothrix\" rel=\"noreferrer\"><em>Leptothrix</em></a> etc, oxidized it into Fe(3) or ferric form; which very easily get <a href=\"https://en.wikipedia.org/wiki/Precipitation_(chemistry)\" rel=\"noreferrer\">precipitated</a> as insoluble compounds. </p>\n\n<hr>\n\n<blockquote>\n <p>Fig 4: Spring acts as iron source.<br>\n <a href=\"https://i.stack.imgur.com/h5D0M.jpg\" rel=\"noreferrer\"><img src=\"https://i.stack.imgur.com/h5D0M.jpg\" alt=\"spring works as source of iron\"></a><br>\n (<a href=\"https://en.wikipedia.org/wiki/Bog_iron\" rel=\"noreferrer\">Wikipedia</a>) , (<a href=\"https://en.wikipedia.org/wiki/File:Iron_bearing_water_in_a_spring.jpg\" rel=\"noreferrer\">Wikimedia</a>) , (<a href=\"https://pubs.usgs.gov/of/2003/of03-346/f5.htm\" rel=\"noreferrer\">USGS</a>) , (<a href=\"https://pubs.usgs.gov/of/2003/of03-346/fig5a.jpg\" rel=\"noreferrer\">USGS url</a>). </p>\n</blockquote>\n\n<hr>\n\n<hr>\n\n<blockquote>\n <p>Fig. 5: <em>Leptothrix</em> sp. , found in ferruginous environment.<br>\n <a href=\"https://i.stack.imgur.com/ABDYc.jpg\" rel=\"noreferrer\"><img src=\"https://i.stack.imgur.com/ABDYc.jpg\" alt=\"*Leptothrix* sp.\"></a><br>\n (<a href=\"https://commons.wikimedia.org/wiki/File:Leptothrix_lichtmikroskopisch.jpg\" rel=\"noreferrer\">Wikimedia</a>) </p>\n</blockquote>\n\n<hr>\n\n<p>The iron components found in bog-iron, is commonly <a href=\"https://en.wikipedia.org/wiki/Iron(III)_oxide-hydroxide\" rel=\"noreferrer\">iron(III) oxyhydroxides</a> (FeO)OH of varying compositions; geologically <a href=\"https://en.wikipedia.org/wiki/Goethite\" rel=\"noreferrer\">Goethite</a> and <a href=\"https://en.wikipedia.org/wiki/Limonite\" rel=\"noreferrer\">Limonite</a>. </p>\n\n<blockquote>\n <p>Fig. 6: Samples of \"bog ore\" from Nassawango Creek show vugs lined with goethite around massive \"ochre\".<br>\n <a href=\"https://i.stack.imgur.com/hchp5.jpg\" rel=\"noreferrer\"><img src=\"https://i.stack.imgur.com/hchp5.jpg\" alt=\"Samples of "bog ore" from Nassawango Creek show vugs lined with goethite around massive "ochre".\"></a><br>\n (<a href=\"https://pubs.usgs.gov/of/2003/of03-346/f5.htm\" rel=\"noreferrer\">USGS</a>) , (<a href=\"https://pubs.usgs.gov/of/2003/of03-346/fig5b.jpg\" rel=\"noreferrer\">URL</a>) </p>\n</blockquote>\n\n<hr>\n\n<p>Sources: \n></p>\n\n<blockquote>\n <ol>\n <li><p>Wikipedia. </p></li>\n <li><p><em>Iron Production in the Viking Age</em>, at <a href=\"http://www.hurstwic.org\" rel=\"noreferrer\">http://www.hurstwic.org</a> \n <a href=\"http://www.hurstwic.org/history/articles/manufacturing/text/bog_iron.htm\" rel=\"noreferrer\">http://www.hurstwic.org/history/articles/manufacturing/text/bog_iron.htm</a> </p></li>\n <li><p>Google books: <a href=\"https://books.google.co.in/books?id=gs0v6pRHlLsC&printsec=frontcover#v=onepage&q&f=false\" rel=\"noreferrer\">Topics in Ecological and environmental microbiology</a>/ Edited by Schmid and Schaechter/ AP; Chapter-37 ---> <a href=\"https://books.google.co.in/books?id=gs0v6pRHlLsC&lpg=PA557&dq=Bog%20iron%20origin%20anaerobic%20reduction&pg=PA557#v=onepage&q=Bog%20iron%20origin%20anaerobic%20precipitation&f=false\" rel=\"noreferrer\">metal precipitation</a> </p></li>\n <li><p>Google Books: <a href=\"https://books.google.co.in/books?id=2zVqBgAAQBAJ&printsec=frontcover#v=onepage&q&f=false\" rel=\"noreferrer\">Environmental Microbiology: Fundamentals and Applications: Microbial Ecology</a>/ Jean-Claude Bertrand/ Springer. \n Chapter 14 (<a href=\"https://books.google.co.in/books?id=2zVqBgAAQBAJ&lpg=PA607&dq=Bog%20iron%20origin%20anaerobic%20reduction&pg=PA607#v=onepage&q=IRON&f=false\" rel=\"noreferrer\">Biogeochemical cycles</a>) </p></li>\n <li><p>Google Books: Bryophyte Biology / Edited by Shaw and Goffinet / Cambridge; \n Chapter 9: <a href=\"https://books.google.co.in/books?id=fuOKCOlRngkC&lpg=PP1&dq=Bog%20iron%20origin%20sphagnum%20goffinet&pg=PA272#v=snippet&q=sphagnum%20iron&f=false\" rel=\"noreferrer\">Mineral nutrition, substratum ecology and pollution</a>/ J. W. Bates </p></li>\n <li><p><a href=\"https://www.jstor.org/stable/20112872?seq=1#page_scan_tab_contents\" rel=\"noreferrer\">Metal depositing bacteria and the distribution of Manganese and Iron in Swamp- waters/ Ghiorse and Chapnick</a>/ jstor.org</p></li>\n <li><p><a href=\"http://Bog%20iron%20formation%20in%20the%20Nassawango%20Creek%20watershed,%20Maryland,%20USA\" rel=\"noreferrer\">Bog iron formation in the Nassawango Creek watershed, Maryland, USA</a>/USGS (<a href=\"https://pubs.usgs.gov/of/2003/of03-346/f5.htm\" rel=\"noreferrer\">photos</a>)</p></li>\n </ol>\n</blockquote>\n"
},
{
"answer_id": 60431,
"pm_score": 2,
"text": "<p>im no biologist, but while not commonly cosidered, calcium IS a metal, so technically skeletons count.\nadditionally, while not technically a metal, limpet teeth are quite impressive.\n<a href=\"http://www.bbc.co.uk/news/science-environment-31500883\" rel=\"nofollow noreferrer\">http://www.bbc.co.uk/news/science-environment-31500883</a></p>\n"
},
{
"answer_id": 85029,
"pm_score": 2,
"text": "<p><a href=\"https://doi.org/10.1111/syen.12253\" rel=\"nofollow noreferrer\">Barden et al (2017)</a> have discovered an extinct species of ant (hell ant) that was alive 95 million years ago that had naturally occurring metal mandibles. Mandibles on ants are essentially the same as fangs on spiders or teeth on humans.</p>\n"
}
] |
9,438 |
<p>The recent <a href="http://www.the-scientist.com/?articles.view/articleNo/36624/title/New-Giant-Viruses-Break-Records/">news</a> about a new supermassive virus being discovered got me thinking about how we define viruses as non-living organisms whilst they are bigger than bacteria, and much more complex than we first gave them credit for. </p>
<p>What biological differences between viruses and cellular organisms have made viruses be deemed non-living?</p>
|
[
{
"answer_id": 9455,
"pm_score": 7,
"text": "<p>If this is a topic that really interests you, I'd suggest searching for papers/reviews/opinions written by <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/?term=Didier+Raoult+mimivirus\">Didier Raoult.</a> Raoult is one of the original discoverers of the massive <a href=\"https://en.wikipedia.org/wiki/Mimivirus\">Mimivirus</a> and his work will lead you to some truly fascinating discussions that I couldn't hope to reproduce here.</p>\n\n<p>The main argument for why viruses aren't living is basically what has been said already. Viruses are obligate parasites, and while plenty of parasites are indeed living what sets viruses apart is that they always rely on the host for the <em>machinery</em> with which to replicate. A parasitic worm may need the host to survive, using the host as a source for energy, but the worm produces and synthesizes its own proteins using its own ribosomes and associated complexes.</p>\n\n<p>That's basically what it boils down to. No ribosomes? Not living. One advantage of this definition, for example, is that it is a positive selection (everyone \"alive\" has got ribosomes) which eliminates things like mitochondria that are sort of near the boundary of other definitions. There are examples on either side of something that breaks every other rule but not this one. Another common rule is metabolism and while that suffices for most cases some living parasites have lost metabolic activity, relying on their host for energy.</p>\n\n<p>However (and this is the really interesting part) even the ribosome definition is a bit shaky, especially as viruses have been found encoding things like their own tRNAs. Here are a few points to think about:</p>\n\n<ul>\n<li>We have ribosome encoding organisms (REOs), so why can't we define viruses as capsid encoding organisms (CEOs)?</li>\n<li>Comparing viruses to a living organism such as a human is absurd, given the massive differences in complexity. A virus, really, is just a vehicle or genetic material, and would be more rightly compared to a sperm cell. Is a sperm cell alive, or is it a package for genetic material that is <em>capable</em> of life once it has infected/fertilized another cell?</li>\n<li>The really large DNA viruses often create cytoplasmic features called virus factories. These look an awful lot like a nucleus. What is a nucleus anyway? Maybe it's just a very successful DNA virus that never left.</li>\n<li>Viruses can get <a href=\"https://en.wikipedia.org/wiki/Sputnik_virophage\">viruses</a>.</li>\n</ul>\n\n<p>I'll wind down here, but suffice to say that while our current definition may have sufficed for a while, and still does, it is no longer quite solid. In particular, there is a theory alluded to above that eukaryotic life itself actually formed <em>because</em> of viruses. I can expand on this if you like, but here are some great sources:</p>\n\n<p>Boyer, M., Yutin, N., Pagnier, I., et al. 2009. Giant Marseillevirus highlights the role of amoebae as a melting pot in emergence of chimeric microorganisms. <em>PNAS</em>. 106(51):21848-21853 (<a href=\"http://dx.doi.org/10.1073/pnas.0911354106\">http://dx.doi.org/10.1073/pnas.0911354106</a>)</p>\n\n<p>Claverie, JM. Viruses take center stage in cellular evolution. 2006. <em>Genome Biology</em>. 7:110. (<a href=\"http://dx.doi.org/10.1186/gb-2006-7-6-110\">http://dx.doi.org/10.1186/gb-2006-7-6-110</a>)</p>\n\n<p>Ogata, H., Ray, J., Toyoda, K., et al. 2011. Two new subfamilies of DNA mismatch repair proteins (MutS) specifically abundant in the marine environment. <em>The ISME Journal</em>. 5:1143-1151 (<a href=\"http://dx.doi.org/10.1038/ismej.2010.210\">http://dx.doi.org/10.1038/ismej.2010.210</a>)</p>\n\n<p>Raoult, D. and Forterre, P. 2008. Redefining viruses: lessons from Mimivirus. <em>Nature Reviews Microbiology</em>. 6:315-319. (<a href=\"http://dx.doi.org/10.1038/nrmicro1858\">http://dx.doi.org/10.1038/nrmicro1858</a>)</p>\n\n<p>Scola, B., Desnues, C., Pagnier, I., et al. The virophage as a unique parasite of the giant mimivirus. 2008. <em>Nature</em>. 455:100-104 (<a href=\"http://dx.doi.org/10.1038/nature07218\">http://dx.doi.org/10.1038/nature07218</a>)</p>\n"
}
] |
[
{
"answer_id": 9439,
"pm_score": 4,
"text": "<p>There are quite some different definitions of being \"alive\", but a common one includes the need to have responsiveness, growth, metabolism, energy transformation, and reproduction (found from the <a href=\"http://www.britannica.com/EBchecked/topic/340003/life\">Encyclopedia Britannica</a>). Viruses depend on host cells to do all this, so seen alone as a virus outside a host cell, they are not alive.</p>\n\n<p>There's <a href=\"http://www.virology.ws/2004/06/09/are-viruses-living/\">another</a> short, but to the point blog entry about this.</p>\n"
},
{
"answer_id": 9445,
"pm_score": 5,
"text": "<p>It is only a question of definition. You can set the boundaries between living things and not living things anywhere.</p>\n\n<p>Some philosophers have argued that using a clear boundary between living and non-living things is not such a good solution. In nature, there would rather be a continuum from a stone to a bacteria.</p>\n\n<p>It is true that in thinking of viruses such as Lausannevirus or Marseillevirus we might be willing to integrate them in the category of living things. These viruses are giant, and even can be parasitized by other viruses.</p>\n\n<p>Viruses are made of proteins and contain nucleic acids (RNA or DNA). If you consider that they are alive, what would you say about viroids? A viroid is just a nucleic acid that is able to infect a host and cause the replication of itself. What about a prion? A prion is a protein that, roughly speaking, has the same consequences as that of a viroid.</p>\n\n<p>I think (one should check the literature, I might be mistaken) that there is a species of parasitoid wasp that produces out of its own genomes, viruses that reduce the host immune system in order to make the caterpillar a suitable habitat for the egg. Is this virus alive? Isn't it just a toxin of the wasp?</p>\n\n<p>I guess one reason for considering viruses as non-living is that we do not know how to branch them in the tree of life! Some might argue by the way that viruses would not at all form a monophyletic group.</p>\n\n<p>There are several people tackling the question of \"what is alive\". Unfortunately, the best book I know on the subject comes from the French literature; it is <a href=\"https://www.amazon.fr/Comment-d%C3%A9finir-vie-Hugues-Bersini/dp/2711748650/ref=sr_1_1?ie=UTF8&qid=1461354538&sr=8-1&keywords=comment%20definir%20la%20vie\" rel=\"nofollow noreferrer\">Comment définir la vie? by Bersini and Reisse</a>. In this field, the most popular authors are Varella and Maturana. Again, if I'm not mistaken, the definitions of life are quite different among philosophers, people having an interest in the origin of life, and people seeking a definition suitable for extra-terrestrial life.</p>\n"
},
{
"answer_id": 9446,
"pm_score": 4,
"text": "<p>I agree with the answers already given, these are the reasons that viruses are not considered alive. I want to point out though that this isn't an area you find 100% agreement on; there is a decent subset of biologists who <em>do</em> consider viruses alive. I would say - completely on the basis of personal observation - that virologists themselves are the group most likely to claim that viruses are alive.</p>\n\n<p><a href=\"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2837877/\">This paper</a> and <a href=\"http://www.scientificamerican.com/article.cfm?id=are-viruses-alive-2004\">this article</a> from the Scientific American have some coverage of the debate if you want to read more.</p>\n"
},
{
"answer_id": 9452,
"pm_score": 2,
"text": "<p>In addition to the good answers given here, I would like to propose a more intuitive argument against viruses being alive.</p>\n\n<p>Viruses are, at one point of their \"life\", simply a piece of DNA (or RNA). Would you consider a piece of DNA to be alive? If so, then are transposons alive? Are chromosomes alive? How about synthesizing a piece of DNA - is that creating life? The answer will probably be \"no\" for most people.</p>\n"
},
{
"answer_id": 9486,
"pm_score": 3,
"text": "<p>Despite great answers from Amory and Remi.b, I want to emphasize this: there is continual debate about the definition of life because <em>\"life\" is not something that exists in the real world</em>. </p>\n\n<p>People seek a definition of life that satisfies an intuitive notion of what alive should mean. They feel that, say, <a href=\"https://en.wikipedia.org/wiki/Intracellular_parasite\">intracellular parasites</a> should be considered alive, but (say) only if they have an enclosing membrane, like <a href=\"https://en.wikipedia.org/wiki/Rickettsia\">Rickettsia</a>, and not if they are just a virus, or just an RNA molecule like a <a href=\"https://en.wikipedia.org/wiki/Viroid\">viroid</a>.</p>\n\n<p>While people have a built-in intuition that, for example, reliably categorizes a tiger as alive and a rock as not alive, that intuition can't be precisely bounded by a definition such that everyone is satisfied by the boundary. There are arrangements of matter in the physical world that fall outside the clear region of the intuitive concept of life, and this leads to continual, unresolvable, argument on what a precise definition of life should be, and what it should include.</p>\n"
},
{
"answer_id": 50511,
"pm_score": -1,
"text": "<p>Good question; science yet don't know anything about \"What is Life\". </p>\n\n<p>Yes. Everything about life we discuss (whatever by a Newton, Descartes or Schrodinger), it is in a level of Sci-fi, or hardly alchemy. Anyone of us don't know actually what is it. </p>\n\n<p>The best characteristic of life is, \"we, the living-creatures, can <strong>sense</strong> . We have <strong>consciousness</strong>\" . </p>\n\n<p>But alas, anyone can judge its own consciousness. We can-not judge someone else or any-other object contains any consciousness or not. We can just <strong>guess</strong> other's consciousness from facial expressions (say cry) , behavior, polygraphs, physiological reactions (respiration, growth, ageing etc... ), complication, informational-content, reproduction, genetic-code and such. \n(<a href=\"https://www.youtube.com/watch?v=evQsOFQju08\" rel=\"nofollow\">https://www.youtube.com/watch?v=evQsOFQju08</a> , Is Your Red The Same as My Red? by Vsauce)</p>\n\n<p>(however a living object can lose consciousness for a while such as when we're chloroformed).</p>\n\n<p>In the same-way, we just <strong>guess</strong> presence of life in other objects from the complication, chemical structure (carbohydrate, proteins, lipid, DNA etc), metabolic reaction etc. and same evolutionary origin . same to us. In strict-logic we can't tell a lovely flying bird contains life and is conscious that an alien-robot is nonliving, lacking consciousness. We can guess, not prove, yet. </p>\n\n<hr>\n\n<p>In the same logic, all virus, viroids and prions (the organisms of \"border zone\") (including biggest viruses) could be (and often is) compared with living-organisms (like we're), due to their similar chemical structure, genetic codes, information content, reaction etc. with us, as-well plausibly same origin with us.</p>\n\n<hr>\n\n<p>There exist too, causes to consider all virus, viroids and prions (including biggest ones). I can call you alive. I can call your one organ (say hand) alive, could call a cell alive. But what we could call 1 protein-molecule? Just like a concrete-mixing machine (known to be nonliving), the protein-molecule is similarly made up of atoms... and nothing else. There is no evidence for \"vital-forces\" also... the protein molecule operates its works just with electromagnetic forces, thermal-collisions etc. There is no \"sign\" of life . In the same-way, a virus, viroid or a prion is just a lump of molecule. And for a big virus? a small hut (nonliving) : big house :: small virus : big virus. A big virus would be similar to a big bottle of nucleic acid.</p>\n\n<hr>\n\n<p>Any more-discussion would be completely opinion-based, but in my-opinion it is better to consider these borderline-organisms as alive, due to more valid-logic such as</p>\n\n<ol>\n<li><p>They're similar with us in chemical structure, genetic code bla bla bla ...</p></li>\n<li><p>They are plausibly same in origin with us.</p></li>\n<li><p>Inert structures, like plant-seeds if contain life, then in same logic we can imagine life in virions etc.</p></li>\n<li><p>We found different level of parasitism in living organisms, such as ATP-parasites (I forgot example and can't find right now), and consider them as alive. So why we'll not consider a \"protoplasm-parasite\" a living-organism?</p></li>\n</ol>\n"
}
] |
9,500 |
<p>If we somehow remove pheromones, <strong>do animals experience a phenomenon similar to human "visual beauty" when looking at members of the opposite sex?</strong> For example, given a set of 20 female ducks observed through a glass panel, would male ducks attempt to court/mate with a small subset of female ducks first(more attractive ones), or is it based on some other criteria (most receptive, random, closest, fittest, pheromones, etc?)</p>
<p>If there is some "visual attractiveness selection criteria", <strong>is there a requirement of certain complexity of the brain and/or visual system for an animal before this phenomenon starts to occur?</strong> </p>
<p>I'm aware of the existence of this question: <a href="https://biology.stackexchange.com/questions/7568/why-does-sexual-selection-evolve-beautiful-features">Why does sexual selection evolve beautiful features?</a>, and my question deals with the members of the same generation, not long-term evolution. </p>
|
[
{
"answer_id": 9503,
"pm_score": 4,
"text": "<p>There are numerous examples of visual attraction in animals. An absolute classic of an experiment, taught to most/all evolutionary biology students, is the <a href=\"http://www.treknature.com/gallery/photo139613.htm\" rel=\"nofollow\">widowbird</a> tail length <a href=\"http://www.nature.com/nature/journal/v299/n5886/abs/299818a0.html\" rel=\"nofollow\">experiment by Andersson</a>. He experimentally manipulated the tail lengths of male widowbirds at random. Some tails were made longer and some shorter. From this experiment Andersson showed that females choose males with longer tails more preferentially. Another classic example is the <a href=\"https://en.wikipedia.org/wiki/Lek_mating\" rel=\"nofollow\">lek mating system</a> where there is a bias in reproductive success towards attractive males, in some cases <a href=\"http://www.sfu.ca/biology/faculty/reynolds/The_Reynolds_Lab/Publications_files/Mackenzie%20et%20al.%20AN%2095.pdf\" rel=\"nofollow\">10-20% of the males get 70-80% of the matings</a>. </p>\n\n<blockquote>\n <p>A lek is an aggregation of males that gather to engage in competitive\n displays that may entice visiting females who are surveying\n prospective partners for copulation. Leks are commonly formed\n before or during the breeding season. A lekking species is defined by\n the following characteristics: male displays, <strong>strong female mate\n choice</strong>, and the conferring of male indirect benefits. Although\n lekking is most prevalent among avian species, lekking behavior is\n found in a variety of animals such as insects, amphibians, and\n mammals</p>\n</blockquote>\n\n<p><a href=\"http://en.wikipedia.org/wiki/Mate_choice#Indicator_traits\" rel=\"nofollow\">Beauty could be a an example of a an indicator trait</a>:</p>\n\n<blockquote>\n <p><strong>Indicator traits</strong> are those that <strong>signal good overall quality of the\n individual</strong>. Traits that are perceived as attractive must reliably\n indicate broad genetic quality in order for selection to favor them\n and for preference to evolve.</p>\n</blockquote>\n\n<p>I'm sure there are some studies in fish, likely guppies or zebra fish, which gave individual fish the opportunity to visually assess potential mates (placing tanks next to each other and observing courtship) which would be very similar to your hypothetical duck example. <a href=\"http://www.jstor.org/sici?sici=0014-3820%281982%2936:1%3C1:SSATEO%3E2.0.CO;2-9&origin=ISI\" rel=\"nofollow\">Despite often being a paradox, female mate choice is well documented.</a> Further, <a href=\"http://en.wikipedia.org/wiki/Mate_choice#Male_mate_choice.2FSex_role_reversal\" rel=\"nofollow\">male mate choice</a> is now coming to light, <a href=\"http://bonduriansky.net/BR-2001.pdf\" rel=\"nofollow\">even in species where female mate choice and male-male competition exists</a>.</p>\n\n<p>I don't think selection on \"beauty\" would require some kind of particularly special neural system, obviously some visual capacity is necessary for visual attraction and some basic neural pathways linked to that. I have done experiments myself in <em>Drosophila simulans</em> which looked at good gene benefits of mating with attractive males (indirect genetic benefits of female mate choice) and another which assessed precopulatory selection (female mate choice) for a secondary sexual character in the same species. Even in such a small-brained species there appears to be some degree of (partially visual) mate choice going on.</p>\n"
}
] |
[
{
"answer_id": 9502,
"pm_score": 3,
"text": "<p>Absolutely. Quality by appearance is sometimes a big part of mate selection and sometimes it is not. </p>\n\n<p>The size and cognitive capacity brain is probably important but not always. Primates are closest to us and have most similar tastes to us, <a href=\"http://www.hup.harvard.edu/catalog.php?isbn=9780674955394\">have varying levels of interest in mate appearance</a>. Most primates have a troupe dominance where a dominant male mates with <em>all</em> the females and sires as many offspring as he can before he loses his place on top. Many smaller primates rely more on sperm competition and the females mate with all the males they can when they are in estrus - the offspring just emerge from the most competitive sperm. Note I studied Sarah Hrdy a while ago. I hear <a href=\"http://en.wikipedia.org/wiki/Robert_Sapolsky\">Robert Sapolsky</a> is another great source of insight on primate/human behavior. </p>\n\n<p>Neither of these modes are quite so focused on visual beauty as our culture is. Other cultures are also not selective based on appearance, e.g. cultures where marriages are arranged would often consider the social and economic relationships between the families more than we do. This is a broad generalization, but just to point out that just looking at someone to decide mate choice isn't as dominant as sometimes it feels. </p>\n\n<p>But to look at some tiny brains I know that snakes often mate in gigantic balls of snake and mate choice is pretty indiscriminate, on the other hand, <a href=\"http://beheco.oxfordjournals.org/content/9/1/33.abstract\">spiders where female choice is dominant, males will experience rejection</a>. This is a bummer for the males because they only often live long enough to offer to one mate. Its probable that the females are not hungry or have recently mated with another male, but just an example to demonstrate that even small brained animals can be discriminating. </p>\n"
},
{
"answer_id": 9554,
"pm_score": 2,
"text": "<p>In addition to the answers stated here, it is also important to remember that we, humans, are more guided by vision than many other animals. Therefore, the idea of separating an animal from a potential mate with glass would also inhibit other important mate selection criteria that other organisms use (calls, pheromones, nest tending, etc.).</p>\n"
},
{
"answer_id": 9584,
"pm_score": 2,
"text": "<p>You seem to be dissociating physical beauty from fitness. In fact, beauty <em>can</em> be taken as a measure of biological fitness. For a classic, if simplistic example, many male humans find large breasts attractive and beautiful, however, large mammary glands are also an indication of fertility and robustness that would imply the prospective mate would be a good mother.</p>\n\n<p>Anything that we consider beautiful in a prospective mate can be interpreted in terms of fitness. Another classic example is symmetry. Humans are attracted to symmetrical faces and bodies. Since we are a symmetrical species, symmetry is an indication of fitness. In other words, lack of symmetry may indicate a developmental problem and by extension decreased fitness.</p>\n\n<p>There isn't really a qualitative difference between the way we define attraction and the way other animals do. In both cases we have instinctive attractions to healthy and fit (in the evolutionary sense) mates. It is simply that our complex society has marked these choices as \"aesthetics\" while we call them \"instincts\" in other animals.</p>\n"
},
{
"answer_id": 45652,
"pm_score": 1,
"text": "<p>Since asking this question, I've learned that <strong>97% of male mammals do not have concept of \"beauty\"</strong> and will mate with every female indiscriminately. These species do not have any paternal investment, so the males are not picky.</p>\n\n<p>In other 3% of mammals (~100 species) and a lot of birds, there is a significant degree of paternal investment in offspring. <strong>Species that have developed a \"pair bond\" mating strategy, have males capable of perceiving \"beauty\" in females</strong> and become much more picky. Humans are a pair bond species. </p>\n\n<p>On the other hand, because mammal females have high investment in their offspring, <strong>without the pair bond females go straight for the top alpha male</strong> to secure his DNA.</p>\n\n<p>The 97% -3% number is quoted multiple times in this podcast on Evolutionary Psychology: <a href=\"https://hosts.blogtalkradio.com/beatyourgenes/2016/03/24/gender-dynamics-biological-differences-of-men-and-women\" rel=\"nofollow\">https://hosts.blogtalkradio.com/beatyourgenes/2016/03/24/gender-dynamics-biological-differences-of-men-and-women</a></p>\n\n<p>There's also <a href=\"https://en.wikipedia.org/wiki/Social_monogamy_in_mammalian_species#Monogamy_in_mammals\" rel=\"nofollow\">this article on social monogamy in mammals</a> that quotes 3-5% figure</p>\n"
}
] |
10,376 |
<p>I'm a maths major and I have an interest in learning biology. I know very, very little; I know how babies are made and that's about it. Could anyone recommend a stimulating text to read for its own sake and also to use to learn biology?</p>
|
[
{
"answer_id": 10386,
"pm_score": 5,
"text": "<p>I found the Campbell Biology textbook to be quite comprehensive and approachable. I think many introductory biology courses use it.</p>\n\n<p><a href=\"http://rads.stackoverflow.com/amzn/click/0321558235\">http://www.amazon.com/Campbell-Biology-Edition-Jane-Reece/dp/0321558235</a></p>\n"
}
] |
[
{
"answer_id": 10378,
"pm_score": 3,
"text": "<p>There are tons of books and it is quite hard to find one that gives such a broad overview. <a href=\"https://www.amazon.ca/Campbell-Biology-9th-Jane-Reece/dp/0321558235/ref=sr_1_2?ie=UTF8&qid=1513808241&sr=8-2&keywords=campbell+biology\" rel=\"nofollow noreferrer\">Campbell Biology</a> is a book that basically covered the first year of my Bachelor degree in biology. I am not sure it would be very stimulating though! If there is a specific branch of biology that interests you, let us know we'll be able to give you a better advice.</p>\n\n<p>As a math Major you might enjoy some fields of biology that are highly mathematized. For example, system biology or theoretical evolutionary biology. For the latter, you might like to read <a href=\"https://rads.stackoverflow.com/amzn/click/0674023382\" rel=\"nofollow noreferrer\">Evolutionary Dynamics: Exploring the Equations of Life</a> book from Martin Nowak. But I am afraid it might not be a nice idea to directly jump into some specific subject before having a good overview of the life sciences.</p>\n\n<p>Otherwise you might appreciate some books of popular (but good level) science such as <a href=\"https://rads.stackoverflow.com/amzn/click/0192880519\" rel=\"nofollow noreferrer\">the Extended Phenotype</a> from Richard Dawkins. This book is very stimulating and I think it starts with some basic definitions of biological concepts such those of \"alleles\" or \"phenotype\".</p>\n\n<p>I gave you two examples of books from the field of theoretical evolutionary biology. For more recommendations in this field, please have a look at <a href=\"https://biology.stackexchange.com/questions/16470/books-on-population-or-evolutionary-genetics\">Books on population or evolutionary genetics?</a>.</p>\n\n<p>Hope this helps a bit!</p>\n"
},
{
"answer_id": 31627,
"pm_score": 2,
"text": "<p>You should check out Richard Dawkins' book The <em>Greatest Show on Earth: The Evidence for Evolution</em></p>\n\n<p>It does focus heavily on evolution but it is an amazing book on biology in general. He covers a wide rage of other topics, from how birds flock so elegantly to dating fossils using dendrochronology. The chapter on embryology is fascinating. </p>\n"
},
{
"answer_id": 31686,
"pm_score": 1,
"text": "<p>The Bible of biology is the Alberts' Molecular Biology of the Cell:</p>\n\n<blockquote>\n <p><a href=\"http://www.ncbi.nlm.nih.gov/books/NBK21054/\" rel=\"nofollow\">http://www.ncbi.nlm.nih.gov/books/NBK21054/</a></p>\n</blockquote>\n\n<p>The Campbell is also pretty good and maybe easier to read..</p>\n"
},
{
"answer_id": 31754,
"pm_score": 2,
"text": "<p>@xuanji offers a good choice with <a href=\"http://rads.stackoverflow.com/amzn/click/0321775651\" rel=\"nofollow\"><em>Campbell</em> Biology</a> if you want a text solid biology textbook. I've got a copy in my library. I would suggest buying a previous edition if you're trying to save money. However, the book could be a bit dry. Reading semi-popular books on topics you are interested about would probably be better approach. </p>\n\n<p>Both @ebrohman and @Remi.b provide good suggestions with Dawkins. I also like Ernst Mayr's <a href=\"http://rads.stackoverflow.com/amzn/click/0465044263\" rel=\"nofollow\"><em>What is evolution</em></a> on the topic of evolution.</p>\n\n<p>For ecology, check out books by <a href=\"http://www.amazon.com/Edward-O.-Wilson/e/B000AQ4776/ref=sr_ntt_srch_lnk_1?qid=1430063182&sr=1-1\" rel=\"nofollow\">E.O. Wilson</a> or <a href=\"http://www.amazon.com/Jared-Diamond/e/B000AQ01ZS/ref=sr_tc_2_0?qid=1430063228&sr=1-2-ent\" rel=\"nofollow\">Jared Diamond</a>.</p>\n\n<p>If you want to learn more about environmental toxicology, Rachel Carson's <a href=\"http://rads.stackoverflow.com/amzn/click/0618249060\" rel=\"nofollow\"><em>Silent Spring</em></a> is a good book to start off with.</p>\n\n<p>If you're looking for a mathematical biology book, Linda Allen has two biomath text books, one on <a href=\"http://rads.stackoverflow.com/amzn/click/0130352160\" rel=\"nofollow\">deterministic models</a> the other on <a href=\"http://rads.stackoverflow.com/amzn/click/1439818827\" rel=\"nofollow\">stochastic models</a>. Murry's also produced some classical mathematical biology <a href=\"http://rads.stackoverflow.com/amzn/click/0387952233\" rel=\"nofollow\">books</a>. Most people would consider these books dry, but as a mathematician, you might like them.</p>\n\n<p>James Watson can be controversial but he's written some interesting books. His <a href=\"http://rads.stackoverflow.com/amzn/click/074321630X\" rel=\"nofollow\"><em>Double Helix</em></a> is a good read. </p>\n\n<p>If you provide what specific type of biology and mathematics you are interested in, I will provide more suggestions. </p>\n"
}
] |
13,595 |
<p>I read a story this week on Richard Lenski who has been 'evolving' <em>E. coli</em> for more than 50,000 generations now. One comment I read was from someone who doesn't accept Evolution who pointed out that we haven't seen a single celled organism 'evolve' into a multi-celled organism. Another person responded and said that a bacteria is not going to evolve into something that isn't a bacteria.</p>
<p>So, if Evolution created single celled organisms and then multi-celled organisms how might that change have happened? And is it possible to recreate that set of driving forces to make a bacteria something other than a bacteria?</p>
<p>To that end, what advantage does being multi-cellular have over being unicellular (if that's even a word)?</p>
|
[
{
"answer_id": 21525,
"pm_score": 5,
"text": "<blockquote>\n <p>How did multicellularity evolved?</p>\n</blockquote>\n\n<p><strong>It is an ongoing field of research - Some insights about the origin of multicellularity</strong></p>\n\n<p>This is a big ongoing field of research. To start with an example, there was relatively recently (2012) an important article by <a href=\"http://www.zoology.ubc.ca/veg/RatcliffEtAl2012.pdf\" rel=\"nofollow noreferrer\">Ratcliff et al.</a> that shows that yeast can quickly evolve multicellularity under selection on the speed they sink to lower water layers. This article is one among many others and is far from being able to explain everything we would like to understand about the evolution of multicellularity. Typically, I think that this yeast species had a multicellular ancestor and we might think that this species would already have fixed alleles (=variants of genes that is fixed meaning that the whole population is carrying this variant today) in the population predisposing this species to easily (re-)evolve multicellularity. Also, they may have kept some standing additive genetic variance in their genome from their past and they would therefore very quickly respond to selection as they don't need de novo mutations. (Sorry if this last sentence was slightly technical).</p>\n\n<p>One of the first traits that we usually refer to when talking about the evolution of multicellularity is the presence of sticky proteins allowing individual cells to paste to each other.</p>\n\n<p><strong>Some insights about the evolution from simple multicellular to more complex multicellular</strong></p>\n\n<p>Then, we could talk about more complex multicellular and argue how do these simple multicellular evolve into some more complex organisms. A common argument is that multicellular can have specialized cells are very could at doing what they're doing as they are specialized. Also, some level of complexity is thought to have raised due to the fact that multicellular organisms tend to have smaller population size than unicellular (see <a href=\"http://www.sciencemag.org/content/302/5649/1401.short\" rel=\"nofollow noreferrer\">Lynch and Conery, 2003</a>). It is important not to confuse evolution of complexity with the evolution of multicellularity although these two notions are somehow related.</p>\n\n<p><strong>What do you mean by multicellularity?</strong></p>\n\n<p>The evolution of multicellularity can be discussed in the context where sister cells form an organism together or when unrelated cells (among the same species or even cells from different species) come together to form an organism. Also, the multicellularity can be discussed at a different level depending on how we want to define multicellularity. Is a stack of cells reproducing individually, working for their own benefit a multicellular? Do we need a division of labor? Do we need a division between germline (reproductive caste) and soma line (non-reproductive case)?</p>\n\n<p><strong>How many times did multicellularity evolve independently?</strong></p>\n\n<p>Some people consider that there are multicellular bacteria (biofilms) but we will avoid discussions that are based on limit-case definitions. Let's talk about eukaryotes. Most Eukaryotes are unicellular and multicellularity evolved many times independently in eukaryotes. To my knowledge, complex multicellularity however evolved only (only?) 6 times independently in eukaryotes.</p>\n\n<ul>\n<li>Metazoa (animals)</li>\n<li>Ascomyceta (fungi)</li>\n<li>Basidiomyceta (fungi)</li>\n<li>Viridiplantae (green plants)</li>\n<li>Florideophyceae (red algae)</li>\n<li>Laminariales (brown algae)</li>\n</ul>\n\n<p><strong>Model organisms and interesting cases to study multicellularity</strong></p>\n\n<p>There are a bunch of specific clades that are particularly interested in studying multicellularity because they present transition states. For example <a href=\"http://en.wikipedia.org/wiki/Volvox\" rel=\"nofollow noreferrer\">Volvox</a> is a chlorophyte genus and the species in this clade present different stages of multicellularity; Some species are exclusively multicellular, some form small groups, some create big colonies, some have some division of labor and some even have separation between the germline and the soma (Some castes don't reproduce). (<a href=\"http://rspb.royalsocietypublishing.org/content/early/2011/12/05/rspb.2011.1999.full\" rel=\"nofollow noreferrer\">ref1</a>, <a href=\"http://icb.oxfordjournals.org/content/43/2/247\" rel=\"nofollow noreferrer\">ref2</a>, <a href=\"http://mbe.oxfordjournals.org/content/23/8/1460\" rel=\"nofollow noreferrer\">ref3</a>, <a href=\"http://www.sciencemag.org/content/329/5988/128.1.short\" rel=\"nofollow noreferrer\">ref4</a>, <a href=\"http://www.sciencemag.org/content/329/5988/223.short\" rel=\"nofollow noreferrer\">ref5</a>, <a href=\"http://www.sciencedirect.com/science/article/pii/S1369526610001585\" rel=\"nofollow noreferrer\">ref6</a>). Yeasts are also a good model organism for studying the evolution of multicellularity. </p>\n"
}
] |
[
{
"answer_id": 13597,
"pm_score": 3,
"text": "<p>For one thing, larger organisms are much more energy efficient. This is what is known as <a href=\"http://en.wikipedia.org/wiki/Kleiber%27s_law\" rel=\"nofollow\">Kleiber's Law</a> where the caloric requirement scales as the 3/4 power to the body mass. </p>\n\n<p>Another thing is that when all the cells cooperate to form a multicellular organism, each given individual is more likely to reproduce and less likely to die due to environmental variation because cooperation creates stability. </p>\n\n<p><a href=\"http://en.wikipedia.org/wiki/Multicellular_organism#Hypotheses_for_origin\" rel=\"nofollow\">There are several theories about <em>how</em> this came about</a>,but those are the elements of <em>why</em>. Collaboration and efficiency improve the chances of survival, which is to say that selection will favor multicellular organisms however they came to be. </p>\n"
},
{
"answer_id": 21550,
"pm_score": 2,
"text": "<p><em>Disclaimer: Not my field of research, and not a field where I know the litterature well. See it as a complement to the other answers.</em></p>\n\n<hr>\n\n<p>A distinct advantage of multicellularity is specialized functions of different cells. This can allow for higher efficiency of e.g. metabolic processes, and also that redundant functions can be removed from some cell lines, since they can be handled by other cells. Therefore, the constituent parts can become simpler, while the resulting organism becomes more complex at the same time. Mathematical modelling of cellular systems have shown how this type of division of labour can evolve from unicellular lines (<a href=\"http://rspb.royalsocietypublishing.org/content/early/2011/12/05/rspb.2011.1999.full\" rel=\"nofollow\" title=\"Ispolatov et al. 2011. Division of labour and the evolution of multicellularity. Proc. R. Soc. B. doi:10.1098/rspb.2011.1999\">Ispolatov et al. 2011</a>), through the steps of aggregation and differentiation from preexisting functions. </p>\n\n<p>An interesting intermediate step that can provide some clues to how multicellularity can evolve, is in cyanobacteria, where some unicellular species can show partial specialization e.g. when part of cellular biofilms. A phylogenetic study of cyanobacteria has also shown that they have reversed from multicellularity to unicellularity at least five times, and most extant cyanobacteria seem to descend from multicellular ancestors (<a href=\"http://www.biomedcentral.com/1471-2148/8/238\" rel=\"nofollow\" title=\"Schirrmeister et al. 2011. The origin of multicellularity in cyanobacteria. BMC Evolutionary Biology 11:45\">Schirrmeister et al. 2011</a>). This means that the evolution of multicellularity is not a one-way process, but seems to be a much more complex process.</p>\n"
},
{
"answer_id": 21554,
"pm_score": 2,
"text": "<p>I STRONGLY encourage to read work from the lab of Nicole King - she studies Choanoflagellates, which are the \"out-group\" for animals - they are, in some sense, the most animal-like single-celled organism that exists. </p>\n\n<p>Chaonos are also amazing because they go through a single to multicellular transition <em>in there own life cycle</em>, so they provide an amazing opportunity to understand when it is more beneficial to be single-celled vs. multi-celled. Currently, one of the working hypotheses of the group is that one of the main drivers of the push towards multicellularity may have just been simple fluid dynamics: the flows around a spherical multicellular \"rosette\" of chaonos bring more food to them. </p>\n\n<p>If you are interested in the evolutionary transition to multicellularity you must read work from the <a href=\"http://kinglab.berkeley.edu/\" rel=\"nofollow noreferrer\">King Group</a>.</p>\n"
},
{
"answer_id": 43091,
"pm_score": -1,
"text": "<p>The eucaryote that became the modern organelle mitochondria, combined with procaryotes. This probably occurred as a result of the mitochondria being absorbed by the parent cell but not destroyed as it usefully created energy rich ATP molecules using Oxygen and Water through respiration.</p>\n\n<p>These were the first Eukaryotic cells, they went on to become Eukaryotic, multicellular life.</p>\n\n<hr>\n\n<hr>\n\n<p>Various benefits to Eucaryotes becoming multicellular include:</p>\n\n<hr>\n\n<p>The volume to surface area of a cell gives cells a natural size of a few micrometers. Larger single cells find it increasingly difficult to absorb enough nutrients or oxygen for the volume of there cytoplasm.</p>\n\n<p>Amoebas can be larger due to being so irregular in shape, this ensures that so nowhere inside the cell is it too far from the cells surface. Various more spherical centimetre scale single celled life also exists in nutrient rich parts of the deep ocean, such as the Valonia Ventricosa.</p>\n\n<p><a href=\"https://en.m.wikipedia.org/wiki/Valonia_ventricosa\" rel=\"nofollow noreferrer\">https://en.m.wikipedia.org/wiki/Valonia_ventricosa</a></p>\n\n<hr>\n\n<p>Another advantage is that structures can form between cells, outside of the cell walls, that can still be protected inside the creatures body. Such a connective network in animals called the extracellular matrix.</p>\n\n<p><a href=\"https://www.khanacademy.org/test-prep/mcat/cells/cytoskeleton/v/introduction-to-cytoskeleton\" rel=\"nofollow noreferrer\">https://www.khanacademy.org/test-prep/mcat/cells/cytoskeleton/v/introduction-to-cytoskeleton</a></p>\n\n<hr>\n\n<p>Note that creatures like the sea sponge are multicellular, but do not have distinct areas of the body such as organs in the same way as animals do.</p>\n\n<p>\"The genes I discuss in my article were not present in the common ancestor of all life on Earth. They do not exist in bacteria, for example. They do not even exist (as far as scientists know) in sponges. Only after the ancestors of cnidarians and bilaterians diverged from sponges did they emerge.\" (A planet of viruses, Carl Zimmer) This is the quote I could find, as I remember, relating to \"bodybuilding\" in many creatures, but not the sea sponge.</p>\n"
},
{
"answer_id": 43156,
"pm_score": 2,
"text": "<h2>If single cells are capable of surviving on their own then why did multicellularity evolve?</h2>\n\n<hr>\n\n<p>This situation can be compared with the evolution of family and society, in a way; during the time of crisis, the survival chances increase when someone stays in a group.</p>\n\n<p>Similar conditions would have resulted in the evolution of multicellularity. The difference between being truly multicellular and just being a group of cells is that in multicellularity, the individual cells cannot survive in the absence of the other. Moreover, different cells in a multicellular organism perform different kinds of functions. However, it is certainly likely that grouping without a strong dependence would have constituted the early stages in the evolution of multicellularity. </p>\n\n<p>One of the complex kinds of microbial colonies is <a href=\"https://en.wikipedia.org/wiki/Biofilm\" rel=\"nofollow noreferrer\">biofilm</a>. In a biofilm different \"regions\" of the colony have different kinds of functional roles; the \"outer\" cells take up nutrients for the colony from the surroundings whereas the inner cells reproduce and keep the colony thriving. Bacteria have also evolved a way of signalling (or \"talking\") to other bacteria (of the same species) by a mechanism known as <a href=\"https://en.wikipedia.org/wiki/Quorum_sensing\" rel=\"nofollow noreferrer\">quorum sensing</a>, which in a way changes the behaviour of the bacteria when then stay in a group.</p>\n\n<p><em><a href=\"https://en.wikipedia.org/wiki/Dictyostelium_discoideum\" rel=\"nofollow noreferrer\">Dictyostelium</a></em> or slime mold (or affectionately called <em>dicty</em> :) ) is an example of early evolution of multicellularity in eukaryotes. When there is plenty of food, dicty stays as unicellular amoeba. However, when there is a shortage of food, the dicty amoebae start grouping up and give rise to a multicellular \"slug\". The dicty slug roams around and when it encounters right conditions (such as humidity), it differentiates to give rise to a \"fruiting body\", which more or less looks like a fungal spore. In a fruiting body some cells form the spores (which will produce new dicties) whereas some cells form the stalk (which supports the spores). Apparently, the choice of what part will a cell become, is random and at this stage the individual dicty amoebae are no more selfish. The aggregation of dicty amoebae is co-ordinated by a signalling molecule called cAMP and this works in a way similar to quorum sensing.</p>\n\n<blockquote>\n <p> <a href=\"https://i.stack.imgur.com/P4xcM.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/P4xcM.png\" alt=\"enter image description here\"></a></p>\n \n <p><hr>\n <sup> Taken from Wikipedia </sup></p>\n</blockquote>\n\n<p><a href=\"https://en.wikipedia.org/wiki/Volvox\" rel=\"nofollow noreferrer\">Volvox</a> is another example of an early stage of multicellular evolution.</p>\n\n<p>To sum up, as you said single cells can very well survive on their own. However, in some situations being multicellular would have given the organism some survival advantages. You should understand that this is just one of the survival strategies and not all organisms needed to adopt this. In fact, there are many more unicellular species in the planet compared to the multicellular ones.</p>\n\n<p>I would reiterate Remi's suggestion that you should have a look at this site called <a href=\"http://evolution.berkeley.edu/evolibrary/home.php\" rel=\"nofollow noreferrer\">Understanding Evolution, hosted by UC Berkeley</a>. </p>\n\n<p>You can also look at this post on our site about a recurrent doubt faced by many students and non-experts in the area of evolution: \"<a href=\"https://biology.stackexchange.com/q/35532/3340\">Why do some bad traits evolve, and good ones don't?</a>\"</p>\n"
},
{
"answer_id": 53576,
"pm_score": 0,
"text": "<p>For the same reason that sociality evolved so many times among animals. There are lots of advantages in having similar fellows. And multicellular organisms are, after all, just a colony, sometimes a society, of individual cells.</p>\n"
}
] |
14,414 |
<p>After my online research on the subject, I learnt that, biologically speaking, many scientists believe that there is no such thing as a race. <em>Homo sapiens</em> as a species is only 200,000 years old, which has not allowed for any significant genetic diversification yet, and our DNA is 99.99% similar. I've read statements that there can be more genetic variation inside a racial group than between different racial groups, meaning that, for example, two individuals from the same "race" can have less in common with each other than with an individual from another "race".</p>
<p><a href="http://en.wikipedia.org/wiki/Race_(human_classification)" rel="noreferrer">Wikipedia on Race (human classification) quote</a>:</p>
<blockquote>
<p>Scientists consider biological essentialism obsolete, and generally discourage racial explanations for collective differentiation in both physical and behavioral traits</p>
</blockquote>
<hr>
<p><strong>Q1:</strong> If <em>Homo sapiens</em> has no races (according to biologists), why are we so different morphologically? (hair/eyes/skin colour and even athletic performance seem to differ between human populations)</p>
<p><strong>Q2:</strong> Is it common for other species too, when genetically close populations have very different morphological traits? Are there any other mammal or animal species that exhibit biological diversity comparable to human diversity, and how do taxonomists treat these species? (excluding intentionally bred domestic species to keep the comparison fair)</p>
<hr>
<p><em>The question has been paraphrased to emphasize that it is the <strong>biological</strong> debate that is in question, not the <strong>sociopolitical</strong>. I.e., why is there no consensus in evidence and opinions of scientists?</em></p>
|
[
{
"answer_id": 14419,
"pm_score": 7,
"text": "<p>Firstly, it's not true that you can't tell racial background from DNA. You most certainly can; it's quite possible to give fairly accurate phenotypic reconstruction of the features we choose as racial markers from DNA samples alone and also possible to identify real geographic ancestral populations from suitable markers.</p>\n\n<p>The reason that human races aren't useful is that they're actually only looking at a couple of phenotypic markers and (a) these phenotypes don't map well to underlying genetics and (b) don't usefully model the underlying populations. The big thing that racial typing is based on is skin colour, but skin colour is controlled by only a small number of alleles. On the basis of skin colour you'd think the big division in human diversity is (and I simplify) between white Europeans and black Africans. However, there is <em>vastly</em> more genetic diversity within Africa than there is anywhere else. Two randomly chosen Africans will be, on average, more diverse from each other than two randomly chosen Europeans. What's more Europeans are no more genetically distinct overall from a randomly chosen African than two randomly chosen Africans are from each other.</p>\n\n<p>This makes perfectly decent sense if you consider the deep roots of diversity within Africa (where humans originally evolved) to the more recent separation of Europeans from an African sub-population.</p>\n\n<p>It's also worth noting that the phenotypic markers of race don't actually tell you much about underlying heredity; for example there's a famous photo of twin daughters one of whom is completely fair skinned, the other of whom is completely dark skinned; yet these two are sisters. This is, of course, an extreme example but it should tell you something about the usefulness of skin colour as a real genetic marker. </p>\n"
}
] |
[
{
"answer_id": 14416,
"pm_score": 4,
"text": "<p><strong>Bias</strong></p>\n\n<p>When you say <code>phenotype</code> you mostly mean \"skin color\", \"size of the nose\", \"hair color\", \"shape of the eyes\", \"height\", and some others. All these traits that we manage to find to explain <a href=\"http://en.wikipedia.org/wiki/Population_stratification\" rel=\"nofollow noreferrer\">population structure</a> among humans. But you forget all the rest of the phenotypic diversity. If you would choose 1000 randomly chosen traits (external morphology and other stuff) and make a <a href=\"http://en.wikipedia.org/wiki/Principal_component_analysis\" rel=\"nofollow noreferrer\">PCA</a>. Will the main axes explain much of the inter-subpopulation (or inter-racial) diversity? I am not sure about that. One cannot use one subset of the total phenotypic or genetic variance and use it in order to define several species within what was previously thought to be one. It is not because two genes are associated with the same population structure that one can define two different species.</p>\n\n<p><strong>scientific observations vs biased intuitions</strong></p>\n\n<p>You say:</p>\n\n<blockquote>\n <p>[..] is it reasonable to use a genetic approach to races and claim that biological races do not exist, while it seems to be a poor indicator, when it comes to comparison of phenotypes of human populations.</p>\n</blockquote>\n\n<p>Similarly, one could say</p>\n\n<blockquote>\n <p>Bats look like birds. We consider them as being mammals just because that is what scientific observations (genetic data or in-depth observation of the phenotypic variance) says. Should we follow scientific explanations when my personal bias intuition tells me that these observations are poor indicators?</p>\n</blockquote>\n\n<p>The answer is yes if you want to increase your knowledge and no if you just want to be comforted into what you think you already know.</p>\n\n<p>I have to confess though that I don't know much about phenotypic or morphological variations among humans. And I'd be curious if someone could give some words about that and whether or not much of the phenotypic and morphological variance is explained by what we consider being racial groups. It might be possible that very little of the total phenotypic variance is explained by racial groups but quite a lot of the face morphological variance is explained by racial groups.</p>\n\n<p><strong>Concept of species</strong></p>\n\n<p>For species that can reproduce exclusively with sex, we tend to use the concept of reproduction isolation to define a species and I really don't think that there is a pair of racial groups are sexually incompatible (however you delimit the racial groups). Eventually, there might have some slight inbreeding depression but I am not sure.</p>\n\n<p>You might want to have a look at <a href=\"https://biology.stackexchange.com/questions/39664/how-could-humans-have-interbred-with-neanderthals-if-were-a-different-species/39669#39669\">this answer</a> to understand the semantic difficulties behind the concept of species</p>\n"
},
{
"answer_id": 14417,
"pm_score": 5,
"text": "<p>Well, that's just it, we <em>don't</em> actually have much phenotypic variation. For example, compare this:</p>\n<p><img src=\"https://i.stack.imgur.com/0KZibm.jpg\" alt=\"Collection of human faces\" /></p>\n<p>to this:</p>\n<p><img src=\"https://i.stack.imgur.com/3bmJzm.jpg\" alt=\"Collection of dogs\" /></p>\n<p>or this:</p>\n<p><img src=\"https://i.stack.imgur.com/gReb7m.jpg\" alt=\"Collection of cat faces\" /></p>\n<hr />\n<p>Or this:</p>\n<p><img src=\"https://i.stack.imgur.com/Xi6tb.jpg\" alt=\"Six human babies\" /></p>\n<p>to this:</p>\n<p><img src=\"https://i.stack.imgur.com/p5fXR.png\" alt=\"Five dogs\" /></p>\n<hr />\n<p><em>This</em> is phenotypic variation:</p>\n<p><img src=\"https://i.stack.imgur.com/9VfSo.jpg\" alt=\"Collection of pigs\" /></p>\n<hr />\n<p>So, as I hope is clear from the images above, phenotypic variation among humans is <em>tiny</em> compared to other species. We just notice small differences much more because, well, it's us so little differences are much more noticeable.</p>\n"
},
{
"answer_id": 14465,
"pm_score": 4,
"text": "<p><em>I decided to summarize a competing hypothesis to make our answers more balanced. I also tried to address the question about the degree of human morphological diversity compared to other animals.</em></p>\n\n<hr>\n\n<p>According to Woodley (2010), it is plausible that <em>H. sapiens</em> does not belong to one species and subspecies (i.e. is polytypic). Some of the data he uses to support this hypothesis could be useful for answering our question. He claims that <em>H. sapiens</em>, which is often considered monotypic, <strong>posses higher levels of morphological diversity, genetic heterozygosity and differentiation than many animal species which are considered polytypic.</strong></p>\n\n<p>Woodley cites a study by Sarich and Miele, who claimed that morphological differences between humans, on average, are equal to the differences among <em>species</em> within other mammalian genera (excluding species bred for domestic purposes), and are typically more strongly marked than in other animals.</p>\n\n<p>However, morphological differences are known to be caused by little genetic differences too, like in the case of domestic dogs, which are still considered to be one species. Therefore, Woodley presented further evidence that looked on these inconsistencies in classification using allele frequencies and genetic diversity.</p>\n\n<p>He presented data from a wide range of studies, which compares genetic diversity of various mammalian species based on heterozygosity (H), which is a common indicator for genetic diversity, and describes whether both alleles are the same or not on a studied locus. According to this data (which you can find in the linked paper):</p>\n\n<ul>\n<li>Chimpanzees exhibited H of 0.63-0.73, which is very similar to H found in humans (0.588 - 0.807), however, chimpanzees are divided into four subspecies.</li>\n<li>Some species like the grey wolf even exhibited a lower H (corresponding to lower genetic diversity) than humans (0.528 vs 0.588 - 0.807), while the grey wolf has been divided into as many as 37 subspecies.</li>\n</ul>\n\n<p><strong>This data suggests that humans are more diverse both morphologically and genetically than some of the other mammalian species that have been divided into subspecies.</strong></p>\n\n<p>References:<br>\nWoodley, M. A. (2010). Is <em>Homo sapiens</em> polytypic? Human taxonomic diversity and its implications, <em>Medical Hypotheses, 74</em>, 195-201. doi:10.1016/j.mehy.2009.07.046 (<a href=\"https://lesacreduprintemps19.files.wordpress.com/2011/06/woodley-2009-is-homo-sapiens-polytypic-human-taxonomic-diversity-and-its-implications.pdf\">full-text PDF</a>)</p>\n"
},
{
"answer_id": 14476,
"pm_score": 4,
"text": "<p>It seems to me that many answers to this question suffer from the nasty habit of \"political correctness\". As a zoologist, I never heard of somebody sequencing the whole DNA of any species to decide when to use or not the term \"race\". If a group of animals comes from a side of a river, and the other comes from the other side, and they have one or a few distinctive features (color of chest pelage, tuffs of hair in the sides of head, etc), that's enough to call them both different races (or even subspecies). Of course some geographical isolation has taken place, although it hasn't been long enough to divide the two (or more) populations into full species. The same logic should be used to humans, right? Maybe some folks believe that, pretending there are no human races, then the question of racism is \"solved\"? Bad logic, to me.</p>\n\n<p>Look at <a href=\"http://www.worldbirdnames.org\" rel=\"noreferrer\">http://www.worldbirdnames.org</a>: they cite 10,518 extant species of birds and 20,976 subspecies. About 2 subspecies per species. How do they do that? (No DNA for most of them.) Subspecies/races are usually from different regions (like human races), their vocalizations are usually different (like human races) and their colors sometimes vary (not as much as in human races). My point is: there is NO SCIENTIFIC REASON to say there are no human races, if we're using zoological reasoning. (Unless we are not animals anymore!)</p>\n\n<p>For mammals, <a href=\"http://www.catalogueoflife.org/col/browse/classification/kingdom/Animalia/phylum/Chordata/class/Mammalia/match/1\" rel=\"noreferrer\">http://www.catalogueoflife.org/col/browse/classification/kingdom/Animalia/phylum/Chordata/class/Mammalia/match/1</a> cite: 4,843 species, 2,998 infraspecific taxa. Again, if someone show me they did complex DNA analysis for most of those infraspecific taxa, and those analysis showed that variation inside races is smaller than between races, THEN I will be forced to agree with them.</p>\n"
},
{
"answer_id": 84807,
"pm_score": 2,
"text": "<p>First you can take a look at this diagram:</p>\n\n<p><a href=\"https://i.stack.imgur.com/vkixy.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/vkixy.jpg\" alt=\"enter image description here\"></a></p>\n\n<p>You can make a google image search for \"Cavalli Sforza\" and get a lot of similar diagrams. This diagram is using a concept known as <a href=\"https://en.wikipedia.org/wiki/Genetic_distance\" rel=\"nofollow noreferrer\">genetic distance</a> by <a href=\"https://en.wikipedia.org/wiki/Fixation_index\" rel=\"nofollow noreferrer\">fixation index</a>. This is a way to measure how different different ethnic groups are genetically.</p>\n\n<p>Basically what you do is you compare how many differences there are on average between two humans from the same population and between two humans from two different populations. The same method can be applied to animals. There is no \"threshold value\" where you can say that two groups of people or animals have become different enough that they can be defined as \"different races\".</p>\n\n<p>Traits such as skin colour are regulated by a very small handfull of genes so even if we have different skin colours that does not mean that we differ much genetically speaking.</p>\n\n<p>Lions and Leopards can have fertile offspring and live basically in the same habitat in Africa. I do not know if crossbreeding is known to have occured in the wild. Probably a hybrid has lower fitness than the original species.</p>\n"
}
] |
14,888 |
<p>Approximately, how many <a href="https://en.wikipedia.org/wiki/Family_%28biology%29">families</a> have been identified?</p>
<p>I've often often come across figures for the total number of species on Earth. Recently, I found myself wondering about the encompassing ranks above them, specifically family, but I can't recall any figures on family and it's a little difficult finding what I want by typing "family" into a Google search. ;)</p>
|
[
{
"answer_id": 59068,
"pm_score": 4,
"text": "<p>The 2011 paper <a href=\"http://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.1001127\" rel=\"noreferrer\">How Many Species Are There on Earth and in the Ocean?</a> indirectly answers this question as well as any other source you'll find I imagine. It estimates how many species there are total based on the rate of discovery of higher taxa; it includes plots of number of taxa over time for the major groups of life in Figure S1. Which gives:</p>\n\n<p>Animalia - 5300 families in 2011 (the plots are given with only one significant figure, the second one's my estimate) (estimated total: 5800)</p>\n\n<p>Chromista - 270 families (estimated total: 360)</p>\n\n<p>Fungi - 550 families (estimated total: 620)</p>\n\n<p>Plantae - 750 families (estimated total: 800)</p>\n\n<p>Protozoa - 280 families (estimated total: 310)</p>\n\n<p>Archaea - 27 families (no estimated total; the number has been increasing exponentially so far)</p>\n\n<p>Bacteria - 300 families (same as for Archaea)</p>\n\n<p>Which gives us a total of 7477 families in 2011, with an estimated total of (ignoring Archaea and Bacteria, who don't really fall in the same kind of classification anyway) 7890 families. (make that <strong>7500 families discovered by 2011</strong> and <strong>8000 estimated in total</strong> given the imprecision involved in my reading the plots).</p>\n"
}
] |
[
{
"answer_id": 14890,
"pm_score": 3,
"text": "<p>I don't know about other groups, but about plants, number of families depends on the system you follow. Recent version of The Plant List (1.1) estimates about 352 000 species of Angiosperms and lists over 400 families. See <a href=\"http://www.theplantlist.org/1.1/browse/A/\" rel=\"noreferrer\">http://www.theplantlist.org/1.1/browse/A/</a> It is very good and reliable source of information. Second very good source about plant systematics is database Tropicos provided by Missouri Botanical Garden and Angiosperm Phylogeny Group. See list of families according to APG3 <a href=\"http://www.mobot.org/MOBOT/research/APweb/\" rel=\"noreferrer\">http://www.mobot.org/MOBOT/research/APweb/</a> and click to \"Families\" on the top of the page. Just note, that there are also synonyms, so that You can't just count the rows. ;-)</p>\n"
},
{
"answer_id": 31883,
"pm_score": 3,
"text": "<p>The Plant List has 642 families listed: <a href=\"http://www.theplantlist.org/1.1/about/#changes\" rel=\"noreferrer\">http://www.theplantlist.org/1.1/about/#changes</a>.</p>\n\n<p>For a quick comparison, Wikipedia lists </p>\n\n<ul>\n<li>522 fish families:\nen.wikipedia.org/wiki/List_of_fish_families</li>\n<li>136 mammal families:\nen.wikipedia.org/wiki/Mammal_classification</li>\n<li>61 amphibian\nfamilies: en.wikipedia.org/wiki/List_of_amphibians</li>\n<li>57 reptile families: en.wikipedia.org/wiki/List_of_reptiles.</li>\n</ul>\n\n<p>This only covers a subset of the total, however (see <a href=\"http://en.wikipedia.org/wiki/List_of_animal_classes\" rel=\"noreferrer\">here</a> for other animal classes). It is relatively difficult to find a good, and relatively complete answer to this, though. </p>\n"
},
{
"answer_id": 31899,
"pm_score": 3,
"text": "<p>The <a href=\"http://www.ncbi.nlm.nih.gov/Taxonomy/taxonomyhome.html/index.cgi?chapter=statistics&uncultured=hide&unspecified=hide&m=0\">NCBI Taxonomy statistics page</a> displays the following information:</p>\n\n<p>There are currently 73540 genera, 331418 species, and 23127 taxa of higher order. Since the number of taxa decreases with the genericity of the taxon, there are probably around 20000 families, give or take a few thousand. </p>\n"
},
{
"answer_id": 59151,
"pm_score": 1,
"text": "<p>I'm adding this as another answer since it's a different source, but <a href=\"https://biology.stackexchange.com/users/87/gaurav\">Gaurav</a> gave this excellent resource as an answer to <a href=\"https://biology.stackexchange.com/questions/59059/number-of-families-in-animal-kingdom\">this related question</a>:</p>\n\n<blockquote>\n <p>The <a href=\"https://www.itis.gov/\" rel=\"nofollow noreferrer\">Integrated Taxonomic Information System</a> (ITIS) is maintained regularly by a consortium of North American governmental agencies, and will give you a <a href=\"https://www.itis.gov/hierarchy.html\" rel=\"nofollow noreferrer\">list of all the classes, orders, families or genera</a> in any of seven kingdoms they recognize. It might be biased towards North American taxa, but it might be quicker to get a list from then rather than extracting them from Wikipedia.</p>\n</blockquote>\n"
}
] |
15,514 |
<p>I've often heard that a population, human or otherwise, will continue to grow as long as there is food available (assuming nothing else is killing them off). It makes sense: if you have food you can live, and if nothing is hunting you you'll survive to reproduce.</p>
<p>I recently designed a piece of software to simulate an ecosystem, with groups of creatures of different species eating and hunting and reproducing alongside each other. It was very simplified (each animal had simple attack/defense/speed/stealth values, etc), but something became rapidly apparent: in every simulation the predators overwhelmed the prey, reproducing until their numbers could not be sustained by the herbivores, and leading to an inevitable die-off of both groups. I could delay the die-off by adjusting different values and initial population counts, but it would always happen eventually. The predators would eat and breed and eat and breed until the entire system collapsed.</p>
<p>At first I thought it was just the product of my over-simplified system, but it got me thinking: <strong>what prevents predators from overpopulating in real life?</strong></p>
<p>It seems like the natural tendency would be for (for example) the sharks to continue breeding and eating until all the fish are gone, or the wolves to eat all the deer, etc. Obviously some predators have predators of their own, but that's just putting off the question: if the hyenas don't overpopulate because the lions eat them, then what's keeping the lions from overpopulating? I can't come up with anything that would prevent the apex predators from growing too numerous, then fighting each other over a dwindling prey population, then dying off entirely when there was no more food to find.</p>
<p>Do predator populations self-regulate to prevent putting undo stress on their prey populations? Or is there some other mechanism to keep the predator hierarchy from becoming top-heavy?</p>
|
[
{
"answer_id": 15516,
"pm_score": 6,
"text": "<p>No, I don't think auto-regulation explain much in the population sizes of predators. Group selection may explain such auto-regulation but I don't think it is of any considerable importance for this discussion.</p>\n\n<p>The short answer is, as @shigeta said</p>\n\n<blockquote>\n <p>[predators] tend to starve to death as they are too many!</p>\n</blockquote>\n\n<p>To have a better understanding of what @shigeta said, you'll be interested in understanding various model of prey-predator or of consumer-resource interactions. For example the famous Lotka-Volterra equations describe the population dynamics of two co-existing species where one is the prey and the other is a predator. Let's first define some variables…</p>\n\n<ul>\n<li><span class=\"math-container\">$x$</span> : Number of preys</li>\n<li><span class=\"math-container\">$y$</span> : number of predators</li>\n<li><span class=\"math-container\">$t$</span> : time</li>\n<li><span class=\"math-container\">$\\alpha$</span>, <span class=\"math-container\">$\\beta$</span>, <span class=\"math-container\">$\\xi$</span> and <span class=\"math-container\">$\\gamma$</span> are parameters describing how one species influence the population size of the other one.</li>\n</ul>\n\n<p>The Lotka-Voltera equations are:</p>\n\n<p><span class=\"math-container\">$$\\frac{dx}{dt} = x(\\alpha - \\beta y)$$</span>\n<span class=\"math-container\">$$\\frac{dy}{dt} = -y(\\gamma - \\xi x)$$</span></p>\n\n<p>You can show that for some parameters the matrix for these equations have a complex eigenvalue meaning that the long term behavior of this system is cyclic (periodic behavior). If you simulate such systems you'll see that the population sizes of the two species fluctuate like this:</p>\n\n<p><img src=\"https://i.stack.imgur.com/ZRImS.png\" alt=\"enter image description here\"></p>\n\n<p>where the blue line represents the predators and the red line represents the preys.</p>\n\n<p>Representing the same data in phase space, meaning with the population size of the two species on axes <span class=\"math-container\">$x$</span> and <span class=\"math-container\">$y$</span> you get:</p>\n\n<p><img src=\"https://i.stack.imgur.com/yidcV.gif\" alt=\"enter image description here\"></p>\n\n<p>where the arrows shows the direction toward which the system moves. If the population size of the predators (<span class=\"math-container\">$y$</span>) reaches 0 (extinction), then <span class=\"math-container\">$\\frac{dx}{dt} = x(\\alpha - \\beta y)\\space$</span> becomes <span class=\"math-container\">$\\frac{dx}{dt} = x\\alpha \\space$</span> (which general solution is <span class=\"math-container\">$x_t = e^{\\alpha t}x_0$</span>) and therefore the populations of preys will grow exponentially. If the population size of preys (<span class=\"math-container\">$x$</span>) reaches 0 (extinction), then <span class=\"math-container\">$\\frac{dy}{dt} = -y(\\gamma - \\xi x)\\space$</span> becomes <span class=\"math-container\">$\\frac{dy}{dt} = -y\\gamma \\space$</span>, and therefore the population of predators will decrease exponentially.</p>\n\n<p>Following this model, your question is actually: Why are the parameters <span class=\"math-container\">$\\alpha$</span>, <span class=\"math-container\">$\\beta$</span>, <span class=\"math-container\">$\\xi$</span> and <span class=\"math-container\">$\\gamma$</span> not \"set\" in a way that predators cause the extinction of preys (and therefore their own extinction)? One might equivalently ask the opposite question? Why don't preys evolve in order to escape predators so that the population of predators crushes?</p>\n\n<p>As showed, you don't need a complex model to allow the co-existence of predators and preys. You could describe your model a bit more accurately in another post and ask why in your model the preys always get extinct. But there are tons of possibilities to render your model more realistic such as adding spatial heterogeneities (places to hide for example as suggested by @AudriusMeškauskas). One can also consider other trophic levels, stochastic effects, varying selection pressure through time (and other types of balancing selection), age, sex or health-specific mortality rate due to predation (e.g. predators may target preferentially young ones or diseased ones), several competing species, etc..</p>\n\n<hr>\n\n<p>I would also like to talk about other things that might be of interest in your model (two of them need you to allow evolutionary processes in your model):</p>\n\n<p>1) <strong>lineage selection</strong>: predators that eat too much end up disappearing because they caused their preys to get extinct. This hypothesis has nothing to do with some kind of auto-regulation for the good of species. Of course you'd need several species of predators and preys in your model. This kind of hypothesis are usually considered as very unlikely to have any explanatory power.</p>\n\n<p>2) <strong>Life-dinner principle</strong>. While the wolf runs for its dinner, the rabbit runs for its life. Therefore, there is higher selection pressure on the rabbits which yield the rabbits to run in average slightly faster than wolves. This evolutionary process protects the rabbits from extinction.</p>\n\n<p>3) You may consider..</p>\n\n<ul>\n<li>more than one species of preys or predators</li>\n<li>environmental heterogeneity</li>\n<li>partial overlapping of distribution ranges between predators and preys</li>\n<li>When one species is absent, the model behave just like an exponential model. You might want to make a model of logistic growth for each species by including <span class=\"math-container\">$K_x$</span> and <span class=\"math-container\">$K_y$</span> the carrying capacity for each species.</li>\n<li><p>Adding a predator (or parasite) to the predator species of interest</p>\n\n<p>... and you might get very different results.</p></li>\n</ul>\n"
}
] |
[
{
"answer_id": 15681,
"pm_score": 3,
"text": "<p>One of the possible adjustments of these mathematical models is to introduce a \"place to hide\", making some (small) percent of the prey population not accessible (or much more difficult to access) for predators. After the number of predators decreases from starvation, prey individuals are relatively safer outside the \"place to hide\" and can grow over this limit before the number of predators increases again. </p>\n"
},
{
"answer_id": 19430,
"pm_score": 4,
"text": "<p>Remi.b's answer is an excellent one, and this should be taken as a supplement to it:</p>\n\n<p><strong>It's possible your simulation is correct</strong></p>\n\n<p>The Lotka-Volterra equations are what is known as a deterministic model, and it describes the behavior of predator-prey systems (in a somewhat simplified fashion) in <em>large populations</em>. Small populations are subject to what is known as stochastic extinction - as the predator and prey curves approach their minimums, they may predict populations less than 1, which in reality are either 0 <em>or</em> 1, and when they're 0...well, someone's gone extinct.</p>\n\n<p>Odds are your simulation is on a small population, and if its a simulation, rather than calculus, you should be seeing those stochastic effects (to be sure - if your simulation keeps track of integer animals, rather than continuous animals, and random chance is involved, this is going to be something you have to worry about).</p>\n\n<p>In a similar model I've been working with, that's a pretty simple adaptation of a L-V model that should, deterministically, result in a stable system like in Remi.b's picture, the predators go extinct 20% of the time, and the prey 80% of the time.</p>\n"
},
{
"answer_id": 23704,
"pm_score": 3,
"text": "<p>You need to add Bell curves to your simulation. The most important curve to simulate is the nutritional quality of the prey though there are plenty more thing to curve like speed and virility for prey and predators both. Nature uses lots of Bell curves so they must be good for something, such as softening the harsh effects of pure exponential growth. I suspect that the more Bell curves you implement the more stable your populations will become. </p>\n\n<p>If the food value of your prey is all equal then there's no reason for your predators to not eat every last one. That's what I do with a plate full of foodstuffs, all equally delicious and with enough surplus that all the bad food can be thrown in the trash. Problems arise when you are forced to eat the trash because there's nothing else to eat.</p>\n\n<p>Let's eat our prey from all 3 sides of the curve. If we eat from the weakest and easiest to catch on the left this makes the prey population stronger and more resistant to the predator. If we eat from the most common on the top the prey rebound more rapidly. If we eat from the most desirable on the right the rapid quality (but not the virility) reduction of the prey population has serious negative health consequences for the predators. Notice how each direction we eat has the necessary corrective action against the predator as a response. Due to the wild randomness of genetics the weak population can always rebound in quality when the predatory pressure eases. Looks like Nature didn't screw that one up either.</p>\n\n<p>An easy example is seen in the human vs plant food supply. Population should rise with no detriment as we produce more and more food, and it would if the quality could stay the same. The population does rise but because the nutritional quality keeps dropping, the detriment is rapidly increasing on numerous health and population charts. </p>\n\n<p>When plants are forced to make do with what little they have, you are forced to make do with what little they provide.</p>\n"
},
{
"answer_id": 60152,
"pm_score": 1,
"text": "<p>What you are missing is that not all prey are equally easy to catch. The old, sick animals living in exposed places are much easier to catch than animals that are young, healthy and living in well-protected places. As the predator catches the easy meat, it becomes progressively harder and harder for the predator to get a meal.</p>\n"
},
{
"answer_id": 70039,
"pm_score": 2,
"text": "<p>This boils down to one main reason: competition. </p>\n\n<p>Animals, in general, don’t like sharing resources with direct competitors, but this violence over food, territory, and in the case of intraspecific relations, breeding rights seems to be more extreme the higher up you go on the food chain. </p>\n\n<p>An excellent example of this regards cougars. A dominant tom cat in Montana, for instance, rules over a domain that can easily exceed a hundred square miles. This territory is several times larger than what he’d require just to feed himself, so why is it so large? It’s quite simple: breeding rights. Within the borders of his, hundred or so square miles of territory are lands also used by two or three females and the cubs he’s fathered with them. Other tom cougars enter at their own risk, as he’d be more than happy to run them out or kill them. The same fate befalls any of his sons who reach maturity, so they either disperse to lands unknown or die trying. Dispersing males naturally die frequently in most species as a result.</p>\n\n<p>Females also defend their territories, but since it’s not advantageous for them to have multiple potential breeding partners, their lands aren’t near as large (maybe forty square miles or smaller), just big enough to keep them and their offspring safe and well fed with all the deer, elk, coyotes, and/or bighorns they need, in addition to smaller prey. Female offspring who disperse have an easier time finding territories than their brothers and are less likely to disperse widely because of this fact. </p>\n\n<p>To answer your question, predators self regulate their populations, often violently. In a stable ecosystem, there’s enough of them to keep their prey in check, but due to factors of real estate, breeding rights, and interactions with other predatory species, they simply don’t overpopulate.</p>\n"
},
{
"answer_id": 73285,
"pm_score": 1,
"text": "<p>If I missed seeing this in one of the other answers, I apologize, but I don't believe anyone has mentioned a very relevant fact about some predators that directly affects their populations at any given time. The fact is that wolves and probably other predators living in a pack-style grouping, allow only the alpha male and female to mate. This obviously severely limits the number of offspring born each year as well as leaving the pack vulnerable to catastrophe when something happens to either or both alphas. This mode of self-regulation is independent of food availability so works in years of abundance as well as famine. </p>\n"
}
] |
15,555 |
<p>So obviously, viruses are nonliving. But when my teacher was teaching viruses in the video (we're doing "flip" learning this semester), the way he described it, it seemed like the viruses responded to their environment in that they moved around until they found a cell of the right type, and then they latched on and hijacked it. </p>
<p>I had always thought of it more like that they were just kind of floating around, carried by the host system (blood in animals for example), until they "bumped into" the right kind of cells and both sets of membrane proteins "docked". But my theory/idea doesn't really make sense because it doesn't account for how viruses would be able to infect bacteria.</p>
<p>But, the idea that viruses propel themselves doesn't make much sense either, because viruses are nonliving, and one of the characteristics of life that they do not meet is that living things acquire and use energy.</p>
<p>In summary my question is, how are viruses propelled? Do they move themselves, or are they moved by external forces?</p>
|
[
{
"answer_id": 15559,
"pm_score": 5,
"text": "<p>All of your reasoning is correct - viruses are <strong>not</strong> motile (i.e. not self-propelled). </p>\n\n<p>I don't understand why you think this would cause a difficulty in the case of bacteria.</p>\n\n<p><strong>Edit in response to comment @Remi.b</strong></p>\n\n<p>Some cursory research on estimating probabilities of collisions between particles engaged in random walks has revealed some very challenging maths. So I decided to simply look at some data.</p>\n\n<p>Remarkably there is a fairly recent paper describing investigations of the kinetics of bacteriophage adsorption.</p>\n\n<blockquote>\n <p><a href=\"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1914437/pdf/303.pdf\" rel=\"noreferrer\">Moldovan, et al. (2007) On Kinetics of Phage Adsorption. Biophysical Journal 93:303–315</a></p>\n</blockquote>\n\n<p>I didn't realise it was still possible to publish papers like this, but in fact it is very interesting. For our current purposes we only need to consider the data presented in Figure 3, which show that when <em>E. coli</em> cells at a density of 10<sup>8</sup> cells ml<sup>-1</sup> are mixed with bacteriophage λ at a density of 5 x 10<sup>4</sup> particles ml<sup>-1</sup>, then 90% of the phage have attached to a bacterial cell within less than 10 min.</p>\n\n<p>Just to relate this to a real life situation, it is estimated that sea water contains bacteria at a density of 10<sup>6</sup> cells ml<sup>-1</sup> and phage at 5 x 10<sup>7</sup> particles ml<sup>-1</sup>.</p>\n"
}
] |
[
{
"answer_id": 15562,
"pm_score": 3,
"text": "<p>You are right, viruses are neither alive, nor are they moving by themselves. They are moved by passive movements (e.g. the bloodstream or movements of the air) until they meet their target cells. This can be either a cell in the human body (for flu viruses these are cells of the respiratory tract for example) or bacteria (for bacteriophages). </p>\n\n<p>For bacteria both can happen, viruses floating around meet a bacteria they can infect or the other way that moving bacteria meet the virus.</p>\n"
},
{
"answer_id": 90881,
"pm_score": 2,
"text": "<p>Viruses move by Brownian motion <a href=\"https://en.wikipedia.org/wiki/Brownian_motion\" rel=\"nofollow noreferrer\">1</a> The definition of temperature is there are an average of about 2 calories (little c) (= 8.3 J) per kelvin, mole, and degree of freedom. <a href=\"https://en.wikipedia.org/wiki/Gas_constant\" rel=\"nofollow noreferrer\">2</a> Multiply that by 1 mole/6.02E23 molecules and you have the Boltzmann constant (1.4E-23 J/(K*DOF). So the virus has three dimensions - three degrees of freedom - of physical translation at 300 K room temperature, to get, say, 900 times the Boltzmann constant or 1.2E-21 J of energy. </p>\n\n<p>Which doesn't sound like much, but kinetic energy = 1/2 mass x velocity squared, so if the virus weighs, say, 100,000 daltons = 100,000/(6.02E23) grams, then you divide the joules by this (converting to kg) to get 0.2 m^2/s^2 - take the square root and you have about 0.6 m/s, or about 1.3 miles per hour. </p>\n\n<p>So the virus ambles along at a walking pace (give or take - see the Boltzmann distribution), requiring NO ENERGY to do so. The caveat is that it has no control over where it goes; this is heat energy. You might say that the virus, like a stealthy flatus in a crowded room, is an agent of chaos (or at least entropy), on a mission to go forth and spread out.</p>\n"
},
{
"answer_id": 98492,
"pm_score": 2,
"text": "<p>The term <em>self-propelled</em> requires some finer qualification in the case of bacteriophages. Although bacteriophages are generally carried via Brownian motion, as described in the other answers, in some of them the attachment process exhibits autonomous propulsion. In particular, they may walk on the surface of a bacteria (see <a href=\"https://www.businessinsider.com/t7-bacteriophage-walks-e-coli-surface-2013-1?IR=T\" rel=\"nofollow noreferrer\">modeling video here</a>) and they inject their genetic material with a <a href=\"https://en.wikipedia.org/wiki/Bacteriophage#Attachment_and_penetration\" rel=\"nofollow noreferrer\">syringe-like motion</a>. <em>In doing so they dispense the energy stored in the viral proteins during their synthesis and the phage assembly</em> - in other words they remain nonliving entities, unable to acquire energy and convert it to useful work, their motion being a programmed one, like that of a released spring.</p>\n"
},
{
"answer_id": 105301,
"pm_score": 2,
"text": "<p>The existing answers are correct. However, there is now one example of a self-propelled<sup><strong>†</strong></sup> virus.</p>\n<p><a href=\"https://www.nature.com/articles/s41586-021-04106-w\" rel=\"nofollow noreferrer\"><strong>Herpesviruses assimilate kinesin to produce motorized viral particles</strong></a></p>\n<blockquote>\n<p>Here, using herpes simplex virus type I and pseudorabies virus as model alphaherpesviruses, we show that a cellular kinesin motor is captured by virions in epithelial cells, carried between cells, and subsequently used in neurons to traffic to nuclei.</p>\n</blockquote>\n<p>Essentially, herpesvirus has been shown to co-opt host-derived <a href=\"https://en.wikipedia.org/wiki/Kinesin\" rel=\"nofollow noreferrer\">kinesin-1</a> to move from the centrosome to the nucleus along microtubules.</p>\n<p><sup><strong>†</strong></sup> It’s not <em>self-propelled</em> in the sense that it encodes its own factors to enable autonomous movement, though the described mechanism is more sophisticated than simple Brownian motion. If flagellar chemotaxis in bacteria is analogous to a boat on open water, then kinesin-propelled motion is like a train ride; you are constrained to the tracks.</p>\n"
}
] |
15,736 |
<p>I had laser eye surgery a decade ago, but in recent years my eyesight has become significantly myopic. I consulted an ophthalmologist to see if this was eye strain because I work at computers a lot, or part of a natural degradation of the eye over time, or both. My ophthalmologist seems to believe that in my case I'm youngish enough that the natural degradation with age is minimal, and that it's mostly eye strain that is my problem. She believes I can get my eyesight back to roughly 90% of my post-surgery sight ability, if I can reduce eye strain. She gave me some eye drops to help with dryness, and recommended various ways to for me to help my eyes recuperate.</p>
<p>I decided to look into eye strain to learn more about what conditions cause it and what can alleviate it. What I learned is that the lens of <a href="http://en.wikipedia.org/wiki/Accommodation_of_the_eye#Theories_of_mechanism" rel="noreferrer">the eye needs to be flatter to accommodate focusing on far objects</a>, and rounded to focus on near objects. The way the lens becomes flat is by using spring-like connective tissue called <em><a href="http://en.wikipedia.org/wiki/Choroid" rel="noreferrer">choroids</a></em> that pull it taught. Attached to these choroids are muscles called <em><a href="http://en.wikipedia.org/wiki/Ciliary_muscle" rel="noreferrer">ciliary muscles</a></em> that stretch the choroids out when they contract. This action causes the choroids to stop pulling on the lens, and the lens will retract into a more rounded shape. So, when the ciliary muscles are relaxed, you can see far. When the ciliary muscles are contracted, you can see close up. <a href="http://www.yorku.ca/eye/ciliary.htm" rel="noreferrer">This diagram from the York University website</a> was the clearest explanation I have come across:</p>
<p><img src="https://i.stack.imgur.com/tM4cr.gif" alt="ciliary muscles and choroids"></p>
<p>Thus, the reason for my current inability to focus on far objects is that so much focusing on close objects, mainly computer monitors, is straining my eyes. In order to regain the ability to focus on far objects, I need to reduce strain and allow the muscles to relax. If they relax, the choroids can pull the eye to the flatter shape needed to see far.</p>
<p>However, I can't reconcile that model with how I understand the mechanics of the other muscles in my body. If I go to the gym and run or lift weights, or in any way expose my muscles to work, they respond by getting stronger without sacrificing the ability to stop contracting. The muscles in my body don't lose the ability to relax, no matter how much I train them. I have never heard of anyone who worked out too hard or too long such that their bicep would remain in a permanent state of contraction.</p>
<p>In fact, in my experience, after a hard workout, it's <em>impossible</em> to prevent my muscles from relaxing and resisting doing more work. When I do a bicep curl at the gym, and I do it to the point that I can't lift the weight anymore, my muscle gives up and I drop the weight. Similarly, if I've spent a long time looking at close up objects, shouldn't my ciliary muscles give up, allowing the choroids to take over, making clear far vision the unavoidable outcome?</p>
<p>The idea that my ciliary muscles need to relax in order to see far also seems to contradict my personal anecdotal experience. Sometimes I am able to see far away, but I can't hold it for more than a few seconds. If I try to maintain focus on far objects for too long, I get an uncomfortable feeling in my eyes that is hard to describe, but it's a form of pain that forces me to give up. My vision goes blurry, and I can only see close objects again. If my bicep worked the same way, it would be as if it hurt to let my arm hang straight down with a weight, and the only way to alleviate it would be to raise the weight, which makes no sense. I feel like the effort is in seeing far, and that when I'm tired, I can only see close up.</p>
<p>It's not that the case that I think that all medical research on the eye has it backwards, it must be that there is some aspect of this that I am not seeing (pun intended).</p>
<p>How can it be that the ciliary muscles, unlike other muscles, lose their ability to relax?</p>
<p>Why is it that my ciliary muscles don't become exhausted and allow the choroids to take over by default?</p>
|
[
{
"answer_id": 15902,
"pm_score": 4,
"text": "<p>First of all, I should correct some points that were misunderstood. \nDon't change the question because this will lead to confusion.</p>\n\n<p>\"The way the lens becomes flat is by using spring-like connective tissue called choroids that pull it taught.\"</p>\n\n<p>In classic ophthalmology you don't need to think about choroid in direct relation to accommodation: choroid is a sponge-like layer between the sclera and retina and in general it is consisted of blood vessels. The anterior part of the choroid continues anteriorly to became a ciliary body which in turn contains ciliary muscle - one circular muscle per eye. From the ciliary body/muscle spread zonules (zonule fibers) and they are fixed on the lens equator. </p>\n\n<p>Physiology: contraction of <strong>ciliary muscle</strong> causes <strong>zonules</strong> to became loosen and <strong>\"free\" the lens</strong> to became more convex and move the focus anteriorly (<em>not choroid contracts itself</em>). If the ciliary muscle relaxes then zonules are tighten up and the lens consequently becomes more flat (less convex) moving the focus posteriorly. In other words you can say it in the terms of depth of focus - convex lens gives less depth, less convex gives more depth of focus.</p>\n\n<p>Thus, the classical choroid layer does not perform any action (look at your choroid related link - there are almost nothing about accommodation).</p>\n\n<p>\"Permanent state of contraction\" can be physiological (=normal) as well as abnormal one, and it is very common in some conditions (muscles spasms). One example is priapism, where corporal smooth muscle contraction causes permanent and dangerous penile erection which can be medical emergency (priapism is by far more complex, so take the explanation like a metaphor). </p>\n\n<p>If we refer to \"accommodation spasm\" there is analogy to \"muscle spasm\" (and partially to priapism), but I should state we believe that spasm of ciliary muscle exists - since we don't see it directly. Probably (and take this sentence as speculation, since I cannot give you reference right now) the causes of this is not a muscle spasm itself, but the state of zonular fibers which cannot come back to their base state. I like the example with iron rod - if you will contract it fast and many times, at some point it can be \"loosen\" as well as fractured (and probably it does happens to zonules too). Probably (I say \"probably\" to underline the point we do not exactly know this), the \"accommodation spasm\" is partially misname and in future the investigations will clarify that.</p>\n\n<p>Probably, you will learn some interesting facts from definition of \"pseudoexfoliation\" syndrome, but I do not explain it here because it is not related directly to the question. From <a href=\"http://en.wikipedia.org/wiki/Pseudoexfoliation_syndrome\" rel=\"noreferrer\">wiki</a> \"has been known to cause a weakening of structures within the eye which help hold the eye's lens in place, called lens zonules\"</p>\n\n<p>Another example for analogy for continued \"spasm\" is the situation when one should care something heavy for a long distance without releasing the grasp - finally one can get not only spastic contraction but also severe ischemic damage to the fingers. </p>\n\n<p>Considering your case, you should know about pathological (degenerative) myopia where the eye expands posteriorly and consequently the focus is before the retina which should be corrected by minus lenses. It is well known fact that myopic eyes have longer axial length then normal eyes. Probably, it is your case.</p>\n\n<p>So, as you can see, the answer to your question is not a clear cut, but assumption. The ciliary muscle does can relax, but probably the problem is more complex then only ciliary muscle related issue.</p>\n\n<p>PS The image you reposted is a little bitconfusing one and is not exact. This one is classical and gives better understanding of the anatomy - </p>\n\n<p><img src=\"https://i.stack.imgur.com/4Bvku.gif\" alt=\"enter image description here\"></p>\n"
}
] |
[
{
"answer_id": 48445,
"pm_score": 2,
"text": "<p>I'm not a eye doctor but I do workout. I would like to say something about your metaphor or comparison from the ciliary muscle to the body muscles. </p>\n\n<p>Let's look at a workout. In a workout, you strain the muscle then relax the muscle repeatedly until you exhaust the muscle. Another part of the exercise is stretching. If you don't stretch, you will lose full range of motion. For instance, if I were to do a regiment of bicep curls for the first time, and I slept that night with my arm cocked, it would be a painful effort to straighten it the next day. If I don't stretch it my arm would stay in that position having limited motion. The muscle is relaxed but it's range has changed. Another example would be, when I was a teen, I did karate and could do the splits. Now-a-days I can not do the splits no matter how much my muscles are relaxed. </p>\n\n<p>Looking at the computer all day isn't comparable to working out a muscle because you don't contract and relax repeatedly. You only contract. </p>\n\n<p>Now let's look at the body muscles in a more relevant metaphor - Tension. Tension is an involuntary reaction. Because you hold the muscle in a contraction state for such a long time, it tends to want to stay contracted without you making the effort. A lot of people hold tension in their neck and shoulders and no matter how much pain it causes them, they can't relax it voluntarily. </p>\n\n<p>Muscles have a mind of there own (muscle memory). To assume you have complete control over them is wishful thinking. I assume that the ciliary muscle is no different. </p>\n"
},
{
"answer_id": 48461,
"pm_score": 2,
"text": "<p>There are a few more things that need to be considered to get a better understanding of the physiology.</p>\n\n<p>The ciliary muscles are not skeletal muscles (voluntary muscles that you can control) but smooth muscles (involuntary muscles which are under the control of the autonomous nervous system, which is self regulated by the parts of brain not under the conscious control). This has several deep implications. </p>\n\n<ol>\n<li><p>Smooth muscles do not hypertrophy - grow and become thick like skeletal muscles - They are more or less constant and their growth/strengthening is more related to hormones than regular contraction/relaxation exercises</p></li>\n<li><p>Smooth muscles are supplied by autonomic nervous system - Parasympathetic system is the main supply. Recently <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/15792840\" rel=\"nofollow\">evidence</a> for sympathetic innervation of ciliary muscles has been found.</p></li>\n</ol>\n\n<p>Generally, there is a balance between the sympathetic and parasympathetic, the balance being driven by the need brain perceives. An imbalance in these systems can cause accommodation problems</p>\n\n<ol start=\"3\">\n<li>This point is speculation based on proved biological laws: Law of tension-stress: This states that if under constant tension, the biological systems grow.</li>\n</ol>\n\n<blockquote>\n <p>Gradual traction on living tissues creates stress that can stimulate and maintain the regeneration and growth of certain tissues. Slow, steady tension of tissue causes them to become metabolically activated, resulting in an increase in their proliferative and biosynthetic functions. These processes are dependent upon two main factors:</p>\n \n <ol>\n <li>The quantity and quality of blood supply to the tissue being mechanically stressed and</li>\n <li>The stimulating effects of tensile forces acting along the lines of muscular contractions because collagen fibers are generally aligned parallel to the vector of tension-stress.\n <sub>source:<a href=\"http://jontristermd.com/for-physicians/the-tension-stress-effect-on-the-genesis-and-growth-of-tissue-2\" rel=\"nofollow\">http://jontristermd.com/for-physicians/the-tension-stress-effect-on-the-genesis-and-growth-of-tissue-2</a></sub></li>\n </ol>\n</blockquote>\n\n<p>This may cause changes in the choroid that may reduce the tension on the zonules causing a semi-permanent/permanent myopia.</p>\n"
},
{
"answer_id": 62881,
"pm_score": 0,
"text": "<p>The ciliary muscle is made of smooth muscle rather than skeletal muscle. These two types of muscles have different mechanisms for contraction and relaxation. Skeletal muscle is relaxed unless it is stimulated by a nerve. Smooth muscle is able to lock itself into a contracted state through a chemical reaction (phosphorylation). It then does the reverse chemical reaction (dephosphorylation) to relax. This is important because smooth muscles do things like keep the urine in your bladder (urinary sphincter), and you don't want that muscle getting tired and giving up.</p>\n"
},
{
"answer_id": 65510,
"pm_score": 1,
"text": "<p>After reading various theories of how the ciliary muscle body works, I came across a convincing new theory by Dr Goldberg, one of reciprocal action. In other words, the lens is only under posterior (rear-inner side) tension when focusing on near objects, but anterior (front-outer side) tension when focusing on distant objects. In both cases the lens is under a form of zonular tension. The ciliary muscle moves forward (near focus) and backward (distant focus), actuating the zonular strings and circular apparatus accordingly. As I have witnessed how I sometimes have to force myself to focus in the distance, I am inclined to believe that relaxation of the ciliary body only leads to a medium focus, and while contraction, either forward and backward, for near and distant focussing respectively. In other words, the ciliary body would also contract slightly for a distant focus, but this contraction would be in opposite direction. There's a video illustrating Dr Goldberg's theory: <a href=\"https://www.youtube.com/watch?v=1yIpyitm6eE\" rel=\"nofollow noreferrer\">https://www.youtube.com/watch?v=1yIpyitm6eE</a>\nI must add that there are theories saying that the zonular fibre gets stretched (permanently longer) when using too much near-vision, so that when ciliary muscle body relaxes, the lens is not held taut enough, causing it to be always convex (nearsighted).</p>\n"
}
] |
16,854 |
<p>Why don't we breathe nitrogen while it makes most of the air?</p>
<p>Why do we always tend to breathe oxygen, not hydrogen and nitrogen?</p>
|
[
{
"answer_id": 16864,
"pm_score": 5,
"text": "<p>I'd argue that we do \"breathe\" all those gases. Air that we inhale (at sea level) is about 78% N$_2$, 20.9% O$_2$, 1% argon, and smaller percentages of CO$_2$, neon, methane, etc. So all those gases are going into the lungs with every breath in.</p>\n\n<p>We take up oxygen preferentially because we have <a href=\"http://proteopedia.org/wiki/index.php/Tutorial%3aHow_do_we_get_the_oxygen_we_breathe\">hemoglobin</a> to bind O$_2$. When hemoglobin binds the oxygen, it upsets the balance and pulls more oxygen across the alveolar membrane. This is aided by pulmonary circulation which carries the blood away. <a href=\"http://highered.mcgraw-hill.com/olcweb/cgi/pluginpop.cgi?it=swf%3a:640%3a:480%3a:/sites/dl/free/0077290828/811360/Hemoglobin_Causes_Net_Diffusion_of_Oxygen.swf%3a%3aHemoglobin%20Causes%20Net%20Diffusion%20of%20Oxygen\">Here's a demo</a> of the diffusion process. </p>\n"
}
] |
[
{
"answer_id": 16856,
"pm_score": 0,
"text": "<p>Basically when air fills our alveoli, by the process of diffusion, only oxygen in the air is taken into the blood stream while the other gases along with the waste CO2 is exhaled. So you do breathe in nitrogen, but it is exhaled as it is by the body. The whole process of the respiratory system is explained <a href=\"http://www.patient.co.uk/health/the-lungs-and-respiratory-tract\" rel=\"nofollow\">here</a> with diagrams. </p>\n"
},
{
"answer_id": 16859,
"pm_score": 5,
"text": "<p>Animals use oxygen as a chemical energy source because oxygen gas can react with many other compounds to form oxides, which releases energy and happen spontaneously.</p>\n<p>Both carbon and nitrogen can be made to react with oxygen, but otherwise they are pretty inert. So of all the gasses in the air present at over a fraction of a percent, oxygen is the only one we can use for energy.</p>\n<p>Nitrogen gas itself (N2) is incredibly chemically inert; N2 requires energy input into it to react chemically. Biometabolism relies upon a chemical release of energy.</p>\n<p>If we had ammonia gas (NH3) in our air it would be a great redox source of energy... taking energy from the ammonia could produce N2. N2 takes <em>a lot</em> of work put into it to get the nitrogen out for other uses.</p>\n<p>Hydrogen (and sulfer) are both possible substitutes for oxygen in the role of redox energy source, but are normally pretty small components of our environment. On another planet they might well be the basis of biometabolism.</p>\n<p>Of course the fact that plants can use carbon dioxide to fix carbon is a different case of biology using a gas out of the air. Its the defining quality of plants!</p>\n<p>The energetics of using CO2 is endothermic - it requires energy input. They have to use sunlight to get the energy to utilize this energy and its very costly energetically. Animals can afford to move and grow because they use oxygen while they eat plants.</p>\n"
},
{
"answer_id": 16867,
"pm_score": 2,
"text": "<p>The bond in oxygen molecules is high energy, and ready to undergo an energy-yielding reaction with other molecules like sugar.</p>\n\n<p>The bond in nitrogen not chemical useful to us...other organisms use energy to \"fix\" nitrogen to make energy rich nitrogen compounds that we <strong>can</strong> use.</p>\n"
},
{
"answer_id": 31573,
"pm_score": 3,
"text": "<p>Nitrogen is much less reactive than oxygen. Indeed, if I haven't totally forgotten my long-ago chemistry courses, most chemical reactions involving N2 are energy-consuming. Thus you get nitrogen compounds produced by lightning, in auto engines, and other places where there's a lot of energy to spare. </p>\n\n<p>Oxygen reactions, OTOH, are energy-producing. You might think instead of fire: most organic stuff will burn (if dried), but it only combines with the oxygen in the air, not the nitrogen.</p>\n\n<p>PS: Indeed, many nitrogen compounds take so much energy to create that they are explosives. Ammonium nitrate, nitroglycerin, trinitrotolulene (TNT), even the potassium nitrate (saltpeter) used to make gunpowder.</p>\n"
},
{
"answer_id": 56485,
"pm_score": 2,
"text": "<p>The other answers seem to be missing the role of oxygen in oxidative phosphorylation, as an organism with aerobic metabolism we use oxygen for its electronegativity. Basically, as we break down glucose energy is released in the form of free electrons, these are \"transported\" for use in the oxidative phosphorylation to create new ATP which is our main form of energy storage. Oxygen eagerly accepts these free electrons at the last step of the oxidative phosphorylation and binds with H+ to form H<sub>2</sub>O. See <a href=\"https://physiology.knoji.com/why-do-we-breathe-oxygen/\" rel=\"nofollow noreferrer\">here</a>.</p>\n\n<p>So without oxygen there would be an accumulation of electrons, stopping the oxidative phosphorylation and forcing us to break down glucose in the (less efficient) anaerobic manner. </p>\n"
},
{
"answer_id": 57035,
"pm_score": 2,
"text": "<p>There are two parts to this answer, and several answers have addressed one or both aspects but I figured I'd put it all in one place.</p>\n\n<p><strong>1) We use oxygen for a purpose that nitrogen is chemically useless for</strong></p>\n\n<p><strong>2) While there <em>is</em> a different purpose we might want to use nitrogen for, it is something that is difficult to evolve (only bacteria have done it) and we can manage without.</strong></p>\n\n<p>Explanations:<br>\n1) We use oxygen because our metabolism uses it for energy. Our metabolism derives chemical energy from the breakdown of complex carbon molecules; this doesn't happen on its own and you need very reactive molecules to interact with those complex carbon molecules and break them down. All organisms do this step-by-step, using successive \"electron acceptors\" to basically strip electrons off of simpler-and-simpler molecules and thus break them down. Molecular oxygen is the most reactive molecule and greedy electron acceptor out there, and allows organisms that use it to get the most energy possible out of a given carbohydrate. That's why aerobic respiration is so useful, and that's what we use oxygen for. Molecular nitrogen has completely different chemical properties; it isn't that electronegative (i.e. greedy for electrons) at all. There are other molecules that can be used as electron acceptors, and are used in various forms of anaerobic respiration: nitrate, sulfate, carbon dioxide... but molecular nitrogen isn't one of them.</p>\n\n<p>For various kinds of anaerobic respiration, see :<br>\n<a href=\"https://en.wikipedia.org/wiki/Microbial_metabolism\" rel=\"nofollow noreferrer\">https://en.wikipedia.org/wiki/Microbial_metabolism</a></p>\n\n<p>2) There IS a purpose for which one could use molecular nitrogen, which is to use it to build nitrogen-based molecules that our body depends on - like DNA, RNA and proteins, which basically do everything in a living organism. No organism uses molecular nitrogen as a source for these; it's much easier to use organic nitrogen compounds like nitrates and ammonia. It can seem silly that such compounds are so limiting, when nitrogen makes up most of the atmosphere! This is less of an issue for carnivores since we get all of our nitrogen needs from eating nitrogen-filled animals, but it's a huge issue for plants. The need for such compounds (and, to a lesser extent, phosphates) is why agriculture needs fertilizer. So why can very very few organisms break down molecular nitrogen ? Because it is a very stable molecule; if you've done chemistry you might know that the two nitrogen atoms in the nitrogen molecule are connected by a triple bond, which is very strong and hard to break. This may be a big reason why the metabolism to break that bond evolved only in bacteria, and all Eukaryotes get by using the bacteria themselves (nitrogen-fixing plants), absorbing nitrogen-filled organisms (carnivores, carnivorous plants - it's the reason they're carnivorous!) or getting by on the organic nitrogen that naturally occurs in the ground thanks to nitrogen-fixing bacteria.</p>\n\n<p><a href=\"https://en.wikipedia.org/wiki/Nitrogen_fixation\" rel=\"nofollow noreferrer\">https://en.wikipedia.org/wiki/Nitrogen_fixation</a></p>\n\n<p>As an aside, the fertilizer humans make uses the Haber process, which converts molecular nitrogen in the atmosphere to ammonia. If you look at the Wikipedia page by the way you'll get an idea of how hard it is to break that triple bond, between the catalysts and the high temperatures and pressures... But through that process you could argue that humanity as a species does \"breathe\" nitrogen.</p>\n\n<p><a href=\"https://en.wikipedia.org/wiki/Haber_process\" rel=\"nofollow noreferrer\">https://en.wikipedia.org/wiki/Haber_process</a></p>\n\n<p>So basically, tl;dr:</p>\n\n<p><strong>1) we don't need to breathe nitrogen</strong><br>\n<strong>2) if we did our bodies still wouldn't because it's really hard to do; no eukaryote does it, except maybe humans themselves but only through technology.</strong></p>\n"
},
{
"answer_id": 57805,
"pm_score": 1,
"text": "<p>As others have pointed out, we <em>do</em> breathe atmospheric nitrogen but we cannot do anything useful with it. </p>\n\n<p>The problem is that the triple-bonded N<sub>2</sub> is very unreactive and almost all animals and plants cannot convert it to anything else. Humans do not have the ability to reduce it to NH<sub>3</sub>, for example, but is would be great if we could. </p>\n\n<p>All forms of life need nitrogen. It is necessary to make protein and DNA, for example. It is also very plentiful. N<sub>2</sub> constitutes about <a href=\"https://en.wikipedia.org/wiki/Atmosphere_of_Earth\" rel=\"nofollow noreferrer\">78% of air by volume</a>, but it is in a form (N<sub>2</sub>) not usable by most forms of life. And therein lies the problem: in order to use atmospheric nitrogen, it needs to be 'fixed', ie converted to a form available to 'normal' metabolic transformation. This is usually taken to mean that N<sub>2</sub> needs to be converted to NH<sub>3</sub>. Very few forms of life have the ability to do this. The 'fixation' of N<sub>2</sub> is also a great industrial problem. </p>\n\n<p>As <a href=\"https://biology.stackexchange.com/a/57035/1136\">outlined</a> by <a href=\"https://biology.stackexchange.com/users/30356/rozenn-keribin\">Rozenn Keribin</a>, the first artificial process to successfully 'fix' N<sub>2</sub> is the <a href=\"https://en.wikipedia.org/wiki/Haber_process\" rel=\"nofollow noreferrer\">Haber-Bosch</a> process, which was developed in the early part of the 20th century, and uses a metal catalyst and high pressures to achieve the following transformation: </p>\n\n<blockquote>\n <p>N<sub>2</sub> + 3 H<sub>2</sub> → 2 NH<sub>3</sub></p>\n</blockquote>\n\n<p>This process <a href=\"https://en.wikipedia.org/wiki/Haber_process\" rel=\"nofollow noreferrer\">remains</a> the main industrial source of NH<sub>3</sub> today, and is a 'mainstay' of the fertilizer industry. During the First World War, it was also an source of NH<sub>3</sub> for the production of ammunition by Germany. For his work in this area, <a href=\"https://en.wikipedia.org/wiki/Fritz_Haber\" rel=\"nofollow noreferrer\">Haber</a> was awarded the <a href=\"http://www.nobelprize.org/nobel_prizes/chemistry/laureates/1918/\" rel=\"nofollow noreferrer\">1918 Nobel prize</a> in Chemistry, a (controversial) honour that has surely stood the test of time. </p>\n\n<p>Biological N<sub>2</sub> fixation is an <a href=\"https://en.wikipedia.org/wiki/Nitrogen_fixation#cite_note-6\" rel=\"nofollow noreferrer\">amazing story</a>, and I'll restrict the discussion to an amazing enzyme: <a href=\"https://en.wikipedia.org/wiki/Nitrogenase\" rel=\"nofollow noreferrer\">nitrogenase</a>. This enzyme catalyzes the ATP-dependent reduction of N<sub>2</sub> to NH<sub>3</sub></p>\n\n<p>(I will not deal with leguminous plants, which can also 'fix' N<sub>2</sub> using a symbiotic relationship with bacteria in root nodules, as I do not know enough about it). </p>\n\n<blockquote>\n <p>In nature, [the] ability to fix N<sub>2</sub> is restricted to a small\n but diverse group of diazotrophic microorganisms that contain the enzyme nitrogenase (Burgess & Lowe, 1996)</p>\n</blockquote>\n\n<p>One type of nitrogenase (that contains molybdenum) catalyzes the following reaction:</p>\n\n<blockquote>\n <p>N<sub>2</sub> + 8 H<sup>+</sup> + 8 e<sup>-</sup> + 16 ATP → 2 NH<sub>3</sub> + H<sub>2</sub> + 16 ADP + 16 P<sub>i</sub></p>\n</blockquote>\n\n<p>Let's analyze this one: that's an eight-electron reduction that uses 16 ATPs just to make two NH<sub>3</sub> from one N<sub>2</sub> ! </p>\n\n<p>Nitrogenases may be classified into <a href=\"https://en.wikipedia.org/wiki/Nitrogenase\" rel=\"nofollow noreferrer\">3 general types</a> depending on metal content: Molybdenum nitrogenase, vanadium nitrogenase and iron-only nitrogenase. (All forms contain iron).</p>\n\n<p>Biological nitrogen fixation was discovered by <a href=\"https://en.wikipedia.org/wiki/Martinus_Beijerinck\" rel=\"nofollow noreferrer\">Martinus Beijerinck</a> and <a href=\"https://en.wikipedia.org/wiki/Hermann_Hellriegel\" rel=\"nofollow noreferrer\">t Hermann Hellriegel</a>. In addition, Beijerinck discovered that tobacco mosaic disease was caused by a virus. Neither received a Nobel prize. </p>\n\n<p><strong>Ref</strong></p>\n\n<p><a href=\"http://pubs.acs.org/doi/abs/10.1021/cr950055x\" rel=\"nofollow noreferrer\">Burgess, B,K. & Lowe, D. J.</a> (1996) Mechanism of Molybdenum Nitrogenase \n<em>Chem. Rev.</em> <strong>96</strong>, 2983−3011</p>\n"
}
] |
16,899 |
<p>I'm trying to look at relationships between parasite and host phylogenetic trees. I have done a bit of searching for software with which to do this, and I have tried using Dendroscope and TreeMap, but can't get to grips with them. </p>
<p>I want to produce something along the lines of this;</p>
<p><img src="https://i.stack.imgur.com/XXsaO.gif" alt="enter image description here"></p>
|
[
{
"answer_id": 16923,
"pm_score": 5,
"text": "<h1>Dendroscope</h1>\n\n<p>Using <a href=\"http://ab.inf.uni-tuebingen.de/software/dendroscope/\" rel=\"noreferrer\">Dendroscope</a>, I opened the provided example file <code>trees.new</code>. This opens a new window with 16 trees in it.</p>\n\n<ol>\n<li>Shift click on the first two trees (<code>Tree1</code> and <code>Tree2</code>).</li>\n<li>Choose <code>Algorithms</code> $\\rightarrow$ <code>Tanglegram...</code></li>\n<li>This will compute the tanglegram and open a new window.</li>\n</ol>\n\n<p>At this point, I get:</p>\n\n<p><img src=\"https://i.stack.imgur.com/4V2KM.jpg\" alt=\"Tanglegram\"></p>\n\n<p>There is nothing special in the <code>trees.new</code> file, just 16 Newick trees. So it looks like all you need is to have your trees in the same file or use <code>File</code> $\\rightarrow$ <code>Add from file</code>. </p>\n\n<p>I think that the tricky part is that your trees have to have the same tip labels, so that they can be lined up optimally. So in your example, <em>Phalacrocorax pygmaeus</em> and <em>Pectinopygus excornis</em> must have been named the same in the original Nexus file and then modified to produce the final figure.</p>\n\n<h1>TreeMap 3</h1>\n\n<p><a href=\"http://sydney.edu.au/engineering/it/~mcharles/software/treemap/treemap3.html\" rel=\"noreferrer\">TreeMap</a> requires some preliminary setup. Basically you create a Nexus file manually. Using the <code>4taxonmatch</code> file from the <a href=\"https://sites.google.com/site/cophylogeny/example-data-files\" rel=\"noreferrer\">examples</a>, you can get the basic layout. You have a <code>HOST</code> block and a <code>PARASITE</code> block. Within each one of those is a <code>TREE</code> block, which contains the Newick formatted tree.</p>\n\n<p>The <code>RANGE</code> block inside the <code>DISTRIBUTION</code> block contains the mapping table. Here <code>p</code> maps to <code>u</code>, etc. This is the connection between host and parasite.</p>\n\n<pre><code>#NEXUS\nBEGIN HOST; \nTREE * Host1 = (u, (v, (w, x))); \nENDBLOCK; \n\nBEGIN PARASITE;\nTREE * Para1 = (p, (q, (r, s))); \nENDBLOCK; \n\nBEGIN DISTRIBUTION; \nRANGE \n p: u, \n q: v, \n r: w, \n s: x\n; \nEND;\n</code></pre>\n\n<p>In contrast, you get the correctly labelled tree directly. See below.</p>\n\n<p><img src=\"https://i.stack.imgur.com/6G1eD.jpg\" alt=\"Tanglegram 2\"></p>\n"
}
] |
[
{
"answer_id": 16900,
"pm_score": 2,
"text": "<p>I have to confess that I know nothing about phylogenetics and the associated software but according to the abstract of <a href=\"http://onlinelibrary.wiley.com/doi/10.1111/zoj.12027/abstract\" rel=\"nofollow noreferrer\">this article</a> it seems that they used <a href=\"http://beast.bio.ed.ac.uk/\" rel=\"nofollow noreferrer\">BEAST</a> to map coalescence of co-evolving hosts and parasites.</p>\n\n<p>Also <a href=\"http://bioinformatics.oxfordjournals.org/content/27/13/i248.abstract\" rel=\"nofollow noreferrer\">this article</a> is probably of highest interest to you as it compares the efficiency of different software to construct tanglegrams</p>\n"
},
{
"answer_id": 20689,
"pm_score": 2,
"text": "<p>You can try the R package <a href=\"http://cran.r-project.org/web/packages/dendextend/\" rel=\"nofollow\">dendextend</a>. The function <code>tanglegram</code> can do the trick. Several associated functions are also available for getting plots with minimum entanglements such as <code>untangle_step_rotate_2side</code>.</p>\n"
},
{
"answer_id": 93809,
"pm_score": 1,
"text": "<p>Jane 4 (software for cophylogeny reconcilation) has a tanglegram viewer with an interactive editor. (<a href=\"https://www.cs.hmc.edu/~hadas/jane/\" rel=\"nofollow noreferrer\">https://www.cs.hmc.edu/~hadas/jane/</a>)</p>\n"
},
{
"answer_id": 93830,
"pm_score": 0,
"text": "<p>I recommend mesquite, which I've used to create phylogeny trees with.\nThere are some intricacies with using it, but there is plenty of documentation on its webpage! \n<a href=\"https://www.mesquiteproject.org/\" rel=\"nofollow noreferrer\">https://www.mesquiteproject.org/</a></p>\n"
}
] |
17,077 |
<p>Why does evolution not make life longer for humans or any other species?</p>
<p>Wouldn't evolution favour a long life?</p>
|
[
{
"answer_id": 17091,
"pm_score": 7,
"text": "<p>Why do we age is a classical question in Evolutionary Biology. There are several things to consider when we think of how genes that cause disease, aging, and death to evolve.</p>\n\n<p>One explanation for the evolution of aging is the <a href=\"http://www.programmed-aging.org/theories/mutation_accumulation.html\"><strong>mutation accumulation</strong> (<strong>MA</strong>)</a> hypothesis. This hypothesis by P. Medawar states that mutations causing late life deleterious (damaging) effects can build up in the genome more than diseases that cause early life disease. This is because selection on late acting mutations is weaker. Mutations that cause early life disease will more severely reduce the fitness of its carrier than late acting mutations. For example, if we said in an imaginary species that all individuals cease to reproduce at 40 years old and a mutation arises that causes a fatal disease at 50 years old then selection can not remove it from the population - carriers will have as many children as those who do not have the gene. Under the mutation accumulation hypothesis it is then possible for mutations to <a href=\"http://evolution.berkeley.edu/evosite/evo101/IIIDGeneticdrift.shtml\">drift</a> through the population.</p>\n\n<p>Another hypothesis which could contribute to aging is the <a href=\"http://en.wikipedia.org/wiki/Antagonistic_pleiotropy_hypothesis\"><strong>antagonistic pleiotropy</strong> (<strong>AP</strong>)</a> hypothesis of G.C. Williams. <a href=\"http://en.wikipedia.org/wiki/Pleiotropy\">Pleiotropy</a> is when genes have more than one effect, such genes tend to cause correlations between traits, height and arm length probably have many of the same genes affecting them, otherwise there would be no <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/8793422\">correlation between arm length and height</a> (though environment and linkage can also cause these patterns)... Back to AP as an explanation for aging, if a gene improves fitness early in life, but causes late life disease it can spread through the population via selection. The favourable early effect spreads well because of selection and, just as with MA, selection can not \"see\" the late acting disease.</p>\n\n<p>Under both MA and AP the key point is that selection is less efficient at removing late acting deleterious mutations, and they may spread more rapidly thanks to beneficial early life effects. Also if there is extrinsic mortality (predation etc.) then the effect of selection is also weakened on alleles that affect late life. The same late-life reduction in the efficacy of selection also slows the rate at which alleles increasing lifespan spread.</p>\n\n<p>A third consideration is the <a href=\"http://www.programmed-aging.org/theories/disposable_soma.html\"><strong>disposable-soma model</strong></a>, a description by T. Kirkwood of life-history trade-offs which might explain why aging and earlier death could be favoured. The idea is that individuals have a limited amount of resources available to them - perhaps because of environmental constraints or ability to acquire/allocate the resources. If we then assume that individuals have to use their energy for two things, staying alive via repair and maintenance (somatic-maintenance) and making offspring (reproductive-investment), then any energy devoted to one will take away from the other. If an individual carries a gene that makes it devote all of its energy to somatic maintenance then its fitness will be very low (probably 0!) and that gene will not spread. If the level of maintenance required to live forever costs more energy than an individual can spare without suffering from low fitness (very likely) or can even acquire and efficiently convert in the first place (also very likely) then high-maintenance alleles will not spread (and aging & death will continue to occur). </p>\n\n<p>To go a little further, it is common for sexes to age differently (this is what I work on) and one possible explanation is that the sexes favour different balances of the trade off between somatic-maintenance and reproductive investment, this can lead to conflict over the evolution of genes affecting this balance and slow the rates of evolution to sex specific optima. <a href=\"http://www.cosmoid.de/zajitschek/papers/Bonduriansky2008FunctionalEcology.pdf\">This paper</a> provides a good review of the area.</p>\n\n<p><strong>To summarise</strong>, evolution has not managed to get rid of death via genetic disease etc. (intrinsic mortality) because the effect is only weakly selected against, and those alleles may provide some early life benefit, and resource limitation may also reduce the potential to increase lifespan due to trade-offs with reproductive effort. Adaptive evolution is not about the <em>survival</em> of the fittest but the <em>reproduction</em> of the fittest - the fittest allele is the one which spreads the most effectively.</p>\n\n<p><strong>EDIT:</strong> Thanks to Remi.b for also pointing out some other considerations. </p>\n\n<p>Another thought is that of altruistic aging - aging for the good of the population (the population is likely to contain related individuals, <em>you</em> are related to all other humans to some degree). In this model aging is an adaptive process (unlike in MA where it is just a consequence of weak selection). By dying an individual makes space for it's offspring/relatives to survive (because resources are then less likely to limit populations). This will stop excessive population growth which could lead to crashes in the population and so, by dying earlier, an individual promotes the likelihood that its progeny will survive. Arguments of altruistic sacrifice are often hard to promote but <a href=\"http://www.researchgate.net/publication/255170953_Viscous_populations_evolve_altruistic_programmed_aging_in_ability_conflict_in_a_changing_environment\">recent work suggests that this is a more plausible model than once thought</a>.</p>\n\n<p><a href=\"http://www.programmed-aging.org/theories/evolvability_theories.html\">Evolvabilty theories</a> also suggest that aging is an adaptive process. These suggest that populations, composed of a mixture of young and old, have biases in how well adapted the members of the population are - where younger individuals are better adapted (because they were produced more recently it is likely that the environment is similar to the environment they are favoured in). Thus by removing the less well adapted individuals from a population via senescence and freeing up resources for younger better adapted individuals, a population evolves more rapidly towards it optimal state.</p>\n"
}
] |
[
{
"answer_id": 17078,
"pm_score": 5,
"text": "<p>This is a very good question.</p>\n\n<p>There is a big ongoing field of research called \"evolution of aging/senescence\" that tackles this question. I won't give you a complete overview of the different hypothesis the could explain why we age but here is a fundamental concept that is to know.</p>\n\n<p>We'll assume that there is some extrinsic mortality, mortality against which a lineage won't ever be able to escape and I think it is not an assumption that is hard to meet. Therefore, an allele that has age-specific effect such as decreasing the fecundity at age 3 will undergo a higher selection pressure and will faster get eliminated from the population than another allele causing the same decrease in fecundity but at age 4 because some individuals would have died between age 3 and age 4. In other words, natural selection is more efficient at lower age than at higher age. Now, imagine in humans an allele that increases the reproductive success of an individual at age 20 by decreasing the survival at age 78. This allele will easily spread in the population. Such alleles are said to have <em>age-specific antagonist pleiotropic</em> effect. And empirical studies have shown that alleles that have antagonist age-specific antagonist pleiotropic exist.</p>\n\n<p>In short, it is because there is some extrinsic mortality that natural selection acts with a different strength at different ages allowing some deleterious allele at old age to fix in the population especially if those alleles have age-specific antagonist pleiotropic effect. You'll find in <a href=\"https://rads.stackoverflow.com/amzn/click/com/0521459672\" rel=\"nofollow noreferrer\" rel=\"nofollow noreferrer\">this book</a> mathematical formulation and more complete discussion of this effect</p>\n\n<p>Other hypotheses exist which are based on lineage selection, group selection or on the mutation-selection balance.</p>\n"
},
{
"answer_id": 17090,
"pm_score": 3,
"text": "<p>There is no selection mechanism that would favor high age.</p>\n\n<p>By the time it's apparent whether or not an individual can reach a high age healthily, they'll have ceased all reproductive activity.</p>\n\n<p>Conversely, people who get cancer at 45 will have likely reproduced already.</p>\n"
},
{
"answer_id": 17095,
"pm_score": 3,
"text": "<p>If you take the line of \"The Selfish Gene - Richard Dawkins\". Evolution doesn't care about individuals, it cares about genes. So as long as the genes are passed along reliably into the future, evolution may do it with 4 generations per 100 years or 100 generations per 100 years.</p>\n"
},
{
"answer_id": 17097,
"pm_score": 4,
"text": "<p>Actually, genetically, there is no reason for animals to continue to exist after they have procreated.</p>\n\n<p>If you look at salmon, they die immediately after procreating, which is probably the most efficient way to carry the best genes to the next generation.</p>\n\n<p>In the case of mammals, they need to teach their offspring where to find food, where to find water and how to avoid dangers.</p>\n\n<p>In the case of humans, that goes into the third generation, so most humans know their parents and their grandparents, and even they live with them in some cultures, since their experiences and ideas are taken as very important.</p>\n\n<p>So maybe the question should be the opposite, why do we live to see our grandchildren grow?</p>\n\n<p>Taking your same question to the opposite: why do people die? Why don't they live forever instead of reproducing? I can think of various reasons for this. Imagine a race that lives forever and another race who have a lot of children early on and then die. Now imagine a contagious disease that spreads among both populations. Which race has the most probability of survival?</p>\n\n<p>Of course, the race that reproduces rapidly has a better chance.</p>\n\n<p>And also, evolution works wonders for the race that reproduces rapidly instead of the race that lives forever. Meaning the number of years a species live has carefully been \"designed out\" by evolution.</p>\n\n<p>Evolution would not work if it didn't stabilize around the best genes. And that's exactly what happens with humans. Most humans have the same traits: live around the same number of years, and have more or less the same abilities, most differences are almost irrelevant.</p>\n"
},
{
"answer_id": 17098,
"pm_score": 4,
"text": "<p>Because evolution isn't about individuals: it's about species. What matters to natural selection isn't how long you live, but how many grandchildren you have. A long lifespan <em>can</em> be an evolutionary advantage, but like any trait, it's only an advantage to the extent that allows you to reproduce more.</p>\n\n<p>It would seem that a longer lifespan would be advantageous anyway, because it would give you more time to reproduce. However, for reasons we don't yet fully understand, it doesn't seem to work out that way in practice. Most organisms (assuming they live long enough) eventually reach an age where they stop reproducing. Even humans do this, and although we've managed to increase the average lifespan quite a bit over the course of recorded human history (to say nothing of the millennia before that), the average age at which people stop reproducing apparently hasn't changed very much.</p>\n\n<p>Why not? What makes <em>this</em> an evolutionary advantage over having more reproductive years? This is one of those things that we haven't really figured out yet. There are a number of competing theories, and the other answers here go into some of them. But the most direct way to answer your question is fairly simple: longer lifespans (and/or reproductive years) haven't given us, or our children, any more success at reproducing. Thus, there is no pressure on the species to live longer, and so it doesn't happen.</p>\n"
},
{
"answer_id": 17119,
"pm_score": 3,
"text": "<p>To an extent it does; in that we live longer than our mouse-like ancestors. So the question becomes: why not keep extending it to immortality.</p>\n\n<p>The key thing is that evolution <em>cares</em> only about the survival of your genes; so if you live for 1000 years or if 10 generations of your family have 1 individual's worth of your genes in each generation (each living for 100 years) this is equivalently successful.</p>\n\n<p>But this assumes it's either-or that an organism can reproduce or live a long time, could it not do both? <a href=\"http://www.washingtonpost.com/wp-srv/national/horizon/june98/microbes.htm\" rel=\"noreferrer\">In principle it could but the resources of a particular niche are limited so in order to avoid mass starvation the reproductive rate must reduce as the average age of the individuals go up</a>.</p>\n\n<p>So this suggests having very long lived individuals is no better than having short lived individuals, but is it at least equal? Sadly not, if fewer new individuals are born then the rate of evolution of that species is reduced. A very long lived species is less able to respond to environmental changes. As such over an evolutionary timescale an extraordinarily long lived animal is likely to be outcompeted by a shorter lived species.</p>\n\n<p>Of course there is a natural breakeven point; there is a considerable cost in bringing an individual from infant to reproductive adult so once they've got there it makes sense to keep them around for a while, but not indefinitely.</p>\n"
},
{
"answer_id": 45880,
"pm_score": 2,
"text": "<p>I am assuming that by longer life, you mean slower aging, because evolution can do little if a mountain falls on a person!</p>\n\n<p>So, why don’t organisms have slower, or better, zero rate of aging?</p>\n\n<p>The theory I am describing is based upon <a href=\"https://www.google.co.in/url?sa=t&rct=j&q=&esrc=s&source=web&cd=3&cad=rja&uact=8&ved=0ahUKEwiDv-PknsHMAhWSkY4KHQ5sChgQFggmMAI&url=https%3A%2F%2Fen.wikipedia.org%2Fwiki%2FLife_history_theory&usg=AFQjCNEDYF9eYirjkBUqeLdbX7vlwYmKkw&sig2=1TqMCZSN79SSZwI6VUgvsg\" rel=\"nofollow noreferrer\">life history theory</a>. Life history theory assumes that:</p>\n\n<ol>\n<li>Resources available to any organism are limited,</li>\n<li>Life processes like ‘reproduction’ and ‘repair and maintenance of the body’ are costly with respect to resource consumption, and resources directed towards one life process must be directed away from the other. Hence a trade off mechanism between the different life processes must exist.</li>\n</ol>\n\n<p>Based on this data, one can infer that given a specie with a given death rate of extrinsic causes (causes beyond that of aging, like getting eaten), one can use a little mathematics to find the average life span of the organism if the organism does not ages. Simple…?</p>\n\n<p>Now, given that the average life span of the non-aging specie is limited, do you really think that the optimum life strategy of the specie would be zero aging? Remember that to not to get old one needs to spend energy, and that all the energy gone in maintaining health will certainly be wasted in the form of dead bodies once the organism dies. </p>\n\n<p>Hence, given a mechanism through which trade off of resources between life processes is possible, the organisms must invest a little more towards reproduction and a little less towards repair and maintenance? Why? Just to reduce the loss of resources in the form of dead bodies and to increase reproductive success, which is what gets counted in the end!</p>\n\n<p>So, indeed, having zero rate of aging has disadvantages! It would be more advantageous if organisms age with a fixed specie specific rate.</p>\n\n<p>Now, time to make few points clear: </p>\n\n<ol>\n<li>This theory assumes Life history theory to be correct. I am not saying- “hello there- this is the correct reason of aging!” I am saying- “This is the correct theory of aging if life history theory is correct!” So, if you do not believe in life history theory, then get busy trying to prove it wrong. The theory I have discussed stands on the shoulder of a giant. On the other hand, if you believe that the theory I discuss does not follows from Life History theory, then lets hear your argument.</li>\n<li>This theory also assumes that aging happens due to lack of repair and maintenance of constantly occurring body damages. The special thing about this theory is that it gives a non-altruistic mechanism through which aging can directly benefit the organism. Hence, this theory makes it easier for us to explain why aging got natural selection- because it has benefits!</li>\n</ol>\n\n<p>I found this theory on <a href=\"https://biology.stackexchange.com/questions/45839/does-reproduction-cause-aging-is-aging-just-a-strategy-to-increase-reproductiv\">this</a> SE question, where the question has now been put on hold due to dubious reasons. Also, the OP mentions this book- <a href=\"http://rads.stackoverflow.com/amzn/click/B01F0HJ6J8\" rel=\"nofollow noreferrer\">Modern Biological theory and experiments on Celibacy</a>, which, I think, was one of the reasons why the question was put on hold!</p>\n"
}
] |
19,762 |
<p>As I understand it, various animal traits have to evolve gradually, but what happens to the species that are "neither here nor there"?</p>
<p>To put it differently, if a species evolved from another, it did so because it's somehow better, right? So why are there examples of the original species not being extinct?</p>
<p>What factors determine weather some species "stick"?</p>
|
[
{
"answer_id": 19764,
"pm_score": 5,
"text": "<p><strong>Short answer</strong></p>\n\n<blockquote>\n <p>Why are there species rather than a long continuum?</p>\n</blockquote>\n\n<p>Three important reasons I could think of are sex, non-uniform adaptive landscape and ancestry.</p>\n\n<p><strong>Long answer</strong></p>\n\n<p>I am not sure I'll answer your question so let me know if I miss your point or if I help!</p>\n\n<p><strong>To start with, you might want to read <a href=\"https://biology.stackexchange.com/questions/39664/how-could-humans-have-interbred-with-neanderthals-if-were-a-different-species/39669#39669\">this answer</a> on the semantic difficulties behind the concept of species</strong> </p>\n\n<blockquote>\n <p>What factors determine whether some species \"stick\"?</p>\n</blockquote>\n\n<p>Natural selection is nothing but differential fitness (fitness is a measure of both reproductive success and survival) among genotypes within a population. Individuals having greater fitness will leave more offsprings and therefore the genes of these individuals increase in frequency in the population. There are few generalities to be made about what <a href=\"http://en.wikipedia.org/wiki/Phenotype\" rel=\"nofollow noreferrer\">phenotypic</a> traits are beneficial in a given population. For example, \"white fur\" is a very good trait for a polar bear but would highly deleterious for a mealworm.</p>\n\n<p>However, there is a thing called <a href=\"https://biology.stackexchange.com/questions/10970/empirical-evidence-for-species-selection\">species selection</a> wherein a given lineage at least, it is possible to identify specific traits that seem to either reduce the extinction rate or increase the speciation rate. This is, for example, the case for polyploidy in angiosperms (<a href=\"http://www.annualreviews.org/doi/abs/10.1146/annurev.genet.34.1.401\" rel=\"nofollow noreferrer\">Whitton and Otto, 2000</a>)</p>\n\n<blockquote>\n <p>if a species evolved from another, it did so because it's somehow better, right?</p>\n</blockquote>\n\n<p>If you observe different extant species you cannot say that any of these species evolve from any other one you can today observe. The correct way of looking at two species is that they share a common ancestor in a given past. Therefore, looking at a cat and a <a href=\"http://en.wikipedia.org/wiki/Eurasian_blue_tit\" rel=\"nofollow noreferrer\">blue tit</a> you cannot say that one species evolved from the other one but you can only say that these two species share a common ancestor (just like any other pair of species) that was neither a cat nor a blue tit. The example is obvious because cats and blue tits are \"not so closely related\" (everything is relative) but the same logic holds for any pair of species.</p>\n\n<blockquote>\n <p>Why are there species rather than a long continuum?</p>\n</blockquote>\n\n<p><strong>Sex</strong></p>\n\n<p>The simplest and most obvious reason why there are species within which individuals are more similar compared to each than to individuals from other species is due to the definition (the most common definition because different definitions exist!) itself of a species. <strong>A species is a group of individuals that can interbreed</strong>. See <a href=\"https://biology.stackexchange.com/questions/39664/how-could-humans-have-interbred-with-neanderthals-if-were-a-different-species/39669#39669\">this</a> for more info on the concept of species.</p>\n\n<p>Take two originally different groups of individuals and allow them to interbreed. Their traits will mix up and you won't be able to tell two different groups apart. All individuals within the new mixed group are a mixture of the individuals from the two previous groups (under some circumstances this process has been sometimes called \"reverse speciation\"). If now you take one single group of individuals. You split them into two groups in the sense that you don't allow individuals from group 1 to mate with individuals from group 2. You will see that after some evolutionary time, the individuals of group 1 will tend to resemble much more to individuals of group 1 (its own group) than to individuals of group 2. If you wait long enough so that these two groups of individuals become different enough so that they can't interbreed any more because they diverged too much, then you have what is called a reproductive isolation and under the common definition of species, you can say that a <a href=\"http://en.wikipedia.org/wiki/Speciation\" rel=\"nofollow noreferrer\">speciation</a> (You may want to have a look to the wiki article for \"speciation\") occurred and therefore you have two new species instead of one ancestral species.</p>\n\n<p><strong>why the two groups tend to diverge through times?</strong></p>\n\n<p>You may wonder \"But why the two groups tend to diverge through times?\". There are several processes that explain that divergence:</p>\n\n<ul>\n<li>Mutations\n\n<ul>\n<li>Different mutations occur in the different groups (just by chance)</li>\n</ul></li>\n<li>Natural selection\n\n<ul>\n<li>The environment differs and the selection pressures differ selecting for different traits in the two species. Also, the accumulation of different mutations affects the selection pressure at other loci.</li>\n</ul></li>\n<li>Genetic drift\n\n<ul>\n<li>Shortly speaking genetic drift is due to random events. Different random events occur between the two populations. For more info about genetic drift, see <a href=\"https://biology.stackexchange.com/questions/14543/why-is-the-strength-of-genetic-drift-inversely-proportional-to-the-population-si\">this post</a></li>\n</ul></li>\n</ul>\n\n<p>If you are not very familiar with these concepts I recommend that you have a look at <a href=\"http://evolution.berkeley.edu/evolibrary/home.php\" rel=\"nofollow noreferrer\">Understanding Evolution (UC Berkeley)</a>.</p>\n\n<p><strong>Adaptive landscape</strong></p>\n\n<p>Note also that there are other reasons for explaining this pattern. One other reason is \"Because the adaptive landscape is not a flat function\". What this means to the layman is that there are some combinations of traits that cannot really be beneficial.</p>\n\n<p><strong>Ancestry</strong></p>\n\n<p>Also, individual phenotypes are not independent of each other and not only for ecological reasons but also because of shared ancestry. If you consider two families, you will easily accept no to see a continuum of phenotypes but two distinct groups (maybe in one family curly hair is common while in the other they all have straight hair).</p>\n"
}
] |
[
{
"answer_id": 19763,
"pm_score": 3,
"text": "<p>Typically when both new and old species still exist it is because evolution pushed the new one into a different habitat or role. </p>\n\n<p>As a hypothetical example reef fish vs. deep water fish and their relative size. Let's say deep water fish evolved into reef fish, but we still have deep water fish. So there were deep water fish that were a little smaller than the rest of the deep water fish, and this gave them access to a new place to hide from sharks, shallow waters near reefs. As time goes on this puts evolutionary pressure on the fish to shrink so as to better hide in the reef, those \"neither here nor there\" fish may have gotten some benefit from being near the reef but the smaller fish got even more benefit and eventually outcompeted the middle species. Vice versa for the deep water fish vs this middle species. It was not as good in deep water so it was outcompeted there as well. This continues until evolution has separated them into two new species.</p>\n\n<p>edit:</p>\n\n<blockquote>\n <p>What factors determine whether some species \"stick\"?</p>\n</blockquote>\n\n<p>Evolution optimizes for the current environment, as long as that environment is stable and the species is a good fit for it then there is little pressure to change. If the environment changes then a species will adapt to it. Here environment is everything relevant to the species: predators, food availability, weather, everything that impacts their life.</p>\n"
},
{
"answer_id": 19765,
"pm_score": 4,
"text": "<p>Nothing happens to them. Organisms exist. They breed with other organisms who are genetically compatible. We humans might try to categorize them according to certain traits, but our labels are just labels, biology isn't governed by them.</p>\n\n<p>Over time, we might see that a population used to have one trait, and its descendants no longer have it, they look different. Nothing earth shattering happened, no bright line was crossed, there was just a change in allele frequencies.</p>\n\n<blockquote>\n <p>if a species evolved from another, it did so because it's somehow\n better, right?</p>\n</blockquote>\n\n<p>No. This is just plain wrong on your part.</p>\n\n<p>It's just different. Maybe it changed so that its traits better match the current environment, or maybe the change was random drift. You can't easily categorize one species as \"better\" than another.</p>\n"
},
{
"answer_id": 19770,
"pm_score": 5,
"text": "<p>Mathematician/computer programmer's answer here:</p>\n\n<p>There <em>is</em> a continuum of different animals — in fact it's pretty fair to say that every animal occupies a different place on this continuum. They're just not <em>uniformly distributed</em> over the continuum; they're clustered around forms that are most likely to survive and reproduce, and the lowest-energy paths between them.</p>\n\n<p>This is because evolution is basically a <a href=\"http://en.wikipedia.org/wiki/Stochastic_optimization\">stochastic optimization</a> algorithm, one that finds the \"best\" set of parameters for maximizing some function by randomly perturbing an initial set of input values. In fact, some of the best optimization algorithms today are based on ideas drawn directly from evolution and called \"evolutionary algorithms\".</p>\n\n<p>In mathematics, given enough time, these algorithms will all converge on one optimum solution and nothing else. Why isn't it like that in nature? Because in mathematics, the \"fitness function\" that we're optimizing for stays the same for a given problem for as long as the algorithm runs. It represents the specific problem we're trying to solve. In nature, there's no outside force imposing a fitness function; an organism's survival depends on millions of factors in its environment which change over time, many of which depend on the survival and properties of the <em>other</em> organisms in its environment (competition, symbiosis, predator/prey relationships, etc.) This is a chaotic system so complex that it could easily go for billions of years without reaching a steady state, and even if it did, external changes (like the odd asteroid impact, to use an extreme example) would still come around to shake things up.</p>\n\n<p>Another reason for the clustering is because a lot of the \"intermediate states\" in the genetic space have a fitness of zero — these are the states between species that can't interbreed, or that have sterile offspring. The categorization of \"species\" is based on this, and although it's not exact, it's still generally true that the more different two creatures are, the less likely they can have viable offspring. This makes evolution more likely to explore the spaces near already-successful organisms, and less likely to produce radical new things by hybridization.</p>\n"
},
{
"answer_id": 23568,
"pm_score": 2,
"text": "<p>Organisms on Earth did not evolve in a homogenous environment. A critical part of speciation (when you go from a single species into two or more) is a reproductive barrier.</p>\n\n<p>This can be a literal, physical barrier - mountain range appears between two populations, valley in the middle of habitat floods and isolates the two halves of the population, a small group is thrown by some catastrophe on a remote island and cannot escape, etc.</p>\n\n<p>It can also be a genetic barrier: Imagine a bird species where males compete for mates with their bright blue crests, and rare mutations occasionally lead to red-crested males which cannot mate at all. If some female birds happen to mate with undesirable red-crested males for a few generations, two parallel sub-populations may develop: Birds which prefer red crests and bird which prefer blue crests. These populations may be very unlikely to interbreed.</p>\n\n<p>There may be more complicated ways of erecting a barrier. For instance, a population of flowering plants that could previously interbreed arbitrarily may find that the ecosystem has experienced some crisis, and now the pollinating insects have become fastidious and only visit certain flowers and not others. Another example: While humans are currently a single species, because of culture (eg. language) certain human subpopulations (such as European nations) are much more likely to breed within themselves than between themselves.</p>\n\n<p>Regardless of how the barrier comes to be, once a barrier can separate a species into sub-populations, the machinery of speciation is set in motion. All species evolve over time in different ways, especially if their environment does not have a very long history of unusual stability. As populations evolve, they try to stay somewhat coherent - the changes tend to be such that they still permit everyone in the population to mate with each other; otherwise they would impose a fitness cost.</p>\n\n<p>However, if two subpopulations are not in contact, there is nothing enforcing compatibility between them. Therefore, as evolution does its work, these are free to wildly diverge from each other. Recall the example of the bird species in which males with blue crests enjoy reproductive success. The color itself is not particularly important, but it is important that the males all have the same color crest and the females prefer the same color. So as these birds evolve, the crest color can slowly drift in hue.</p>\n\n<p>Now let's say you took these birds, and set a few of them free in one continent, and another group free on another continent. Again, over time, the crest color will shift. However, there is nothing stopping from the color in continent A from shifting to red while the color in continent B shifts to green. There is, after all, no advantage to being compatible with a population you are not in contact with.</p>\n\n<p>The example above is largely behavioral, but non-behavioral examples are also possible. A very fundamental process is fertilization: Eggs have an ECM made up of proteins unique to that species, while sperm have enzymes to digest the coat of their own species. Because of this, cross-species fertilization is very difficult. Again, once you erect some kind of barrier between two populations, the systems of coat proteins and enzymes in the gametes of either population may evolve in divergent ways - they evolve in small steps, so that the interaction partner protein can always keep up, but compatibility with the isolated population is not selected for, and if the isolated groups are reunited after a very long time their gametes may end up becoming unable to fertilize each other.</p>\n"
},
{
"answer_id": 80982,
"pm_score": 0,
"text": "<p>I shall introduce you to the phenomena called <a href=\"https://en.wikipedia.org/wiki/Ring_species\" rel=\"nofollow noreferrer\">ring species</a></p>\n\n<p>Examples include gulls, Ensatina salamanders, house mouse, etc</p>\n\n<p>A ring species is a series of adjacent populations that can interbreed with each other. \nSay population A, B, C, D, E. </p>\n\n<pre><code>A can interbreed with B\nB can interbreed with A and C\nC can interbreed with B an D\nD can interbreed with E\n</code></pre>\n\n<p>All very good. Sounds like a regular species. But here is the weird part. The populations furthest from each other cannot interbreed. ie Population A cannot interbreed with Population E.</p>\n\n<p>A and E are by definition different species.\nAnd yet, population A and E are linked, genes can flow between A and E via adjacent populations.</p>\n\n<p>What is most likely happening is that there is a gradual change in gene variation between populations, so that there is gradually increasing barrier between successful hybridization. This barrier increases until the terminal ends of the ring cannot hybridize.</p>\n\n<p>Furthermore, if any intermediate population within the ring were to go extinct, and break the ring, the two ends of the ring would become two separate species.</p>\n\n<p>A ring species is a snapshot of one species that is one local extinction event away from becoming two species.</p>\n"
}
] |
19,873 |
<p>Would I be able to genetically modify a plant at home? What equipment will be necessary? I think it might be a fun change from the 'norm' of regular hybridisation, to try some inter-family gene insertion, instead of staying within a genus. Are some plants easier to modify than others?</p>
|
[
{
"answer_id": 19875,
"pm_score": 4,
"text": "<p>Well, that depends on your home. ;) I think it is not an easy process.</p>\n\n<p>There are <strong>two main methods</strong> that are used to genetically modify plants:</p>\n\n<p><strong>Using the bacterium</strong>, Agrobacterium tumifaciens, as a vector for the DNA. Agrobacterium has the ability to infect plants and insert DNA into a plant's genome. It causes crown gall tumours in natural infections. This method has mainly been used to modify broad leaved plants, such as sugar beet and oilseed rape, but is now also being applied to monocot species, such as maize and rice</p>\n\n<p><strong>Particle bombardment</strong> or biolistics where the DNA to be inserted is coated on minute gold particles and fired into plants cells. This approach is used for monocot plants such as maize and rice</p>\n\n<p>Here I found simple step by step article, but lil bit old. may be there are new methods for this process.\n<a href=\"http://www.popsci.com/science/article/2011-01/life-cycle-genetically-modified-seed\">How To Genetically Modify a Seed, Step By Step</a></p>\n"
}
] |
[
{
"answer_id": 19874,
"pm_score": 2,
"text": "<p>Yes, It is.</p>\n\n<p>An Indian Company IndieBB can help you get one.\n<a href=\"https://www.indiegogo.com/projects/indiebb-your-first-gmo\" rel=\"nofollow\">IndieBB: a DNA system designed to help you and your friends to explore genetic engineering and synthetic biology by making fluorescent bacteria at home.</a></p>\n"
},
{
"answer_id": 21430,
"pm_score": 2,
"text": "<p>Yes it is. The easiest plant to transform would be Arabidopsis, which can be transformed by agrobacterium using the floral dip method. The process would be as follows:\n1. Design a gene sequence you wish to insert into the plant\n2. Synthesize (or otherwise acquire the DNA)\n3. Insert the DNA into your agrobacterium, at home you would use a cold snap transformation process described here: <a href=\"https://www.youtube.com/watch?v=PvkfIECvyqs\" rel=\"nofollow\">https://www.youtube.com/watch?v=PvkfIECvyqs</a> This can be done at home using a dry ice bath.\n4. Then use the floral dip method to insert the dna into the plant. This involves growing a plant to just the right age when it is flowering and dipping the Arabidopsis flowers into a solution of the agrobacterium.\n5. Then grow the flowers to seed and grow the seeds on a suitable select able marker (which you designed into your DNA plasmid).</p>\n\n<p>The specific experimental conditions needed to do all this are too long for this answer, but you can look them up online as all the procedures are standard.</p>\n\n<p>Plants which result from this process would not be legal to release into the wild due to USDA regulations.</p>\n\n<p>Engineering other plants, depending on the species, can be more complex but could possibly also done at home. There are even designs online for an open source gene gun if you didn't want to use agrobacterium.</p>\n"
},
{
"answer_id": 21499,
"pm_score": 2,
"text": "<p>genetic modification can be done with mutations. A mutation is a permanent change in the sequence of DNA. In order to obtain an observable effect, mutations must occur in gene exons, or regulatory elements. Changes in the non-coding regions of DNA (introns and junk DNA) generally do not affect function.</p>\n\n<p>Mutations can be caused by:</p>\n\n<ul>\n<li>external (exogenous) factors, such as chemicals and radiation </li>\n</ul>\n\n<p>or</p>\n\n<ul>\n<li>endogenous (native) factors</li>\n</ul>\n\n<p>Mutations can be advantageous and lead to an evolutionary advantage of a certain genotype..this will be a solution for your plant modification..</p>\n\n<p>A mutagen is a physical or chemical agent that changes the genetic material, usually DNA, of an organism and thus increases the frequency of mutations above the natural background level.</p>\n\n<p>chemical mutagens:</p>\n\n<ul>\n<li>Bromine </li>\n<li>Sodium azide</li>\n<li>Psoralen</li>\n<li>Benzene</li>\n</ul>\n\n<p>long term treatment plant with mutagens caused mutations some might be advantage\nthen select advantage ..\n As many mutations cause cancer, mutagens are therefore also likely to be carcinogens!</p>\n"
},
{
"answer_id": 23935,
"pm_score": 1,
"text": "<p>Not to forget that simple cross breeding your plants the Mendelian way also modifies their genetic make up, as @souvik bhattacharya indicates in his comment. No equipment necessary, no chemicals, no ethical issues.</p>\n"
}
] |
20,437 |
<p>recently i got into a debate with <a href="https://hinduism.stackexchange.com/posts/comments/4386?noredirect=1">this</a> question on hinduism.se ,</p>
<p>as the link given above shows, are sperms considered as living or non-living </p>
<p>as far as my knowledge is concerned, sperms undergo locomotion, senescence, more over the best thing to say they are living is they contain genome, i.e. haploid sets of chromosomes</p>
<p>so in short are sperms living or non-living</p>
|
[
{
"answer_id": 20442,
"pm_score": 3,
"text": "<p>The question of what is living is nothing but a matter of definition. We can only tell you what are the standard definitions of what is a living thing but no absolute truth exist behind these definitions. Therefore, I am afraid that all discussions here will bring anything new to your ethic or religion related discussion.</p>\n\n<p>I want to argue that the @user137's answer is very misleading for two reasons. First, he based his discussion exclusively on the \"reproduction ability\" definition of life. Second because his definition of reproduction might be misleading as well.</p>\n\n<p>Reproduction is not only cell division obviously. Following this same definition one would not consider a human to be a living things but only to be a collection of living (and non-living) things. It is important to understand that a spermatozoid is just one phase of a life-cycle. This phase yield to the next phase. That's it. It seems weird to say that a kid is not alive just because he cannot reproduce. It seems weird to say that a grandmother is not alive because it cannot reproduce. You can say however that a kid is a living thing that cannot reproduce and at another moment of its life cycle it will be able to reproduce (assuming it will survive to this age). One should not think of spermatozoids as something totally detached from the human phase as we know it. These things just form a cycle and it seems to me miseleading to say that a part of this cycle is not alive. Saying such thing would yield someone to think that two living things create non-living things that by fusion will become alive. That seems weird. But again, it is nothing but a matter of definition. I cannot say that user137 is wrong, I cannot only say that his definition seem neither useful, intuitive nor common among biologists.</p>\n\n<p>You may want to have a look to life-cycle and to understand what are the haplontic and diplontic phases with a bunch of wikipedia readings.</p>\n\n<p>Other concepts such as the ability to synthesize its own components, having a boundary between interior and exterior and ability to response to environmental stimulis are often used in order to define what is a living thing and what is not.</p>\n"
}
] |
[
{
"answer_id": 20438,
"pm_score": -1,
"text": "<p>One requirement most biologists have to consider something living is the ability to reproduce. This is why viruses are generally not considered alive. They contain proteins and DNA or RNA, but require infecting a host cell and hijacking its replication machinery to reproduce itself.</p>\n\n<p>Fully differentiated sperm cells cannot divide and therefore can't reproduce. Their only role is delivering DNA cargo to an oocyte and creating an embryo. An individual sperm cell is just as alive as an individual neuron or muscle cell. These require nutrients and energy, carry out metabolism, perform functions, contain DNA, but a plate of neurons won't grow into a human.</p>\n"
},
{
"answer_id": 20447,
"pm_score": 2,
"text": "<p>Sperm are unquestionably alive, according to all or most sensible definitions of life (They move around, they have goals, they eat things, they die). They are not, however, a human or animal life. </p>\n\n<p>Vineet Menon has a shaky grasp of species definitions, and I'd like to correct some misunderstandings. Chromosome number is not that useful in distinguishing different species. There are a large number of genetic disorders that alter your chromosomal count without making you not a human being. (<a href=\"http://en.wikipedia.org/wiki/Klinefelter_syndrome\" rel=\"nofollow\">Klinefelter</a>, <a href=\"http://en.wikipedia.org/wiki/Turner_syndrome\" rel=\"nofollow\">Turner</a>, <a href=\"http://en.wikipedia.org/wiki/Edwards_syndrome\" rel=\"nofollow\">Edward</a>, <a href=\"http://en.wikipedia.org/wiki/Down_syndrome\" rel=\"nofollow\">Down</a>, etc.) It's also worth noting that all mosses are haploid except during the sporophyte stage of their life cycle, when they're diploid. I doubt Vineet Menon intends to categorically declare mosses 'not alive'.</p>\n\n<p>Your blood is alive, and your feces is also thriving with bacteria. Some yogurt is alive, most cheese is alive. All fermented beverages are alive, or were once. Bread dough is alive. The argument you linked to is debating whether or not they are alive enough to qualify as a macroscopic living thing for ethical purposes, which is an entirely different question. A chicken definitely qualifies, single-celled algae like spirulina, mushrooms, and yeast do not. Eggs, fertilized or not, seem to be somewhere in the middle. It is a continuous spectrum with people and cats and chickens and things at one end, and viruses and tuberculosis and dirt at the other. Eggs and sperm and mushrooms I would put somewhere in the middle.</p>\n\n<p>So whether the answer to the question 'Are gametes alive?' is unquestionably yes;\nThe answer to the question of whether or not that makes them 'a life' is up to you.</p>\n"
},
{
"answer_id": 20455,
"pm_score": 2,
"text": "<p>Sperm, in my opinion can't truly be considered \"alive\"...but they are living. Bear with me before you skip my answer. </p>\n\n<p>A cell can be considered a \"living\" thing since It has RNA/DNA, it imbibes nutrition, it grows and is destroyed, we cannot say however that it is alive. It has a specific set of instructions coded into the RNA which it follows till its death (which is also protein,and hence RNA, mediated). Alive is a term reserved for organisms and not single haploid somatic cells. On the other hand...sperms have spiral mitochondria hence they contain RNA.\nIn short..yes..they can be considered living</p>\n"
},
{
"answer_id": 20460,
"pm_score": 2,
"text": "<p>Damn.. this is getting into a huge debate.</p>\n\n<p>There are different levels of life. What we mean by living when we say living is generally an <strong>Organism</strong>.</p>\n\n<p>This is highly debatable. If you say viruses are nonliving because they need a host then almost every hetertroph is nonliving because they need the support of autotrophs. </p>\n\n<p>An organ is living as long as it remains inside the body; similarly a cell in a multicellular organism can be considered alive only if it remains associated with the multicellular whole.</p>\n\n<p>So is a single man alive?? Well he can eat, carry out metabolism, form a habitat but he cannot reproduce. Man as an organism is alive as he can sustain cell division and metabolism within himself but in that restricted zone human population is dying. He is living because he has the <strong>potential</strong> to reproduce. It is same as a lone enzyme- it can carry out its metabolism but will one day degrade unless it is re-formed. </p>\n\n<p>Sperm on the other hand is just a vehicle- it doesn't have the potential to sustain itself; its sole aim is to deliver the potential to the egg so that life can be created.</p>\n\n<p>To conclude- the question of what is \"life\" is purely philosophical. A more scientific question would be - \"What is a stable, self-sustaining and dynamic biological system\"</p>\n"
},
{
"answer_id": 20531,
"pm_score": 2,
"text": "<p>Your best chance of actually reaching an answer <strong>for yourself</strong> (*) to this is by parallel.</p>\n\n<p>Do you consider independetly-living single-celled organisms alive? This includes bacteria, amoeba, bacteria, some parasites such as plasmodium (the malaria germ), and more.</p>\n\n<p>Sperms are not quite independently-living single-celled organisms. They have many things in common with the ones mentioned above: they move, metabolise, communicate and sense, and most importantly they can cease to do all those things, i.e. they do what we commonly call, \"die\".</p>\n\n<p>The main difference is, they don't reproduce themselves, they are the reproduction vessel for a larger organism.</p>\n\n<p>There is absolutely no objective way to decide whether that difference is sufficient to decide that all those single-celled creatures are alive and sperms aren't, it's a question of definition. You might even decide that you don't consider bacteria or anything that exists commonly as single cells \"alive\", and thus this whole approach is pointless. In any case, it's not a biological question and thus should be discussed somewhere else.</p>\n\n<p>(*) For yourself because there is no false or correct answer as long as nobody can get more than two people to agree on a definition of life.</p>\n"
}
] |
20,657 |
<p>Some people say that it's awful that humans eat animals. They feel that it's barbaric, because you're killing life and then on top of that, you're eating it, and that you should eat vegetation instead.</p>
<p>But isn't vegetation life too? Personally, I see no difference between animals and veg as all life has cells, dna etc</p>
<p>So my question is, is it possible for humans to live healthy long lives without eating any type of life, i.e no animals, no plants, no cells (dead or alive) etc? If it is possible, how would it be done?</p>
|
[
{
"answer_id": 20664,
"pm_score": 7,
"text": "<p>The answer to your question is <strong>yes</strong> it is certainly possible. </p>\n\n<p>At one time it was thought that there was something special about \"organic\" chemicals which meant that they could not be artificially synthesised out of fundamental elements. In 1828 Frederick Wöhler synthesised urea (CO(NH<sub>2</sub>)<sub>2</sub>) which is often taken as the first demonstration that the organic v inorganic distinction was not a sound one (for more on this see the <a href=\"https://en.wikipedia.org/wiki/W%C3%B6hler_synthesis\">Wikipedia article on Wöhler synthesis</a>.</p>\n\n<p>As far as we know all essential human nutrients can be synthesised from inorganic ingredients, even complex molecules such as Vitamin B<sub>12</sub>.</p>\n\n<p>Other contributors have pointed out that organic pathways for synthesising our food have evolved over long periods to be very efficient - at least in the conditions prevailing on Earth. You haven't ruled out copying biochemical pathways using chemicals that are entirely of inorganic origin. Anyone trying to do this seriously could create glucose (for example) by artificially creating enzymes (perhaps via artificial DNA) to do the job. The thing is that we already have self-replicating and repairing machines to do that already (plants).</p>\n\n<p>There might be circumstances when we needed to use artificial synthesis. I can think of two science-fiction stories that deal with this question, the first of which goes into some detail:</p>\n\n<ul>\n<li><a href=\"https://en.wikipedia.org/wiki/The_Moon_Is_Hell!\">The Moon is Hell</a> by John W. Campbell, in which astronauts are stranded on the moon and forced to make food from what they find there.</li>\n<li><a href=\"https://en.wikipedia.org/wiki/Technical_Error\">Technical Error</a> by Arthur C. Clarke, in which a man is accidentally rotated through the fourth dimension. His employers contemplate the difficulty caused by the \"handedness\" of many biological molecules meaning they would have to artificially synthesise many of his foods.</li>\n</ul>\n\n<p>It may be that a future expedition to Mars (say) might have to think about these things.</p>\n\n<p>A little searching fails to come up with standard inorganic syntheses of glucose and similar substances. The reason for this is almost certainly because it is so easy to use organic inputs. Glucose is easily made by the hydrolysis of starch. Starch is very common and cheap. Even l-glucose is usually made out of organically derived precursors (or sometimes even using d-glucose).</p>\n\n<p><strong>UPDATE: sources etc</strong>\nOne problematic question is: where do you get your input for making nutrients? As others have pointed out, exactly where to draw the line is difficult. </p>\n\n<p>This problem starts in defining what is alive in the first place. Do you count viruses (which can go down to a few thousand base pairs of RNA) or satellite viruses (STobRV has only 359 base pairs) or prions? In a sense these are \"just\" very large molecules. But then really simple bacteria are not many orders of magnitude more complex. As an aside most systems of ethics that do not permit eating meat do not make an alive/non-alive distinction, choosing some other aspect such as sentience, though Jainism comes close to doing so.</p>\n\n<p>The second problem is, if we reject living things as sources of food, how far removed from those living things are we allowed to get? You say no cells in any state including \"dead\". That would exclude (say) fruit even though most fruits are expressly created by plants in order to be eaten (and in some cases must be eaten) - something that vegans, jains, fruitarians and others would be happy with eating. If we could use dead material things would be much easier.</p>\n\n<p>But would you also include hydrocarbons (coal, oil, gas) which were once living organisms? If you do, then you are in difficulty because terrestrial carbon is recycled through the biosphere. All CO2 was (to a close approximation) once a part of a living thing. If you take that position then of course you are going to have to go off-planet to find your source chemicals and your problem becomes very much harder.</p>\n\n<p>I was assuming that you were restricting yourself to consuming cells that retain some of their cell structure but had not completely degraded. If that is where you draw the line then there are ample sources of raw materials on earth.</p>\n\n<p>Genetic modification is much more science fiction though not entirely impossible. Some nutrients could be made by humans without much difficulty. Our inability to manufacture vitamin C is down to one missing enzyme (L-gulono-gamma-lactone oxidase) which is present in most vertebrates (I think of mammals only guinea pigs, humans and some bats are unable to synthesise it). You could certainly imagine some very careful genetic modification changing humans so they no longer need to consume vitamin C.</p>\n\n<p>But photosynthesis would be much harder. Chloroplasts (which do the job in most plants) are really a very primitive form of life living in plant cells which may independently reproduce (and for that reason might be excluded by you - they aren't \"cells\" but they have membranes). They could easily end up in conflict with our mitochondria (since intracellular conflict between organelles is possible) and you would need to do enormous amounts of work to make human cells co-operate with them properly.</p>\n\n<p>More in keeping with your theme would be adding photosynthetic systems directly to human cells along with a suite of enzymes to manufacture all the things we cannot. That is of course in principle scientifically possible (since plants do it) but much harder than it looks. Living systems are very complicated and small changes can have unexpected consequences. Even very minor genetic modifications are problematic. The human autotroph is likely to be some way off.</p>\n"
}
] |
[
{
"answer_id": 20659,
"pm_score": 5,
"text": "<p>Living organisms can be divided into hetrotrophs and autotrophs. Autotrophs like plants and algae are able to produce complex <em>organic</em> compounds from relatively simple <em>inorganic</em> components. They are satisfied with sunlight, water and other abiotic stuff and do not need to consume \"life\".</p>\n\n<p>We -- along with all other animals -- are not autotrophs, but heterotrophs. This means that we cannot produce organic compounds by ourselves but need to 'reuse' the ones that are produced by autotrophic organisms. That's why no human will ever be able to live without consuming other life.</p>\n"
},
{
"answer_id": 20660,
"pm_score": 2,
"text": "<p>It may be feasible to live without consuming anything that was alive, but it would be incredible difficult.</p>\n\n<p>For example, all humans need to consume glucose to survive. Glucose is the only food source used by cells in the brain. Plants are the easiest source of food source for glucose. If we can't get glucose from plants, then we would need to synthesize it without the aid of enzymes or any sort of organism. A quick google search does not yield any hits for how this synthesis could be performed. Probably because it is so easy to get a plant to make the sugars for us.</p>\n\n<p>Now think about all the amino acids, vitamins, fats, and minerals that we would also need to synthesize or extract without any organism intervention.</p>\n\n<p>You have gone from the good intention of not harming another organism to the creation of a whole chemical industry dedicated to the production of nutrients for people.</p>\n\n<p>Think about this as well. When you poop, a lot of the poop is actually dead bacteria that was living in your gut. </p>\n"
},
{
"answer_id": 20661,
"pm_score": 3,
"text": "<p>Depends on how you define \"life\"? Is unfertilized chicken eggs alive?</p>\n\n<p>What about cow milk? Well there are bacteria in it. What if you get rid of that bacteria? Then some people would not be able to utilize lactose...</p>\n\n<p>Also as <code>Bez</code> mentioned rice grains are quiescent, meaning they are in a dormant state and not really \"alive\" but again depends on how you define \"life\". Even top biologist have trouble defining \"life\" and there exist many competing definitions of \"life\". All of them have their advantages and disadvantages, but there is no universal definition of life on which all biologists would agree.</p>\n\n<p>If you consider everything above as \"life\" then it is not really possible for humans to survive without consuming other life.</p>\n\n<p>If only we could sustain chloroplasts in our epidermis layer we would be able to synthesize sugars for ourselves. But then we would become little green men...</p>\n\n<p>So it is much better to respect your meat. Whenever you eat meat just be conscious that something had to die to produce that meat. Be grateful for that lost life and realize that part of it will live in you.</p>\n"
},
{
"answer_id": 20670,
"pm_score": 2,
"text": "<p>It is entirely possible to live without consuming life using only current technology. In fact, there is a company called <a href=\"http://www.soylent.me/\" rel=\"nofollow\">Soylent</a> which has developed a food substituent designed to replace all eating, entirely. The philosophy of that company is that – food is just a collection of chemicals for the body to process, and that as long as the body gets all of the necessary chemicals, it will survive fine. That is exactly what soylent aims to do – the powdered mix they produced has all the chemicals necessary for human life. </p>\n"
},
{
"answer_id": 20671,
"pm_score": 3,
"text": "<p>Question: Is it possible for humans to live healthy long lives without eating any type of life, i.e no animals, no plants?</p>\n\n<p>First, according to a <a href=\"http://www.biology-online.org/dictionary/Living_thing\" rel=\"nofollow\">definition of a living organism</a>(biology-online), milk is not live, because it does not have an ability to reproduce itself, among other...</p>\n\n<p>My claim: If you consider milk and honey non-live (no DNA), then, yes, humans can survive for some time by consuming only these, and water. An example are infants, who can live exclusively on human breast milk and water for more than 1 year.</p>\n\n<p>This is <a href=\"http://nutritiondata.self.com/facts/dairy-and-egg-products/95/2\" rel=\"nofollow\">human milk composition</a> (Nutritiondata), from which you can see it contains all <a href=\"http://www.nutrientsreview.com/glossary/essential-nutrients\" rel=\"nofollow\">essential nutrients</a> (Nutrientsreview) (essential amino acids, fatty acids, vitamins and probably all essential minerals - not all essential minerals are listed in Nutritiondata milk composition, though).</p>\n\n<p>But to actually prove that humans can or cannot \"live healthy long lives\" by consuming only milk and honey, one would need to do a human trial...and I'm not aware of any.</p>\n"
},
{
"answer_id": 20672,
"pm_score": 4,
"text": "<p>Your question is phrased somewhat ambiguously as to whether you're asking about the theoretical possibility, the feasibility, or the practical ability in everyday life.</p>\n\n<p><strong>1) Theoretically, yes.</strong> It is chemically possible to produce all substances that humans need to survive without the use of living organisms in the process. In the end, biological systems use chemical processes, so at the very least it would be possible to isolate the biological (enzymatic) machinery and use it without the live organism around it. The latter is within current biotechnological capabilities.</p>\n\n<p><strong>2) Feasibly, no.</strong> Going through the hassle of making all those substances in that way would probably be less efficient than simply using the biological (live) systems that already exist and are very efficient at it - in particular, plants.</p>\n\n<p><strong>3) Practically, no.</strong> Using only currently commercially available products (i.e. things you could buy right now), you will probably not be able to source a full human diet without relying on some live organism at some point in its production exactly because of number (2) above.</p>\n"
},
{
"answer_id": 20684,
"pm_score": 4,
"text": "<p>Even on a purely synthetic diet, your body would still use living cells as an energy source. Our bodies contain more bacterial cells than human, mostly contained in our gut. These microbes process any nutrients we ingest and when they die, we absorb their cellular components as nutrition. </p>\n\n<p>The lining of the gut is the most rapidly dividing population of cells in the body. Unlike skin cells, when these die, our intestines recycle much of this as nutrition. Throughout the rest of our bodies, when a cell dies, its components are recycled: red and white blood cells, mucosal membranes, invading microbes, etc. </p>\n\n<p>When you kiss, engage in intercourse, there's also an exchange of living cells which die in the process.</p>\n\n<p>Abstaining from organic food, human contact will not stop the fundamental processes of autophagy, apoptosis, digestion, cell turnover of both our own and microbial cells. </p>\n"
},
{
"answer_id": 20688,
"pm_score": 2,
"text": "<p>Well, technically if you are eating something from a plant or animal without killing that plant or animal, then technically you would not be \"consuming life\" as nothing as been killed. Fruits, for example, can be removed from the tree without harming it and in fact are meant to be removed as that is how the tree reproduces. Ditto with berries, melons, squash, cucumbers, peppers, beans, seeds, nuts, etc.</p>\n\n<p>As for animal products I think only milk and honey would qualify as technically an egg is a future animal. </p>\n\n<p>So yes, I would say that it is completely possible to live a healthy life without once killing another living thing.</p>\n"
},
{
"answer_id": 20719,
"pm_score": 3,
"text": "<p>No.</p>\n\n<p>It is possible but extraordinarily impractical to <em>nourish yourself</em> without killing animals, plants or even bacteria, as many have explained in detail.</p>\n\n<p>However, your immune system constantly kills pathogens that infect your body. What's worse, the macrophages literally catch and eat these bacteria alive, so you are very much \"consuming\" them.</p>\n\n<p>You could live in a bubble, but even then there are bacteria in your gut. In your gut, they are not attacked by your immune system, but they can sometimes get through the gut lining into the body, where they <em>are</em> attacked. They could also escape from you anus into the environment, and then end up elsewhere in your body.</p>\n\n<p>Even if you had a magic force field keeping the gut flora inside the space of your intestinal lumen, they could still mutate and <em>become</em> immunogenic, then get consumed by your macrophages. Anyhow, collectively, <a href=\"http://discovermagazine.com/galleries/zen-photo/m/microbiome\">your gut flora has more cells than your body</a>, so is it really fair to say \"you\" did not consume any life when this symbiotic bacterial mass living inside you (more like <em>you</em> are the parasite living <em>outside it</em>) consumes some of its own cells?</p>\n\n<p>But let's say you get rid of your gut flora, too. It's a hell of a life, and you wouldn't wish it on your enemy, but it solves that problem. Now only human cells are present inside your bubble. What happens when eventually your cells mutate and you get cancer? There are natural killer cells that will try to consume the cancer. So you have still consumed life.</p>\n\n<p>Let's say you made yourself immune to cancer. That's impossible, but let's say you made your DNA polymerase so high fidelity that it takes millions of years for even a single mutation to occur (this is also almost impossible). Your body still has to kill cells through apoptosis as part of maintaining its own function. Again, to conserve resources, these cells are literally <em>swallowed</em>. It's debatable whether an apoptotic cell is alive, but it is <em>made</em> to die by influence of other cells, so this is very analogous to killing a chicken and eating it. In principle.</p>\n\n<p>The answer is no, but your question becomes meaningless if you define \"life\" scientifically. It is only possible to live without consuming life if \"life\" means <em>only plantae, metazoa and fungi</em>. But that is not what it means, because at least <a href=\"https://en.wikipedia.org/wiki/Ahimsa_in_Jainism#Important_constituents\">some Eastern religions</a> <em>do</em> consider eating microbes to be \"consuming life\".</p>\n\n<hr>\n\n<h2>Lame, boring answer</h2>\n\n<p>The Universe has a finite reserve of (dis)entropy. When that runs out, no more life can exist, because all life must increase entropy. Even on Earth, by simply being alive you are taking up space that could be used by other organisms. To be alive you require some form of energy; even if this energy is solar, you would still be using up energy that could have been used by a plant.</p>\n\n<p>By simply existing, you are irreversibly destroying vital resources necessary for other life. Thanks to you, at least some life somewhere will be left without resources and starve. Therefore you cannot exist without harming life.</p>\n"
},
{
"answer_id": 20803,
"pm_score": 2,
"text": "<p>Honey is produced from nectar that does not contain any living cells and carefull beekeeper should be able to take at least some from the hive without killing any bees. However bees themselves will also consume pollen that is alive.</p>\n\n<p>It also may be possible to feed on fruits; while cells there are still alive, they are about to die soon without any prospects of future surviving. If you really do not want to harm the plant in any way, take the seed from the fruit and plant it somewhere. Fruits are for seed propagation only and the plant should really not have any pretensions to you afterwards.</p>\n\n<p>Dead leaves in the autumn may contain the needed materials; unfortunately they are not edible directly and would need some pre-processing technology.</p>\n"
}
] |
20,709 |
<p>A vast majority of humans get at least some grey hair as they age. As far as I know this applies to both genders and all races. Presumably this means that at least some grey haired humans have noticeable reproductive advantage, or maybe they had it in the recent past.</p>
<p>Theoretically, because this feature is so prevalent, there must be a strong evolutionary pressure to keep it. Am I right? If so, what is it?</p>
|
[
{
"answer_id": 20715,
"pm_score": 4,
"text": "<blockquote>\n <p>Presumably this means that at least some grey haired humans have\n noticeable reproductive advantage, or maybe they had it in the recent\n past.</p>\n</blockquote>\n\n<p>No it doesn't. Natural selection is not that strong, it doesn't optimize every single possible physical trait towards maximum reproducing.</p>\n\n<p>And as others have mentioned, having lots of grey hair usually happens after reproduction is over. Historically, lots of women did a lot of reproducing before they had any grey hair.</p>\n"
}
] |
[
{
"answer_id": 20721,
"pm_score": 2,
"text": "<p>I do not think there is a reproductive advantage in gray hair - it's the other way around: </p>\n\n<p>Normal colored hair has a reproductive advantage.\nBut it also has a cost in terms of substances needed to build it.</p>\n\n<p>I make the assumption here that grey hair - which is often also more sparse - has a lower cost in terms of material. </p>\n\n<p>I think we are investing the cost for the part of the live that is exposed to direct evolutionary reproductive pressure.</p>\n\n<p>Later, we do not longer invest the cost.</p>\n\n<p>That makes sense if we assume that hair becoming gray is a process of degradation. </p>\n\n<p>It is not supported by an investment, but by the absence of an investment, following from absence of evolutionary pressure.</p>\n"
},
{
"answer_id": 22017,
"pm_score": 2,
"text": "<p>Grey hair is one of many age related traits. Other traits showing a positive correlation with age include Parkinson's, cancer, and Alzheimer's. There are two key theories as to why age-related disease & decline occurs. But the key message is just because something evolves, it doesn't mean it's advantageous.</p>\n\n<p>First of all is mutation accumulation (MA) theory. This theory basically suggests that as we age there is less likelihood that selection can remove the alleles that cause genetically determined aging. If we consider something like cancer, which is clearly deleterious it becomes clearer, though grey hair may be deleterious (reduces fitness) it is at least less obvious. If a cancer has early onset, affects people aged 10, then it is highly unlikely to spread through a population because those carrying the allele are unlikely to reproduce. If a cancer has late onset, causing cancer at 60 years old, then there is a much lesser chance it will affect reproductive success - most 60 year olds don't have more children in the future. In the case of MA the effect of selection is weak if a trait reduces survival post-reproduction. The same could be true of grey hair, even if it is costly it's arrival late in life is not that surprising.</p>\n\n<p>The other theory is antagonistic pleiotropy (AP) which suggests that genes which improve fitness might reduce survival. For example, the genes that cause cancer at age 60 might also make you better at attracting mates, fertilising, and raising offspring. In this case it would be beneficial to carry the cancer gene (from an evolutionary perspective). I think there is some evidence (but can't find it right now) that grey hair is associated with higher fitness, in that case it could be that grey hair has evolved directly because of sexual selection (people might prefer silver haired partners) or because of AP - grey haired people are better at other fitness related things because of pleiotropy.</p>\n\n<p>So to answer your question: direct selection is not necessarily the reason that grey hair has evolved, it could be because of mutation accumulation or pleiotropic gains associated with the genes affecting grey hair.</p>\n\n<p>You can read more about <a href=\"https://biology.stackexchange.com/questions/17077/why-does-evolution-not-make-our-life-longer/17091#17091\">these theories of aging in this answer and for references.</a></p>\n"
},
{
"answer_id": 74047,
"pm_score": -1,
"text": "<p>My theroy is that gray hair allowed a predator to pick out the weak one in the group and focus on it as a possible food source allowing the younger ones to escape and survive. </p>\n\n<p>Gray hair is also a signal to a potential mate that you might not be providing young healthy genes. </p>\n\n<p>Both of these could have allowed our species of human to succeed over others. </p>\n"
},
{
"answer_id": 78899,
"pm_score": 0,
"text": "<p>I think grey hair does have an evolutionary advantage related to Vit D. Vit D is crucial to life and severe deficiency may lead to death. The main source of this vitamin is the production in skin cells through exposure to UV light. </p>\n\n<p>As you might know, humans who live in colder climates with limited sun exposure lost the pigmentation in their skin. This is to allow more UV rays to reach the deeper layers of skin to produce Vit D. Humans living in sunny areas had the opposite need as their skin pigmentation is protective against skin cancer, and it still allows enough UV rays to produce Vit D in sunny areas. This is why people with pigmented skin living in cold climates are recommended to take Vit D oral supplements, and why people with less pigmentation in hot climates are more vulnerable to skin cancer.</p>\n\n<p>Grey hair allows more UV rays to reach the skin due to the lack of pigmentation in the hair. Humans in general need more Vit D as they age and start becoming vulnerable to osteoporosis and fractures. This explains why grey hair commonly starts at age 40-50 when the bones start to become increasingly weaker.</p>\n"
}
] |
20,912 |
<p>Throughout high school, I remember learning about Darwin's theory of evolution as if it were near-fact. But something always seemed wrong about the ideas presented.</p>
<ul>
<li>Survival of the fittest</li>
<li>Random mutation</li>
<li>Natural Selection</li>
</ul>
<p>All of these things seem to account for some margin of evolutionary progress, but I always remained skeptical that the extremely complex features of life could have formed from these methods alone, even after hundreds of millions of years.</p>
<p>Here's what I notice:</p>
<p>Any time a species has needed the development of a specific feature to survive, it has developed that feature, and that feature precisely.</p>
<hr>
<p>I'm going to use this example:</p>
<p><strong>Turtles on an island where shrubbery grew higher up developed longer necks, to reach the leaves.</strong></p>
<p>I imagine that turtle looking up at that food, and sub-consciously wishing to get to it, constantly straining, for its entire lifetime. </p>
<hr>
<p>It seems plausible to me that we (advanced life) could have a biological mechanism to "write" needed alterations into either our own DNA or our reproductive DNA over time, triggering the very specific evolutionary developments necessary to our survival without relying on random mutation.</p>
<p>My question:</p>
<p><strong>Is this possible?</strong> Does any similar mechanism exist that we know of? <em>If not, how can so many specific (advanced) evolutionary leaps be otherwise explained?</em><br></p>
|
[
{
"answer_id": 20913,
"pm_score": 6,
"text": "<p>This entire answer will be long, so read the short part first, then read the rest if you (or anyone else) is curious. Citations are included in the long section. I can include additional citations in the short section if needed.</p>\n\n<p><strong>Long Story Short</strong></p>\n\n<p>Your question touches on some common misconceptions about how the evolutionary process. Organisms don't \"want\" to evolve traits. Traits evolve through the biological processes of random mutation and natural selection. </p>\n\n<p>Organisms do not \"want\" to evolve traits. (Well, OK, I'd love to evolve an extra pair of hands but that is not possible.) Natural selection works by modifying existing traits. Your turtle can stare all she wants at food out of reach but she will not evolve a longer neck. Instead, natural variation exists among neck lengths of the turtles because of variation of the genes that determine features related to overall boxy size. Those individuals with longer necks may be able to get a bit more food, live a little longer, and reproduce a little more. They will pass along their genes to their offspring, so perhaps more of their offspring will also have longer necks. Over many generations, the turtles may have somewhat longer necks. </p>\n\n<p>A common misconception is that the traits of organisms are precisely adapted for a specific need. They are not, for a few reasons. First, natural selection occurs relative to the current environment. Adaptations that work well in one environment may not be so useful in another environment. Environments are rarely stable over evolutionary time so traits are subject to constant change. </p>\n\n<p>Next, as mentioned above, natural selection can only work on what traits are present. While an extra set of arms would be handy, I am a tetrapod. My four appendages, along with the appendages of all other tetrapods, trace back to our common ancestor. The appendages of all tetrapods are modifications of that ancestral trait. </p>\n\n<p>Finally, organisms haven't \"sampled\" the entire realm of possible mutations and combinations of mutations. In other words, a certain mutation or set of mutations might actually be able to adaptively improve a particular trait in the current environment but, if the mutations never occur, then the improvement can never happen.</p>\n\n<p>We only need to look at ourselves to realize how imperfectly adapted we are. We get bad backs and knees because our bodies weren't designed to walk upright. We evolved from quadrupedal organisms. This has happened so recently that changes in the structure of our knees and backs haven't yet evolved (and may never). Search the internet for the \"blind spot\" eye test. We have a mass of blood vessels in <em>front</em> of the retina of our eyes, which reduces our visual accuity. We often have to have teeth pulled from our jaws because the flattening of our face (relative to our australopithicine ancestors) has shorted our jaws. We don't have as much room for our teeth but we have not evolved a reduced number of teeth.</p>\n\n<p>As for human technology being able to make direct changes to our DNA to improve our adaptability, I would say no. While I do not have the ability to see into the future, the complexity of our genome, and more specifically how genes are regulated, suggests to me this would be a very daunting if not impossible task. See the long answer below for more on regulatory genes but the gist is that a small set of regulatory genes control most of the other genes (including other regulatory genes). The interactions are extremely complex and we have a detailed understanding of very few of these interactions. I speculate that affecting one such gene in a \"positive\" way is very likely to have many unintended negative consequences. </p>\n\n<p>Below are some simple math and other ideas to show you how mutations can lead to the many adaptive traits that you see among the diversity of life on earth.</p>\n\n<p><strong>Long Story</strong></p>\n\n<blockquote>\n <p>how can so many specific (advanced) evolutionary leaps be otherwise explained?</p>\n</blockquote>\n\n<p>Mutations occur at random throughout the genome. Most mutations will be neutral. That is, they are neither bad or good from an evolutionary viewpoint. The mutations are neutral because the genome for most organisms is non-functional. Mutations that occur in the functional regions of DNA (i.e., protein-encoding and related regions) are more likely to be detrimental (bad) because the mutation may negatively affect the function of the protein or even the ability to produce the protein. However, some mutations are beneficial. The mutation may actually enhance the functionality of the protein or even produce new proteins. </p>\n\n<p>A couple of factors have to be considered regarding mutations. The mutation <em>rate</em> is very low. For example, <a href=\"http://www.pnas.org/content/99/2/803.long\" rel=\"nofollow noreferrer\">Kumar and Subramanian (2002)</a> compared the DNA sequences of 5669 protein-encoding genes from 326 species of mammals. Their results suggested that the average mutation rate among mammals is 2.2 x 10<span class=\"math-container\">$^{-9}$</span> per base pair (bp) per year. This means that, on average, a point mutation has changed each DNA nucleotide position in the mammalian genome slightly more than twice (2.2 times) every billion (10<span class=\"math-container\">$^9$</span>) years. That's a lot of time!</p>\n\n<p>However, this same rate occurs in every individual in the population, so you have to consider the population sizes of the organisms. So, let's do a simple exercise. Consider a species like the <a href=\"http://www.hhmi.org/biointeractive/making-fittest-natural-selection-and-adaptation\" rel=\"nofollow noreferrer\">rock pocket mouse</a> or another small mammal that has a very short generation time. For this simple example, let's assume the generation time is one year. That means that the mutation rate of 2.2 x 10<span class=\"math-container\">$^{-9}$</span> per bp per year would then correspond to 2.2 x 10<span class=\"math-container\">$^{-9}$</span> mutations per bp per generation. Generation time is important because new mutations are inherited only through reproduction.</p>\n\n<p>Assume the average mammalian diploid genome is about 6 billion (6 x 10<span class=\"math-container\">$^9$</span>) nucleotides in size. The number of heritable mutations that occur in a single offspring is</p>\n\n<p><span class=\"math-container\">$$(6 \\times 10^9) \\times (2.2 \\times 10^{-9}) = 13.2.$$</span></p>\n\n<p>Next, assume that about 2.5% of the mammalian genome is composed of functional, transcribed sequences that may affect the phenotype (the traits of the organism). That means that, of all the mutations that occur in every offspring every generation, about 2.5% could potentially affect the phenotype. That is,</p>\n\n<p><span class=\"math-container\">$$13.2 \\times 0.025 = 0.33.$$</span></p>\n\n<p>Still a small number. But, now we have to account for population size. Small mammals, like mice and voles, generally have large population sizes. Assume that the population of rock pocket mice contains 100,000 reproducing individuals. If so, then</p>\n\n<p><span class=\"math-container\">$$0.33 \\times 100,000 = 33,000,$$</span> </p>\n\n<p>which is the number of new heritable mutations that could occur in the population. Most of these mutations will be detrimental and removed from the population by natural selection but, if even a small fraction of these new mutations are beneficial, then natural selection can cause these beneficial mutations to increase rapidly in frequency in the population during future generations.</p>\n\n<p>In humans, <a href=\"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1461236/pdf/10978293.pdf\" rel=\"nofollow noreferrer\">Nachman and Crowell (2000)</a> estimated that the average mutation rate was 2.5 x 10<span class=\"math-container\">$^{-8}$</span> mutations per bp per generation (not year), by comparing the genomes of humans and chimps. If we assume the same genome size and effective human population size of 500,000 individuals, then applying the same math suggests that 1,875,000 new mutations that potentially affect phenotype occur in the human population every generation. Again, only some of these will be beneficial but that is still the possibility of a number of new beneficial mutations. In evolutionary terms, a mouse or human generation is the blink of an eye.</p>\n\n<p>How long would it take for a beneficial mutation to spread through a population? That depends on two things. How beneficial is the mutation (called the strength of selection, <em>s</em>) and the population size? To estimate how long it would take for a beneficial mutation to spread through a population, we can use the formula,</p>\n\n<p><span class=\"math-container\">$$t = \\frac{2}{s}\\mathrm{ln}(2N_e),$$</span></p>\n\n<p>where <span class=\"math-container\">$t$</span> is time in generations, <span class=\"math-container\">$s$</span> is the strength of selection, and <span class=\"math-container\">$N_e$</span> is the effective population size (number of reproducing individuals). For the strength of selection, let's assume <span class=\"math-container\">$s=0.01$</span>, which is weak but positive natural selection. Going back to our rock pocket mice with <span class=\"math-container\">$N_e = 100,000$</span>, then the beneficial mutation would be spread throughout the population in only 2441 generations (remember, we're talking evolutionary time so 2000 years is nothing). If <span class=\"math-container\">$N_e = 10,000$</span>, the mutation spreads in only 1981 generations. If we increase the strength of selection t 0.2, then the times are 122 and 99 years for population sizes of 100,000 and 10,000 years, respectively.</p>\n\n<p>These \"back of the napkin\" calculations show just how quickly even weakly beneficial mutations can appear and spread throughout a population. Yet, this doesn't include other types of mutations like gene duplications that can also allow new proteins to evolve. For example, human ability to see red colors is due to a simple gene duplication <a href=\"http://cichlid.umd.edu/cichlidlabs/kc/Teaching/Visionpdfs/Nathans1986.pdf\" rel=\"nofollow noreferrer\">(Nathans et al. 1996</a> and references therein). This duplication also explains the common form of red-green colorblindness.</p>\n\n<p><em>Whew!</em></p>\n\n<p>There's yet more to our mutational story. Consider humans and chimps, which are nearly identical from a genetic standpoint (between 96-99% depending on how you calculate it) yet they appear very different. If humans and chimps diverged from their common ancestor within the past five million years, how could they differ so much? This question was initially posted by [King and Wilson (1975)]. They argued that mutations to structural proteins (like those that compose bones and muscles) would not be enough to explain the phenotype differences between humans and chimps. The proposed that <a href=\"http://www.nature.com/scitable/topic/gene-expression-and-regulation-15\" rel=\"nofollow noreferrer\">regulatory genes</a> are the key to understanding the big differences. Regulatory genes are those that control other genes, by turning them on or off and other important functions. Changes to the regulatory genes can cause fairly rapid changes to the phenotype. </p>\n\n<p>This understanding has led to the broad (and fascinating) field of <a href=\"http://evolution.berkeley.edu/evolibrary/article/evodevo_01\" rel=\"nofollow noreferrer\">evolutionary developmental biology</a>. This field focuses on how mutations in regulatory genes associated with development (from embryo to adult) have had a long-term evolutionary impact. The field is rich with examples, but one cool one is associated with duck feet and bat wings. Let's begin with the embryo. Most vertebrate embryos have membranes between the digits (fingers and toes) during an early stage of development. For most vertebrates, the membranes are lost later in development. The small flaps of skin you have between your fingers are the remnants of your embryonic membranes. </p>\n\n<p>A set of regulatory genes called BMPs (and a couple of others) are responsible for causing the loss of the membrane in vertebrates. However, through different sets of mutations, the BMPs are not able to function in duck feet and bat hands. Thus, they both end up with membranes between their digits (<a href=\"http://www.pnas.org/content/103/41/15103.long\" rel=\"nofollow noreferrer\">Weatherbee et al. 2006</a>). Thus, two different mutations block the same set of developmental genes, leading to novel adaptations in two very different types of vertebrates. One final example is the evolution of bird feathers from scales. As you may know, birds are evolved from dinosaurs. It turns out that bird feathers and alligator scales (alligators are birds closest <em>living</em> relative) use the same regulatory genes to develop. The genes are BMP2 and SHH (sonic hedgehog for fans of the old computer game) (<a href=\"http://prumlab.yale.edu/sites/default/files/harris_etal_2002.pdf\" rel=\"nofollow noreferrer\">Harris et al. 2002</a>). Other regulatory genes underlie the different types of feathers, like downy feathers and flight feathers (Harris et al. 2002).</p>\n\n<p><strong>Literature Cited</strong></p>\n\n<p>Harris, M.P. et al. 2002. <em>Shh-Bmp2</em> Signaling module and the evolutionary origin and diversification of feathers. Journal of Experimental Biology 294: 160-178.</p>\n\n<p>King, M.-C. and A.C. Wilson. 1975. Evolution at two levels in humans and chimpanzees. Science 188: 107-116.</p>\n\n<p>Kumar, S. and S. Subramanian. 2002. Mutation rates in mammalian genomes. Proceedings of the National Academy of Sciences USA 99: 803-808.</p>\n\n<p>Nachman, M.W. and S.L. Crowell. 2000. Estimate fo the mutation rate per nucleotide in humans. Genetics 156: 297-304.</p>\n\n<p>Weatherbee, S.D. et al. 2006. Interdigital webbing retention in bat wings illustrates genetic changes underlying amniote limb diversification. Proceedings of the National Academy of Sciences USA 103: 15103-15107,</p>\n"
}
] |
[
{
"answer_id": 20914,
"pm_score": 4,
"text": "<p><strong>About your question</strong></p>\n\n<p>This kind of very basic question has the drawback to need a very long answer. In consequence, your question might get some close vote. I'll do my best to help but you might want to look at some source of information as an introduction to evolutionary biology. A book eventually or Khan academy maybe.</p>\n\n<p><strong>Darwin's evolution theory</strong></p>\n\n<p>The expression \"Darwinian evolution theory\" easily yield to misunderstanding because Darwin was probably the most important scientist (and one of the first if not the first) to develop evolution theory but not the only one. Evolution theory is not anymore Darwin's evolution theory.</p>\n\n<p><strong>What is Natural Selection? Lewontin Recipe</strong></p>\n\n<p>You list:</p>\n\n<pre><code>- Survival of the fittest\n- Random mutation\n- Natural Selection\n</code></pre>\n\n<p>It is a list of different concepts that might be present in evolutionary biology but its nothing like a recipe for evolution to occur. This list I think already shows some point you misunderstood about evolution. The Lewontin recipe is a good way in order to understand what is natural selection and when it occurs. The Lewontin recipe says that natural selection occurs whenever:</p>\n\n<ol>\n<li>Individuals in a population vary in terms of a given trait</li>\n<li>This trait has some (additive) heritability. <a href=\"https://biology.stackexchange.com/questions/16576/can-i-force-evolution-in-a-group-of-cells-by-removing-all-the-smaller-cells/16578#16578\">Here</a> is one of the several posts that explain the concept of heritability. It might be slightly a post that is a bit advanced for you though but shortly speaking it means that offspring are more similar to their parents more than they are to other non-kin individuals in the population.</li>\n<li>The fitness varies (not necessarily linearly) as the trait varies.</li>\n</ol>\n\n<p>Simple example:</p>\n\n<ol>\n<li>In a population, there are blue pens and red pens</li>\n<li>Reproduction is asexual and blue pens create other blue pens while red pens create other red pens.</li>\n<li>blue pens make more offspring than red pens.</li>\n</ol>\n\n<p>In such a situation, natural selection occurs yielding the frequency of the blue pens to increase in the population while the frequency of red pens will decrease.</p>\n\n<p><strong>What is evolution?</strong></p>\n\n<p>Evolution is not only natural selection. It is for example very important to consider random events. One of them is <em>mutation</em>, another is <em>genetic drift</em> (I am not trying to list every parameter that influence evolution but only to give you a sense of why natural selection is different than evolution with a goal of explaining why a trait that is needed do not necessarily appear). Both mutations and genetic drift explain why a species will not necessarily be perfectly adapted to its environment.</p>\n\n<p><em>Mutations</em></p>\n\n<p>In the broad sense mutation is any change in the DNA sequence. Some changes are more likely to happen than other but in any case, the likeliness of these changes to happen is not dependent on the consequence they will have on the phenotype (shortly speaking, a phenotype is how an individual looks like) and on the reproductive success. So mutations occur randomly and the specific mutation that would be needed in the population may not occur. Therefore saying, if a trait is needed (in the sense of \"if a trait would be beneficial\"), then a mutation will occur to make this trait existing is totally wrong. You may be surprised by the level of adaptation of life but this does not mean that what they needed was created with the purpose to help these individuals surviving but it only means that random mutations occur, most of them are deleterious (decrease the reproductive success) while few of them are beneficial (increase the reproductive success) and those that are beneficial are more likely to rise in frequency in the population.</p>\n\n<p><em>Genetic drift</em></p>\n\n<p>If the change in frequency of mutations would depend exclusively on natural selection, then I would not have said before that a beneficial mutation is more likely to raise in frequency but I would have said that a beneficial mutation will raise in frequency. An intuitive explanation of what is genetic drift can be found on <a href=\"https://biology.stackexchange.com/questions/14543/why-is-the-strength-of-genetic-drift-inversely-proportional-to-the-population-si/14545#14545\">this post</a>. It will also allow you to understand why a small population undergo a more random change in frequency of their genes that are big population.</p>\n\n<p>Therefore, when you say that you noticed that <code>Any time a species has needed the development of a specific feature to survive, it has developed that feature, and that feature precisely</code> is wrong. You only noticed that species has some level of adaptiveness if I can say so. It is very hard to imagine what new mutation would be beneficial of a given individual in a population but there are in reality many mutations that are beneficial that has never occurred or that has disappeared because of genetic drift. Also, as it is implied in the Lewtontin recipe different individuals have different traits yielding to different reproductive success. If you do not consider mutations that have never occurred but only to sites in the genome that are polymorphic (where different variants exist in the population), then it is worth knowing that any single individual carries quite a lot of deleterious variants. These deleterious mutations explain many genetic diseases. No, we are not perfect.</p>\n\n<p><strong>About your question again</strong></p>\n\n<p>Hope that helps a bit. But I would need days in order to explain further what evolution is. It is a bit field in biology. Your question is a bit too broad and as I said at the beginning you should seek some information by yourself and come back to this site with a question that can be more quickly answered.</p>\n\n<p>Hope that helps!</p>\n"
},
{
"answer_id": 20916,
"pm_score": 3,
"text": "<p>Short answer version:</p>\n\n<blockquote>\n <p>It seems plausible to me that we (advanced life) could have a\n biological mechanism to \"write\" needed alterations into either our own\n DNA or our reproductive DNA over time, triggering the very specific\n evolutionary developments necessary to our survival without relying on\n random mutation.</p>\n</blockquote>\n\n<p>No, it's not. Despite what your feelings tell you, despite what you wish the case might be, there is no evidence in molecular biology to suggest that such a mechanism exists, there is no evidence that such a mechanism is required to explain the different phenotypes we see. </p>\n"
},
{
"answer_id": 20918,
"pm_score": 3,
"text": "<blockquote>\n <blockquote>\n <p><strong>Any time a species has needed the development of a specific feature to survive, it has developed that feature, and that feature precisely.</strong></p>\n </blockquote>\n</blockquote>\n\n<p><strong>This statement is clearly false. The dinosaurs didn't develop what they needed, did they?</strong> </p>\n\n<p>It turned out that on this occasion, the mammals happened to be best adapted to the conditions at the time, just as the fish had managed to get the upper hand over the large arthropods and the ammonites previously. </p>\n\n<p><strong>In hindsight many of nature's solutions seem wonderfully elegant, but they were arrived at by luck under intense pressure to survive.</strong> The fact that our eye is designed with blood vessels on the front of the optical surface instead of the back is an example of a design that could have been done better if thought out from scratch. There are many vestigial features from previous generations which persist, even though they are no longer needed. Notice that flatfish hatch with eyes on opposite sides of their head and one eye then migrates to be on the same side as the other, and whale embryos that have teeth which have disappeared by the time they are born, etc.</p>\n\n<p><strong>Natural selection is a combination of lucky mutations which happen to fit in with the prevailing conditions.</strong> It's a tough world out there. Even the plants are strangling each other, as can be seen on this video: <a href=\"https://www.youtube.com/watch?v=aNjR4rVA8to\" rel=\"nofollow noreferrer\">https://www.youtube.com/watch?v=aNjR4rVA8to</a></p>\n\n<p><strong>The turtle didn't have much time to stare longingly at the leaves he couldn't reach.</strong> Some other turtle with a slightly longer neck came and ate them. And he got bigger and stronger and fought with the first turtle so he got to mate with all the females. And so the next generation of turtles had longer necks than the last. </p>\n\n<p><strong>It's easy to forget, with our comfortable lives, what a struggle nature is. The reason for this is that humans as a species have developed the most devastating weapon of all: cooperation.</strong> Compared to most other organisms, we treat other individuals of the same species pretty well (most of the time) <em>and</em> we actually <strong>teach</strong> each other how to do things. While some other species cooperate among individuals, humans have taken this to a whole new level. As a result, we have been able to eradicate many species which pose a threat to us and bring many other species which are useful to us under control. </p>\n\n<p><strong>If you want to know why this didn`t happen before:</strong> humans evolved from an ape-like creature that, due to changes in its environment, came down out of the trees and started walking on the ground. This creature then had its hands free to use tools, and by sheer chance this combination of factors made a bigger brain advantageous, so this creature (which was already social, like apes but unlike octopi, one of the few other creatures blessed with the ability to perform complex manipulations) became even more intelligent and began to educate its offspring in how to control its environment. </p>\n\n<p><strong>There is nothing in biology which enables the mutation of genes to be directed. Finally, human technology has developed to the point where it may be possible to modify genes directly.</strong> However, there are significant ethical issues regarding the use of this technology. The termination of an \"imperfect\" human is frowned upon because it is considered that all members of the species should be given the best chance to survive. Besides, <strong>it is not at all clear if there is really ever such thing as a \"defective\" gene.</strong> For example carriers of the gene responsible for sickle cell anaemia have increased resistance to malaria.</p>\n\n<p>Anyway, <strong>long before humans were able to manipulate genes directly, they were able to produce massive changes in the phenotype of dogs in a remarkably small number of generations.</strong> There is a breed of dog adapted to every possible use. An unfortunate consequence is that <strong>the gene pool in each breed is rather small, leading to breed-specific illnesses.</strong> If these breeds were left alone it would take many generations for mutations to allow their genotypes to diversify again. And who knows what the final animal would look like?</p>\n\n<blockquote>\n <blockquote>\n <p><strong>It seems plausible to me that we (advanced life) could have a biological mechanism to \"write\" needed alterations into either our own DNA or our reproductive DNA over time, triggering the very specific evolutionary developments necessary to our survival without relying on random mutation.</strong></p>\n </blockquote>\n</blockquote>\n\n<p><strong>There is no evidence for such a mechanism, and it is very unclear how a mutation could be proved beneficial without being tested in the environment. What there is, is a way of mixing and matching genes, so that the best ones can propagate throughout the population.</strong> Unicellular organisms do this by a variety of means. <strong>For multicellular organisms the way of doing is sexual reproduction.</strong></p>\n\n<p><strong>The cost of this is enormous.</strong> Look at a flowering plant. That flower has evolved exclusively to enable pollination, typically by insects. In some cases, virtually all the plant's energy goes into making that flower and relatively little into making the actual seeds. Plants do have a particular problem exchanging genes because they do not move about. Stationary animals, such as the barnacle, also have similar problems. The barnacle solves this by having a \"penis\" several times longer than its body length so that it can copulate with its neighbour without moving from its spot. In humans, fully half the population is male and therefore unable to bear offspring. </p>\n\n<p><strong>Asexual reproduction is far more efficient at producing offspring but does not enable the interchange of genes. The offspring are clones of their parent and therefore have the same genetic strengths and weaknesses.</strong> Asexual reproduction does exist, even in some animals, but exclusively asexual reproduction would preclude the spread of beneficial mutations. <strong>That's why organisms invest so much energy in sex.</strong></p>\n\n<p>Aphids are a good example of an animal that reproduces both sexually and asexually. At the boom times of the year, aphids reproduce asexually and are actually born as already pregnant females! When the availability of food slows down, they switch to the slower, sexual reproduction system with males and females.</p>\n\n<p>In many animals, males must demonstrate their good health in order to be able to mate with the females (who are choosy, because they have to take the cost of bearing the young.) In many large herbivorous mammals, this is done by males fighting. Male birds often display their health by elaborate plumage, the classic example being the peacock. It is debatable whether such a conspicuous waste of resources is really beneficial to the species, but the females have evolved to select males in this way. In some fish, there is only one male in a group, and when something happens to him, the biggest healthiest female actually changes sex to become a male.</p>\n\n<p><strong>So, if an organism were able to program its own genes, why invest so much energy in sexual reproduction?</strong></p>\n"
},
{
"answer_id": 20933,
"pm_score": 2,
"text": "<p>The answer provided by Mike Taylor is just perfect and complete. </p>\n\n<p>However, I'd like to add some thoughts of my own in a more colloquial style:</p>\n\n<ul>\n<li><p>Survival of the fittest is not always true. There is also \"survival of the luckiest\" (e.g. the fittest is showing off in the beach with the other turtles and is struck by lightning). </p></li>\n<li><p>Reproduction is not that simple and many times the female mates with several mates (apart from the fittest one) and a paternal test should be procured. </p></li>\n<li><p>Mutation changes are not always gradual (i.e. the turtles might develop a long neck in just one generation).</p></li>\n<li><p>Mutations don't always lead to a phenotype change. Sometimes, depending of the environment, the phenotype change doesn't occur. For example, the turtles might only grow a long neck if the live in a sunny island.</p></li>\n<li><p>Not all mutations are beneficial and not all beneficial mutations have an impact on survival (e.g. many actors/actresses are not very tall although they reproduce successfully).</p></li>\n</ul>\n\n<p>In my opinion there are many shades of grays in between the ideas behind evolution.</p>\n\n<p>The features of the \"fittest\" are sometimes lost by random reasons as the listed above, and the features of the \"less fitted\" are sometimes transmitted. </p>\n\n<p>And finally, sometimes, an organism develops (or is developing) a mechanism to alter the genes directly (e.g. human beings). Where would that lead? Does evolution mean something anymore?</p>\n"
},
{
"answer_id": 20936,
"pm_score": 1,
"text": "<p>To add to the previous answers that treat specifically of the biological Darwinism, there is also <strong>Universal Darwinism</strong> which postulates that evolution is a natural phenomenon that appears when a set of conditions and constraints are present. And indeed, it has successfully been applied to a number of fields (see below the quote), which seems to imply that evolution is not a property of the evolving individuals (as you implied) but <strong>a property of the system</strong> where the individuals evolve (as long as the individuals satisfy a few special properties, namely variation and heredity, see below).</p>\n\n<p>Here's the definition from Wikipedia:</p>\n\n<blockquote>\n <p>At the most fundamental level, Charles Darwin's theory of evolution states that organisms evolve and adapt to their environment by an iterative process. This process can be conceived as an evolutionary algorithm that searches the space of possible forms (the fitness landscape) for the ones that are best adapted. The process has three components:</p>\n \n <ul>\n <li>variation of a given form or template. This is usually (but not necessarily) considered to be blind or random, and happens typically by mutation or recombination.</li>\n <li>selection of the fittest variants, i.e. those that are best suited to survive and reproduce in their given environment. The unfit variants are eliminated.</li>\n <li>heredity or retention, meaning that the features of the fit variants are retained and passed on, e.g. in offspring.</li>\n </ul>\n \n <p>After those fit variants are retained, they can again undergo variation, either directly or in their offspring, starting a new round of the iteration. The overall mechanism is similar to the problem-solving procedures of trial-and-error or generate-and-test: evolution can be seen as searching for the best solution for the problem of how to survive and reproduce by generating new trials, testing how well they perform, eliminating the failures, and retaining the successes.</p>\n \n <p>The generalization made in \"universal\" Darwinism is to replace \"organism\" by any recognizable pattern, phenomenon, or system. The first requirement is that the pattern can \"survive\" (maintain, be retained) long enough or \"reproduce\" (replicate, be copied) sufficiently frequently so as not to disappear immediately. This is the heredity component: the information in the pattern must be retained or passed on. The second requirement is that during survival and reproduction variation (small changes in the pattern) can occur. The final requirement is that there is a selective \"preference\" so that certain variants tend to survive or reproduce \"better\" than others. If these conditions are met, then, by the logic of natural selection, the pattern will evolve towards more adapted forms.</p>\n \n <p>Examples of patterns that have been postulated to undergo variation and selection, and thus adaptation, are genes, ideas (memes), neurons and their connections, words, computer programs, firms, antibodies, institutions, quantum states and even whole universes.</p>\n</blockquote>\n\n<p>Also, you may be interested in some terminology associated with this theory, for example for John Maynard Smith an individual that can evolve in an evolvable system is called a <em>Unit of evolution</em> [1]. This shows how much abstract and generalizable evolution can be.</p>\n\n<p>[1]: Fernando C, Vasas V, Szathmáry E, Husbands P (2011) Evolvable Neuronal Paths: A Novel Basis for Information and Search in the Brain. PLoS ONE 6(8): e23534. doi: 10.1371/journal.pone.0023534</p>\n"
},
{
"answer_id": 21855,
"pm_score": 2,
"text": "<blockquote>\n <p>\"I imagine that turtle looking up at that food, and sub-consciously\n wishing to get to it, constantly straining, for its entire lifetime.</p>\n \n <p>It seems plausible to me that we (advanced life) could have a\n biological mechanism to \"write\" needed alterations into either our own\n DNA or our reproductive DNA over time, triggering the very specific\n evolutionary developments necessary to our survival without relying on\n random mutation.\"</p>\n</blockquote>\n\n<p>That is a pre-Darwin idea of evolution called \"<a href=\"http://en.wikipedia.org/wiki/Inheritance_of_acquired_characteristics\" rel=\"nofollow noreferrer\">inheritance of acquired characteristics</a>\" or Lamarckism after it's creator French natural philosopher Jean-Baptiste Lamarck. Lamarck postulated that given the use of tissues altered those tissues e.g. lifting weights makes muscles bigger, then an organisms descendants would benefit if everything the parent's tissues \"learned\" could be passed on. </p>\n\n<p>There are actually epigenetic factors in cells that selectively turn genes on or off or otherwise modify their use generation to generation. But this is not evolution because the genes are always there, ready to be used if needed and no new information is ever created. </p>\n\n<p>The flaws in Lamarckism are that, even if the mechanism existed to transmit acquired characteristics, how would it know what characteristics led to what outcome? How could it distinguish positive changes from negative ones? </p>\n\n<p>Most fatally, how could an organism evolve a system that was not related to an existing behavior? For the turtle to stretch its neck, it must desire to eat the leaves and exert effort to do so. How did it acquire the behavior of desiring to eat the leave in the first place? Going forward, if the plants it does eat goes away, how would it ever find another food source? It wouldn't desire to eat inedible plants so it would never exert itself to do so and would never pass that exertion on to it's young. </p>\n\n<p>The hiccup in your understanding of Darwinism is that you've got it backwards. Species don't find solutions and evolve. It's not something species do. It's something that <strong><em>happens</em></strong> to species, a force from the outside. It's not analogous to humans setting down to consciously solve a problem. </p>\n\n<p>Darwin was originally going to use the analogy of \"wedging\" instead of \"natural selection.\" He wanted to emphasize that it was the environment squeezing in on species that formed them. (Today we think of wedges largely for their splitting power but in but in Darwin's day, if you wanted to compress something you used a wedge hammered in from the side. It was a common tool that performed the same jobs as jacks and hydraulics do today.) But he went with the anthropomorphic analogy of nature being an animal breeder selecting for traits for reproductive success and a lot of misunderstandings followed. </p>\n\n<p>Evolution is not random. Only variations themselves are random. The selection of them is not. It's like shooting dice. The fall of the dice is random but only certain values of dice are winning number and are \"selected.\" The same mutation might show up in every generation for millions of years but produce no change until the environment changes to make the mutation useful. </p>\n\n<p>Species have no existence independent from their environment. The environment squeezes them into a specific form, one that best satisfies the demands of the Second Law of thermodynamics. If the environment doesn't change, then the organism won't either. From that perspective, adaptation is about as amazing as a rock rolling downhill. (That would look pretty fantastic if you didn't know about gravity.) </p>\n\n<p>Imagine you had never seen clay and never seen molding. Your walk along a stream bank lined with clay. Walking one way you pass a blank stretch of clay. After you pass, a leaf falls into the claw and creates a near perfect imprint before being blown away. When you return past that spot, it looks like the clay has somehow altered itself, against all probability, into an exact mirror duplicate of a leaf. How you might wonder, could the clay possibly know how to exactly duplicate the shape of a leaf? </p>\n\n<p>But the clay did nothing. The clay did not alter to fit the leaf, the force of the falling leaf altered the clay. </p>\n\n<p>Likewise, species do not evolve themselves, they are evolved by external forces. Species seem to miraculous fit their ecological niches but, just like the clay, did nothing to shape themselves to the niche. Just as the clay will be passively shaped by the pressure of molding, species have no choice but to assume the forms they do. </p>\n\n<p>It's not survival of the <em>fittist</em> but survival of the <strong><em>fitted</em></strong>. </p>\n"
},
{
"answer_id": 36635,
"pm_score": 0,
"text": "<p>There are indeed massive evolutionary control systems integrated into DNA. They constitute the major force for efficient change in living beings. </p>\n\n<p>Random DNA mutations are not as beneficial as controlled ones, you can see random single gene mutations at work in medical books: Anemia, cancer, cheese smelling sweat, no sweat glands, skin conditions, scales, brittle bones, lactose tolerance, These are all examples of mutations of single proteins and single growth hormones and so on. </p>\n\n<p>Instead of random DNA mutations, life-forms control their rate of change and types of variations in very efficient ways, changes in color, longer and shorter bones/arms/legs which you can see in humans, physical maturation times, length and quantity of hair, all these things are safe for an animal to have lots of genetic variation with. Changes in bone length vary more than 10 percent in a single generation of humans, but changes like lactose tolerance occur only every 100ds of generations. Therefore there are hundreds of genes for controlling growth hormones as it's selection-important. If color changes become important to an animal, for example, birds, fish, and butterflies, then hundreds of genes are devoted to color. If color is not important, for example, northern and snow animals, then few gene changes are devoted to color, The many Color genes of a tropical animal would go dormant very fast if it were exposed to snowy conditions.</p>\n\n<p>It makes sense for DNA to favor developments that encourage reproduction and survival in variable settings, and indeed DNA is supercharged to deliver mostly useful morphological and chemical changes in large numbers. Plants, conversely, need to change their chemicals alot to attract and repel animals, whereas animals do not need to attract other animals for food, only to defend themselves, that one reason why animals have a lot less chemical variety than plants. Only Chinese use animals for medicine, and there are few aspirins and sedatives derived from animals. Animals cannot produce powerful random chemicals because their nervous system hormones and cell walls are less robust than cellulose cells and plant hormones. Otherwise, animals would have more variable smell and taste, but all mammals taste similar.</p>\n\n<p>It's the same with computer evolution. If you tell a computer program to vary DNA randomly or to create life-forms randomly, it will have epileptic, disorganised animals that flop around, roll around, hit walls, and that is not what animals do to evolve. If you equip a computer evolution program with DNA tool kits copied from nature, you will much faster have meaningful animals... i.e. simple locomotive insects. If you tell the computer to use sinusoidal limb movements like fish fins, millipede legs, insect legs, using nerve impulses, and to create metameric life forms, you will have alot more success than just adding limbs onto random parts of the body, using random pattern nerve impulses and so on. </p>\n\n<p>It's not an easy thing to study, as it is very complex. I would love some statistics and journals regarding types of evolutionary changes that are prevalent in different life-forms.</p>\n"
}
] |
20,992 |
<p>From what I understand, your body needs certain amounts of vitamins and minerals to maintain health. Why can't we just take enough pills to obtain these vitamins and minerals?</p>
|
[
{
"answer_id": 20993,
"pm_score": -1,
"text": "<p>This is more of a biochemistry question and to be honest its a little bit out of my league because I have not had the necessary grad classes to explain nutrition but indeed I will try.</p>\n<p>Unknown metabolite cofactors and things like ionization, oxidation and state of matter are the reason that straight up vitamins are rejected by the body and cause really expensive urine and a difficult time otherwise excreting.</p>\n<blockquote>\n<p>Metabolism involves a vast array of chemical reactions, but most fall under a few basic types of reactions that involve the transfer of functional groups. This common chemistry allows cells to use a small set of metabolic intermediates to carry chemical groups between different reactions. These group-transfer intermediates are the loosely bound organic cofactors, often called coenzymes.</p>\n<p>Each class of group-transfer reaction is carried out by a particular cofactor, which is the substrate for a set of enzymes that produce it, and a set of enzymes that consume it. An example of this are the dehydrogenases that use nicotinamide adenine dinucleotide (NAD+) as a cofactor. Here, hundreds of separate types of enzymes remove electrons from their substrates and reduce NAD+ to NADH. This reduced cofactor is then a substrate for any of the reductases in the cell that require electrons to reduce their substrates.</p>\n<p>Therefore, these cofactors are continuously recycled as part of metabolism. As an example, the total quantity of ATP in the human body is about 0.1 mole. This ATP is constantly being broken down into ADP, and then converted back into ATP. Thus, at any given time, the total amount of ATP + ADP remains fairly constant. The energy used by human cells requires the hydrolysis of 100 to 150 moles of ATP daily, which is around 50 to 75 kg. In typical situations, humans use up their body weight of ATP over the course of the day. This means that each ATP molecule is recycled 1000 to 1500 times daily.</p>\n</blockquote>\n<p>-<a href=\"http://en.wikipedia.org/wiki/Cofactor_(biochemistry)#Cofactors_as_metabolic_intermediates\" rel=\"nofollow noreferrer\">wikipedia</a></p>\n<p>If you did not like that explanation of cofactors maybe you will this:</p>\n<blockquote>\n<p>Whole foods offer three main benefits over dietary supplements:</p>\n<p><strong>Greater nutrition</strong>. Whole foods are complex, containing a variety of the micronutrients your body needs — not just one. An orange, for example, provides vitamin C plus some beta carotene, calcium and other nutrients. A vitamin C supplement lacks these other micronutrients.</p>\n<p><strong>Essential fiber</strong>. Whole foods, such as whole grains, fruits, vegetables and legumes, provide dietary fiber. Most high-fiber foods are also packed with other essential nutrients. Fiber, as part of a healthy diet, can help prevent certain diseases, such as type 2 diabetes and heart disease, and it can also help manage constipation.</p>\n<p><strong>Protective substances</strong>. Whole foods contain other substances important for good health. Fruits and vegetables, for example, contain naturally occurring substances called phytochemicals, which may help protect you against cancer, heart disease, diabetes and high blood pressure. Many are also good sources of antioxidants — substances that slow down oxidation, a natural process that leads to cell and tissue damage.</p>\n</blockquote>\n<p>-<a href=\"http://www.mayoclinic.org/healthy-living/nutrition-and-healthy-eating/in-depth/supplements/art-20044894\" rel=\"nofollow noreferrer\">The great Mayo Clinic</a></p>\n"
}
] |
[
{
"answer_id": 21338,
"pm_score": 3,
"text": "<p>I think the piece of missing information here is the distinction between <a href=\"http://fnic.nal.usda.gov/food-composition/macronutrients\" rel=\"nofollow noreferrer\"><i>macro</i>nutrients</a> and <a href=\"http://www.who.int/nutrition/topics/micronutrients/en/\" rel=\"nofollow noreferrer\"><i>micro</i>nutrients.</a> The info from Mayo clinic quoted in the <a href=\"https://biology.stackexchange.com/a/20993/9268\">another answer</a> addresses some reasons why whole foods might be better than pills for obtaining micronutrients (i.e. vitamins and minerals). While this may be true, most of it remains to be conclusively demonstrated (arguably). However, one clear reason “why….you need a healthy diet on top of that” is (unarguably) to obtain the fat, protein, and carbohydrates that your body uses to create energy. Unlike the minerals that act as cofactors, these macronutrients are the substrate. They are broken down to create the ATP that keeps everything running and they are built up to create the very structure of the body. </p>\n\n<blockquote>\n <p>The energy that is consumed in the form of food or drinks can either be stored in the body in the form of fat (the major energy store), glycogen (short-term energy/carbohydrate reserves), or protein. . . to be used by the body to fuel energy-requiring events. *</p>\n</blockquote>\n\n<p>These are called <i>macro</i>nutrients because they are required in gram quantities — hundreds or even thousands of times more massive than the requirements for most <i>micro</i>nutrients. As such, they don’t fit in a pill. As tragic as it is, we must keep eating. </p>\n\n<hr>\n\n<p><sub>\n*Gibney, M. J., & Nutrition Society. (2009). <em>Introduction to Human Nutrition.</em> Chichester, West Sussex, U.K.: Wiley-Blackwell.\n</sub></p>\n"
},
{
"answer_id": 23101,
"pm_score": 1,
"text": "<p><em>The Question:</em> Why can't we just take enough pills to obtain these vitamins and minerals?</p>\n<h3>We don't know enough about nutrition.</h3>\n<p>There are about <a href=\"http://www.nutrientsreview.com/glossary/essential-nutrients\" rel=\"nofollow noreferrer\">45 essential nutrients</a>, which you need to consume to be healthy and live. You can get all of them from food without thinking about them. I'm not sure if currently there are a lot of supplements on the market that contain all essential nutrients. Also, we may currently still not know which all nutrients are essential, so we may miss some when designing multivitamin/mineral pills.</p>\n<h3>Food is easier!</h3>\n<p>A healthy adult who regularly consumes both plant and animal foods in reasonable variety and amount does not really need any vitamin/mineral supplements. And you need to eat foods to get calories. Yes, you could make supplements to substitute calorific content; imagine some sort of carbohydrate powder. But why complicate this when food is readily available, much cheaper, and easier?</p>\n"
},
{
"answer_id": 35830,
"pm_score": 1,
"text": "<p><strong>TL;DR : Food gives the human body much more than simply vitamins & minerals. A healthy diet is essential to overall healthiness, not just this one aspect of it.</strong></p>\n\n<h2>Micronutrients</h2>\n\n<p>The component you're asking about - vitamins & minerals - are referred to as \"<a href=\"https://en.wikipedia.org/wiki/Micronutrient\" rel=\"nofollow\">micronutrients</a>\", and is only a quarter or so of what the body <a href=\"https://en.wikipedia.org/wiki/Healthy_diet\" rel=\"nofollow\">needs</a>. Micronutrients are the vitamins like <a href=\"https://en.wikipedia.org/wiki/Vitamin_A\" rel=\"nofollow\">Vitamin A</a>, <a href=\"https://en.wikipedia.org/wiki/B_vitamins\" rel=\"nofollow\">Vitamin B</a>, <a href=\"https://en.wikipedia.org/wiki/Vitamin_C\" rel=\"nofollow\">Vitamin C</a>, etc. but it's also trace elements like zinc, iron, iodine, and many other metals that the body requires in very small quantities.</p>\n\n<p>This is the part of the diet that most people actually overlook, and is what pills like the \"once-a-day\" vitamin are intended to supplement.</p>\n\n<h2>Macronutrients</h2>\n\n<p>Much of what we get from food falls in the category of \"<a href=\"https://en.wikipedia.org/wiki/Nutrient\" rel=\"nofollow\">macronutrients</a>\". These nutrients are the actual building blocks of the body - things like fats, proteins, calcium, carbon, hydrogen, etc. A lot of macronutrients are required on a daily basis, and it would be difficult to condense these into a pill form. An average-sized pill would have to be taken 5-6 times a day in order to provide even a less-than-average amount of macronutrients for the average person.</p>\n\n<h2>Digestion</h2>\n\n<p>The human body is designed to be an engine. The act of eating is hard-coded into human physiology, and the act of digesting food kick-starts a great many processes throughout the body. Digestion is a rather efficient process, and it's one that only works properly when it has enough food to break down. A handful of pills could never fuel this process correctly, since they would simply dissolve in the stomach and never require any kind of breaking down.</p>\n\n<h2>Psychological</h2>\n\n<p>Lastly, food & drink have a psychological component to them as well. The human brain is wired so that it desires food on a psychological level. The physical act of eating something soothes that desire in a way that a pill never could. One of the greatest obstacles to someone trying to lose weight is this very component - even when their body technically has what it needs from vitamins, supplements, or shakes, this psychological aspect of hunger makes them want food anyway.</p>\n"
},
{
"answer_id": 55783,
"pm_score": 0,
"text": "<p>Your answer is in Cellular Respiration which is the production of ATP (energy storage molecules). Food is Carbon and Hydrogen. The body needs carbon and hydrogen for cellular respiration. Carbon and Hydrogen are not in vitamin pills they are in food.</p>\n"
}
] |
23,873 |
<p>This is a cross-cutting question but I think its core is about biology. Our society's need for energy is dramatically growing and we are messing up with our environment to answer them. Maybe another way to proceed would be to use the primary energy source that is the sun in the same way as it has been used throughout the ages: photosynthesis.</p>
<p>I know the energy effiency is not as good as a solar panel's but it could clearly be compensated by volume. I found surprisingly little information about harvesting energy from photosynthesis which is why I began to wonder where we are at today. </p>
<p>Thanks!</p>
<p><strong>Edit</strong>
I meant transforming the chemical energy generated by photosynthesis into electrical energy. For instance, the first algae powered building was unveiled at the International Building Exhibition hosted in Hamburg. This is a whole different approach.
The most basic example of what I would like to talk about seems to be the algae powered lamp that has (apparently) been developped. In other words, it seems that some sort of plant solar panels are under development and I don't understand how it's done.</p>
|
[
{
"answer_id": 23882,
"pm_score": 4,
"text": "<blockquote>\n <p>The most basic example of what I would like to talk about seems to be\n the algae powered lamp that has (apparently) been developped.</p>\n</blockquote>\n\n<p>I think you misunderstood the idea. That lamp uses <a href=\"http://en.wikipedia.org/wiki/Bioluminescence\">bioluminescence</a> and not electric power. Normally living cells don't like to give you energy. The trick we use is anaerob fermentation. Without the presence of oxygen (good electron acceptor) they cannot extract more energy from compounds like ethanol, etc... so they get rid of them. After that we can \"burn\" these compounds with oxygen and get a lot of energy. So currently there is no solution which uses sunlight and microbes to produce electricity directly, however it might be possible.</p>\n\n<p>There are many ways to use photosynthesis in order to produce energy.</p>\n\n<ul>\n<li>The simplest way to burn the plant itself when it has grown enough. You can burn wood, energy plants (e.g. energy grass), etc... and use a generator.</li>\n<li>A more sophisticated approach to ferment biomass and produce methane, ethanol, etc... which you can burn. This works very well by starch (e.g. corn bioethanol), and there is active research about <a href=\"http://en.wikipedia.org/wiki/Cellulosic_ethanol_commercialization\">cellulose conversion</a>.</li>\n<li><p>There is active research about <a href=\"http://en.wikipedia.org/wiki/Artificial_photosynthesis\">artificial photosynthesis</a> as well.</p>\n\n<ul>\n<li>You can feed microbes with electric power coming from a photovoltaic system (solar panel), so they can produce ethanol, methane, etc... This might be better than storing energy in batteries.</li>\n<li>You can use electric power coming from solar panels to split water. After that microbes can use the hydrogen as electron donor to fix $CO_2$, so they can create ethanol, etc... </li>\n<li>You can use light to split $CO_2$ into $CO$ and $1/2O_2$. You can use $CO$ in biological systems to create ethanol, etc... You can use $CO$ in shift reaction to create $H_2$. It is a new technology to use copper nanoparticles to convert $CO$ into ethanol in a completely artificial system.</li>\n</ul></li>\n</ul>\n\n<p>You can use a photovoltaic system instead of photosynthesis if you need electric power instead of chemical compounds.</p>\n\n<p>Related articles:</p>\n\n<ul>\n<li>2011 - <a href=\"http://onlinelibrary.wiley.com/doi/10.1002/adma.201004393/abstract?deniedAccessCustomisedMessage=&userIsAuthenticated=false\">Light Absorption Enhancement in Thin-Film Solar Cells Using Whispering Gallery Modes in Dielectric Nanospheres</a></li>\n<li>2010 - <a href=\"http://onlinelibrary.wiley.com/doi/10.1111/j.1758-2229.2010.00211.x/abstract?deniedAccessCustomisedMessage=&userIsAuthenticated=false\">Powering microbes with electricity: direct electron transfer from electrodes to microbes</a></li>\n<li>2008 - <a href=\"http://www.sciencedirect.com/science/article/pii/S0958166908001341\">The microbe electric: conversion of organic matter to electricity</a></li>\n<li>2011 - <a href=\"http://aem.asm.org/content/77/9/2882.short\">Electrosynthesis of Organic Compounds from Carbon Dioxide Is Catalyzed by a Diversity of Acetogenic Microorganisms?</a></li>\n<li>2011 - <a href=\"http://pubs.rsc.org/en/content/articlelanding/2011/mt/c1mt00042j#!divAbstract\">Metal centers in the anaerobic microbial metabolism of CO and CO2</a></li>\n<li>2014 - <a href=\"http://link.springer.com/chapter/10.1007/978-1-4939-1148-6_13\">From Ionizing Radiation to Photosynthesis</a></li>\n<li>2012 - <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/22487129\">Biological conversion of carbon monoxide to ethanol: effect of pH, gas pressure, reducing agent and yeast extract.</a></li>\n<li>2014 - <a href=\"http://www.nature.com/nature/journal/v508/n7497/full/nature13249.html\">Electroreduction of carbon monoxide to liquid fuel on oxide-derived nanocrystalline copper</a></li>\n<li>2009 - <a href=\"http://pubs.acs.org/doi/abs/10.1021/ar9001679\">Molecular Approaches to the Photocatalytic Reduction of Carbon Dioxide for Solar Fuels</a></li>\n<li>2014 - <a href=\"http://aaqr.org/VOL14_No2_March2014/8_AAQR-13-09-OA-0283_533-549.pdf\">Comparison of CO2 Photoreduction Systems: A Review</a></li>\n<li>2013 - <a href=\"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3627189/\">Leaf-architectured 3D Hierarchical Artificial Photosynthetic System of Perovskite Titanates Towards CO2 Photoreduction Into Hydrocarbon Fuels</a></li>\n<li>2009 - <a href=\"http://pubs.acs.org/doi/abs/10.1021/ja905797w\">Water-Gas Shift Reaction Catalyzed by Redox Enzymes on Conducting Graphite Platelets</a></li>\n</ul>\n"
}
] |
[
{
"answer_id": 23875,
"pm_score": 3,
"text": "<p>It is not possible to do this directly. Indirectly, it is possible, this is actually done by harvesting fruits - they contain the energy of the sunlight conserved in chemical compounds like sugars or starch and their cellular structures. The basic process for this is <a href=\"http://en.wikipedia.org/wiki/Photosynthesis\">photosynthesis</a>.</p>\n\n<p>The products from the fields are used technically to produce gas by fermentation, which then can be burned to produce electricity. Read reference 1 for more details.\nWhat is also done is the use of sugar cane (done widely in Brazil) or <a href=\"http://www.pjoes.com/pdf/19.2/323-329.pdf\">corn</a> to produce ethanol which is then used in the fuel of cars. See references 2-4.</p>\n\n<p>Besides these technical processes, there is of course still the possibility to simply burn whole plants or the wood of trees, which is also the result of the fixation of sun energy.</p>\n\n<p>References:</p>\n\n<ol>\n<li><a href=\"http://www.pjoes.com/pdf/19.2/323-329.pdf\">Biogas Production from Maize Grains and Maize Silage</a></li>\n<li><a href=\"http://journeytoforever.org/biofuel_library/Pimentel-Tadzek.pdf\">Ethanol Production Using Corn, Switchgrass, and Wood; Biodiesel\nProduction Using Soybean and Sunflower</a></li>\n<li><a href=\"http://en.wikipedia.org/wiki/Ethanol_fuel_in_Brazil\">Ethanol fuel in Brazil</a></li>\n<li><a href=\"http://en.wikipedia.org/wiki/Corn_ethanol\">Corn ethanol</a></li>\n</ol>\n"
},
{
"answer_id": 23876,
"pm_score": 3,
"text": "<blockquote>\n<p>I found surprisingly little information about harvesting energy from\nphotosynthesis</p>\n</blockquote>\n<p>Photosynthesis does not produce energy as such, it produces <strong>sugars/carbohydrates/chemical energy</strong>, which the plant then converts into energy via respiration.</p>\n<p><img src=\"https://i.stack.imgur.com/DwZfS.png\" alt=\"enter image description here\" /></p>\n<hr />\n<p>You can burn the sugar to produce heat. But this is basically what your doing when you burn a plant. So no, photosynthesis cannot be used (directly) to produce electrical energy.</p>\n<hr />\n<p>In a <a href=\"http://news.stanford.edu/news/2010/april/electric-current-plants-041310.html\" rel=\"nofollow noreferrer\">Standford university research</a> they did successfully harvest electrictity from photosynthesis:</p>\n<blockquote>\n<p>The Stanford research team developed a unique, ultra-sharp\nnanoelectrode made of gold, specially designed for probing inside\ncells. They gently pushed it through the algal cell membranes, which\nsealed around it, and the cell stayed alive. From the\nphotosynthesizing cells, the electrode collected electrons that had\nbeen energized by light and the researchers generated a tiny\nelectrical current.</p>\n</blockquote>\n<p>But it goes on to say:</p>\n<blockquote>\n<p>Ryu said they were able to draw from each cell just one picoampere, an\namount of electricity so tiny that they would need a trillion cells\nphotosynthesizing for one hour just to equal the amount of energy\nstored in a AA battery. In addition, the cells die after an hour.</p>\n</blockquote>\n<p>So this is be no means practical at the moment</p>\n"
},
{
"answer_id": 23896,
"pm_score": 1,
"text": "<p>Another alternative is using plants to generate biomasse using photosynthesis and letting bacteria convert that into electricity.</p>\n\n<p>There is research being done about this method and you can read more about it on the following websites:</p>\n\n<ul>\n<li><a href=\"http://www.plantpower.eu/\" rel=\"nofollow\">http://www.plantpower.eu/</a></li>\n<li><a href=\"http://plant-e.com/technology.html\" rel=\"nofollow\">http://plant-e.com/technology.html</a></li>\n</ul>\n"
},
{
"answer_id": 23923,
"pm_score": 0,
"text": "<p>Everyone's looking at photosynthesis for direct energy conversion, but it's not the only approach. Another function of most plants is to pump water up to altitude, to serve its own needs. </p>\n\n<p>Tap into that - picking plants where the sap is watery, not inconveniently sticky like maple syrup, resinous, or likely to congeal into rubber, and you have at least hypothetically, the potential for micro hydro power...</p>\n\n<p>I'm making no claims for energy density or efficiency.</p>\n"
},
{
"answer_id": 24146,
"pm_score": 1,
"text": "<p>I can highly recommend Prof David MacKay's online book <a href=\"http://www.withouthotair.com/\" rel=\"nofollow\">http://www.withouthotair.com/</a>\nwhere puts things into perspective. You can find him on YouTube and TED too.</p>\n\n<p>e.g. <a href=\"http://www.withouthotair.com/c18/page_103.shtml\" rel=\"nofollow\">http://www.withouthotair.com/c18/page_103.shtml</a> \"Can we live on renewables\"</p>\n\n<pre><code>POWER PER UNIT LAND OR WATER AREA\nWind 2 W/m2\nOffshore wind 3 W/m2\nTidal pools 3 W/m2\nTidal stream 6 W/m2\nSolar PV panels 5-20 W/m2\nPlants 0.5 W/m2\nRain-water\n (highlands) 0.24 W/m2\nHydroelectric\n facility 11 W/m2\nGeothermal 0.017 W/m2\n</code></pre>\n\n<p>Table 18.10. Renewable facilities have to be country-sized because all renewables are so diffuse.</p>\n\n<p>So it doesn't look good for plants as direct energy source (except for food) (in UK at least)...(or most renewable things for that matter).</p>\n\n<p>Essential reading for anyone interested in energy.</p>\n"
}
] |
24,090 |
<p>Corneas are donated and transplanted, but not the eyeball. </p>
<p>I don't understand. What is the purpose of donating a cornea without an eyeball to a blind person?</p>
|
[
{
"answer_id": 24101,
"pm_score": 4,
"text": "<p>No-one can re-implant an entire eye, because the optic nerve has been severed in one who has lost an eye. A cornea can't be grafted to a glass eye. But blindness isn't only caused by loss of the entire orbit. It's also caused by cloudy corneas, which is the purpose of eye-banks.</p>\n\n<p>The optic nerve is a cable of nerve fibers that carry visual information from the eye to the brain. In adult mammals, any damage to the optic nerve caused by injury or disease tends to be permanent, because the cells that form the optic nerve cannot regenerate. Any injury or disease that involves optic nerve damage can lead to permanent loss of vision. Obviously the loss of an eye would sever the optic nerve.</p>\n\n<p>However, if the future holds success for optic nerve regeneration, it would also open the door for entire-eye transplantation. In which case, a new cornea might come in handy.</p>\n"
}
] |
[
{
"answer_id": 24092,
"pm_score": 2,
"text": "<p>The eyeball is basically the sclera that surrounds the delicate inner structures of the eye (<a href=\"http://en.wikipedia.org/wiki/Eye\" rel=\"nofollow\">see wiki on the eye</a>). The cornea is the transparent window in front of the pupil that transmits light to the retina. It needs replacement when it turns opaque, often due to damage or infections. The cornea can be replaced on its own, without the need for transplanting other tissues of the eye, as an opaque or otherwise damaged cornea does not necessarily mean that other structures of the eye are damaged. If the light-sensitive parts are damaged, including the exceptionally rare case that the entire eye ball is missing, corneal transplants have obviously no use.</p>\n\n<p>Eye banks are necessary to properly retrieve and store eyes. They extract, preserve, and dispatch corneas when necessary (<a href=\"http://en.wikipedia.org/wiki/Eye_bank\" rel=\"nofollow\">eye bank wiki</a>).</p>\n"
},
{
"answer_id": 24105,
"pm_score": 4,
"text": "<p>You are asking two questions that you think are connected but are actually not.</p>\n\n<blockquote>\n <p>Question 1 - What is the use of eye banks?</p>\n</blockquote>\n\n<p>Answer: It's to store corneas for transplant for people with cornea damage.</p>\n\n<blockquote>\n <p>Question 2 - What use is cornea transplant to a completely blind person?</p>\n</blockquote>\n\n<p>Answer: It depends. If the blindness is due to clouded cornea (several diseases cause this) then replacing the cornea will reverse the blindness. If the blindness has other causes then cornea transplant is of no use to the person.</p>\n"
},
{
"answer_id": 24109,
"pm_score": 4,
"text": "<p>I used to work at an eye bank so I have a bit of knowledge about this, though some of it may be out of date.</p>\n\n<p>There are several aspects to an eye bank. The corneas are one of the primary things that are kept for transplantation. Of course, this will not repair blindness in someone that has problems in other areas of the eye, but corneal transplants are helpful for people who have corneal damage for one reason or another (such as a foreign object, age, or disease damaging the cornea.)</p>\n\n<p>Beyond this, small parts of the sclera (the white part of the eye) are also sometimes used to patch damage (though generally this is not because of unexpected trauma, but because of reconstruction from other surgeries, such as valve implantation because of glaucoma.)</p>\n\n<p>Finally, of course, many people would not understand what the purpose of the organization was if it was called a \"Cornea Bank\". \"Eye Bank\" is more descriptive.</p>\n"
},
{
"answer_id": 24118,
"pm_score": 2,
"text": "<p>In addition to providing tissue for transplant, eye banks also provide tissue from all parts of the eye to medical schools and universities for teaching and research purposes. There are many medically relevant questions that can only be answered by examining human tissue, and eye banks facilitate this research.</p>\n"
},
{
"answer_id": 24119,
"pm_score": 2,
"text": "<p>It seems to me that really your whole question seems to be much simpler than it seems and it is just</p>\n\n<p>\"why are eye banks called eye banks when they can't transplant eyes, just bits of them like corneas\"</p>\n\n<p>The answer is:</p>\n\n<p>In the english language and in various cultures, the names of things often have a loose and not entirely accurate relationship to the product at question. For example a person might be a screw loose mentally but that doesn't mean a physical screw, etc, etc.</p>\n\n<p>English is not a consistent scientific logical language for describing the world.</p>\n"
}
] |
24,126 |
<p>Does each cell contain only a single copy of its genome? Or are there ever 'extra' copies present. </p>
<p><strong>Reason behind question</strong>: <em>Wondering whether gene mutations could be corrected by referencing a 'backup copy'.. If such a thing exists..</em></p>
|
[
{
"answer_id": 24127,
"pm_score": 5,
"text": "<p>As a quick answer, yes, most human cells carry 2 copies of the genome and are known as <a href=\"http://en.wikipedia.org/wiki/Ploidy#Diploid\">diploid</a> cells. One copy comes from each of your parents, so they aren't identical, but usually pretty close. Sperm and egg cells only carry one copy of the genome and are known as <a href=\"http://en.wikipedia.org/wiki/Ploidy#Haploid_and_monoploid\">haploid</a>. During fertilization the 2 cells merge their copies and make a diploid zygote. At the <a href=\"http://en.wikipedia.org/wiki/Chromosome#Human_chromosomes\">chromosomal</a> level, humans have 23 chromosomes, so a diploid cell has 2 copies of each so a total of 46.</p>\n\n<p>As far as repairing damaged DNA, using one chromosome to repair its damaged counterpart is known as <a href=\"http://en.wikipedia.org/wiki/Homologous_recombination\">Homologous Recombination</a>.</p>\n"
}
] |
[
{
"answer_id": 24128,
"pm_score": 3,
"text": "<p>Diploid cells contain two copies of the genome. Additionally, each copy of the genome can have multiple copies of certain genes. Which can provide a level of protective redundancy.</p>\n\n<p>However, there are a number of potential problems with having multiple copies of portions of the genome such as trisomy disorders (e.g. Down Syndrome). Which is why therapy like you describe is still highly experimental.</p>\n"
},
{
"answer_id": 24139,
"pm_score": 3,
"text": "<p>Addition to other answers.</p>\n\n<p>Usually a human cell is diploid. Sometimes there might be extra copies of a chromosome and this phenomenon is called aneuploidy (Downs Syndrome, Klinefelter's syndrome etc). This always has deleterious effects because of changes in stoichiometries of different gene products (dosage effect). </p>\n\n<p>Some other organisms also tolerate polyploidy (more than two copies of the entire genome) — salamanders and a lizard whose name I can't remember right now.</p>\n\n<p>Would an extra copy help in providing a functional gene when the other copy is mutated?</p>\n\n<p>Yes and it is the case with all recessive mutations. The effect of loss of function is not seen because the other allele is providing a functional copy (sometimes the dosage is reduced and it affects the system in subtle ways).</p>\n\n<p>However, it the mutation is dominant then extra copies won't help much. For example, a mutation that leads to the formation of a toxic or hyperactive protein (gain of function), then extra copies may at best reduce the overall relative concentration of the bad allele but cannot eliminate its ill effects. </p>\n"
},
{
"answer_id": 24148,
"pm_score": 2,
"text": "<p>To address the \"reason behind the question\" - no, this doesn't work as you seem to assume it does. It is the whole point of sexual reproduction to have two slightly different copies of the genome. Mutations are not \"corrected\" within an organism, because they are not considered a bad thing per se. Mutations are \"corrected\" across generations, in the sense that maladaptive mutations are selected out of the gene pool, because their carriers don't manage to reproduce well. </p>\n\n<p>If there were a mechanism in the cell which would decide that \"this copy of the genome is 'correct', this is 'incorrect', I will replace all differing places in the 'incorrect' copy with the information from the 'correct' copy\", evolution would never have happened. </p>\n\n<p>An individual has two genome copies, and each of them gets transcribed from. If one of them contains a mutation with negative effects, then it's bad luck for the individual. The purpose of the two genome copies is to increase genetic variability, not to reduce it. </p>\n"
},
{
"answer_id": 24507,
"pm_score": 1,
"text": "<p>Most of the above answers are incorrect.</p>\n\n<p>The definition of the genome is all of the encoding genetic material. An individual human genome includes two full sets of 23 chromosomes as well as mitochondrial DNA. There is one copy of this genome in most human cells. A few exceptions:</p>\n\n<ul>\n<li>Red blood cells don't have nucleuses and have no chromosomes. They don't have a copy of the genome.</li>\n<li>Human sperm cells have only one set of 23 chromosomes. This is not the complete genome of the individual.</li>\n<li>Despite comments above, human egg cells have a full two sets of chromosomes until ovulation. The fertilized zygote gets one set of chromosomes from an egg cell and one set from a sperm cell. However, the actual egg cell in the ovaries has a full two sets of chromosomes which don't all get transferred to the zygote.</li>\n<li>There is genetic variation between cells due to damage and copying mistakes.</li>\n<li>Some living humans are chimeric and are often unaware of this. They are individuals formed from distinct egg/sperm combinations. That adds extra complexity to this answer.</li>\n</ul>\n"
}
] |
28,177 |
<p>Lately I have seen a number of unrelated "scientific" debates over whether certain substances should be outlawed because they are toxic to humans. My initial, informal reaction is usually to respond that anything is toxic to humans if you give them a sufficiently large dose.</p>
<p>However, formally I don't know if that's really true for <em>everything</em> a human being could ingest in some way. I started to wonder if there were some substances that our body could handle unlimited amounts of without any negative consequences.</p>
<p>As this question has been (correctly) identified as a bit vague, I'll try to explain what i'm looking for. For the purposes of this question, I'm willing to ignore the limitations of actually ingesting a given substance in "the usual way". For example, if you can't physically drink enough of some liquid fast enough to kill you without your stomach filling up and vomiting, but that same liquid injected intravenously <em>could</em> be lethal, I could consider that toxic. I also recognize that the body can only physically contain a certain volume of stuff, after which sheer pressure would cause it to fail; I'm more interested in "biochemical toxicity" as opposed to any physical damage (I just don't know the term for what I'm looking for.)</p>
<p>In other words, one of my goals is to learn if, under laboratory conditions, a properly motivated researcher could <em>always</em> find a dose that would be toxic, regardless of the impracticality of a real person ingesting that dose under normal circumstances.</p>
<p>So, with that qualification, my ultimate question is:</p>
<p><strong>Is there any substance we know of that is completely non-toxic to humans at arbitrarily large doses ingested over an arbitrarily short period of time?</strong></p>
|
[
{
"answer_id": 28179,
"pm_score": 6,
"text": "<p>I’ll answer this theoretically, since that’s how it has been posed. And if we’re ignoring practicalities, we may as well posit that the substance in question will be introduced directly into the bloodstream (This is, of course, simple to do in reality, but not how most people consume their non-toxic substances.) The easiest way to show that any unspecified substance can be toxic at an unlimited volume is to invoke the human body’s mechanisms for volume homeostasis.</p>\n\n<p>As mentioned in <a href=\"https://biology.stackexchange.com/a/24406/9268\">this answer</a>, the human kidneys functioning optimally can produce up to ~ 25 L/day of urine.<sup>1</sup> This would require complete suppression of <a href=\"http://en.wikipedia.org/wiki/Vasopressin\" rel=\"nofollow noreferrer\">ADH</a> (anti-diuretic hormone, a.k.a. arginine vasopressin), which would occur only if the “toxin” load were markedly hypotonic (think water).<sup>2</sup> There is therefore a theoretical maximum <strong>volume</strong> of any substance that can be dealt with by the body, which is something less than 25 L per day. (For any substance <em>other than</em> water, the maximum will be lower because ADH will not be as fully suppressed by a less hypotonic load.) </p>\n\n<p>A volume of any substance introduced into the bloodstream (including a product precisely mimicking the constituents of the bloodstream itself!) will overwhelm the body’s homeostatic mechanism. This will result in edema which is unpleasant and, in the case of <a href=\"http://www.nlm.nih.gov/medlineplus/ency/article/000140.htm\" rel=\"nofollow noreferrer\">pulmonary edema</a>, certainly pathologic - a “toxidrome” in your scenario. In the case of hypotonic fluids, serum osmolality will also fall causing <a href=\"http://en.wikipedia.org/wiki/Hyponatremia\" rel=\"nofollow noreferrer\">hyponatremia</a> with all of its consequences.</p>\n\n<p><strong>Summary</strong>: No, the human body can not tolerate an unlimited volume of anything, therefore there is no substance that is non-toxic \"at any dose.\" </p>\n\n<hr>\n\n<p><sub>\n1. Christopher Lote. (2012). Principles of Renal Physiology. Springer New York.\n</sub> </p>\n\n<p><sub>\n2. No, you may not drink 25 liters of water per day. For one thing, urine can not be made with a tonicity of 0 to balance this (more like 60 mOsm/kg minimum). Additionally, ADH can rarely be completely suppressed, yielding a somewhat more concentrated urine and therefore lower tolerance for hypotonic intake before serum osmolality is compromised.\n</sub></p>\n"
}
] |
[
{
"answer_id": 28178,
"pm_score": 3,
"text": "<p>There is a problem with definition of toxicity — things that are dangerous in large amounts aren't usually called toxic. In spite of this, you're right: everything can be dangerous to a human in large enough amounts, or if delivered improperly.</p>\n\n<p>For example, <a href=\"https://en.wikipedia.org/wiki/Water_intoxication\" rel=\"noreferrer\">even water can be toxic if drank too much</a>. Also, when it gets into the lungs, it may cause drowning.</p>\n\n<p>On the other hand, air, while necessary in lungs, is dangerous if present as a gas in the bloodstream.</p>\n\n<p>BTW, even botox (being one of the strongest poisons) <a href=\"https://en.wikipedia.org/wiki/Botulinum_toxin\" rel=\"noreferrer\">is used in medicine in very small doses</a>.</p>\n"
},
{
"answer_id": 28182,
"pm_score": 4,
"text": "<p>It depends largely on the method of administration. If you are atomizing the substance and delivering it via water vapor, many, many substances have no known LDLo (lowest dose required to kill a member of the tested population). Almost any substance in existence has the potential to kill you if it is diluting your bloodstream via direct intravenous injection or oral consumption; however, when it comes to inhalants, many substances cannot kill you. </p>\n\n<p>Since your question was specific to intoxicants, here's a couple of examples: There is no LDLo level of Tetrahydrocannabinol (the active ingredient in marijuana) when delivered via atomization. There is also no known LD50 (a similar, albeit somewhat less reliable, metric) for lysergic acid diethylamide (commonly referred to as LSD). For psilocybin (the active ingredient in \"magic mushrooms\"), the LD50 is high enough that an average person would need to ingest around 6 pounds before cause for concern.</p>\n\n<p>Other far more dangerous substances that can kill with vastly lower amounts include anything that speeds or slows the heart rate: most specifically, cocaine (including crack), opiates (including morphine, heroin, and various pain pills), and any amphetamine, methamphetamine or derivative substance, or other stimulant (crystal meth, ADHD medication, and even caffeine or ephedrine). Of course, the most common killer categorically from a historical perspective is alcohol.</p>\n"
},
{
"answer_id": 28193,
"pm_score": 2,
"text": "<p>The inert gasses Helium and Neon are non-toxic when administered through inhalation, so long as the patient's oxygen supply is sufficient. They are also non-toxic when injected, so long as the injection is slow enough for them to be dissolved in the bloodstream.</p>\n\n<p>You can be killed by them through various means (asphyxiation through oxygen displacement, rapid injection causing an air embolism, rapid decompression causing decompression sickness, and so on), but since the cause of death is unrelated to the chemical properties of the substance involved, it's not accurate to call this \"toxicity\" (unless you're <a href=\"http://xkcd.com/1260/\" rel=\"nofollow\">XKCD</a>).</p>\n\n<p>Other inert gasses (Argon, Krypton, Xenon) may be toxic at high pressures: although I haven't found an LD50 for any of them, they can all induce <a href=\"https://en.wikipedia.org/wiki/Nitrogen_narcosis\" rel=\"nofollow\">nitrogen narcosis</a>, and Xenon is usable as a general anesthetic.</p>\n"
},
{
"answer_id": 28195,
"pm_score": -1,
"text": "<p>Vitamin C won't kill you no matter how much you get into your body as long as it is enough to help prevent arterial wounds and atherosclerosis(This happens in people with scurvy or vitamin C deficiency because of how cholesterol is used to help repair the wounds and this can lead to a complete blockage of the artery and thus an infarction of all the tissue that artery supplies. So if you don't want to have an MI, one of the things you have to do is get vitamin C into your system. </p>\n\n<p>Another example of this is chloride ions. While having high chloride ions might cause there to be a slower reaction time(since chloride acts as an inhibitor in neurons) it itself won't kill you. Yes it might affect the muscles by not having them contract as much as they are supposed to but this is naturally cured by urinating out more chloride and thus more sodium which can lead to a sodium deficiency which is bad because your body needs sodium in order to function. With a low amount of it it you wouldn't be able to think clearly or even have a normal heart rhythm which might lead to bradycardia from a higher pottasium concentration in the heart. </p>\n"
},
{
"answer_id": 28199,
"pm_score": 2,
"text": "<p>not even AIR, because if you force too much you will explode it depends on how extreme is the \"any dose\" statement</p>\n\n<p>water is also toxic in large Ingestible amounts</p>\n\n<p>and since we go into theoretical application the answer would be dark matter </p>\n\n<p>so the final answer is nothing , because the human body has evolved to exist in some equilibrium, so too much of one thing even if is harmless it itself ( like water, or proteins ) it causes an imbalance, and as a result it becomes \"toxic\"</p>\n"
},
{
"answer_id": 28206,
"pm_score": 1,
"text": "<p>Even simple water is \"toxic in high amounts\" as kidneys can remove 25 l per day at most. All other substances are probably even more \"toxic\".</p>\n"
},
{
"answer_id": 58914,
"pm_score": -1,
"text": "<p><sub>This is not really a substance, but anyway.</sub></p>\n<h1>Neutrino</h1>\n<p>Neutrinos are ghostly particles that barely interact with any matter. Therefore, no sufficient amount of neutrino (that human can ever collect) can kill you. To have a lethal dose of neutrino radiation, you must stand <strong>inside</strong> the outer layout of a giant star that creates a supernova.</p>\n<p>Source: XKCD, <a href=\"https://what-if.xkcd.com/73/\" rel=\"nofollow noreferrer\">Lethal Neutrinos</a></p>\n"
}
] |
29,679 |
<p>Does the brain really function like a computer as in, ultimately every response is related to a binary sequence based on whether particular neurons fire or not?</p>
|
[
{
"answer_id": 29685,
"pm_score": 5,
"text": "<p>First of all, I would like to point out that making analogy between digital computers and the brain is often very misleading.</p>\n\n<p>That being said, my answer is, some scientists believe so, some don't.</p>\n\n<p>Several things to consider:</p>\n\n<ol>\n<li><p>Some neural systems are not spiking. C. elegans for example has a nervous system that is entirely analogue. Human nervous system also contains neurons with graded responses (mostly in the sensory front-end though).</p></li>\n<li><p>Spiking neurons may be binary at each time point, but time itself is continuous. Firing at 0.003 seconds later can represent something different. (in contrast to the usual synchronous digital architecture of computers)</p></li>\n<li><p>The neuron doctrine is sometimes challenged. Glial cells that do not fire may have important functions for information processing. See:</p>\n\n<ul>\n<li>Bullock, T. H., Bennett, M. V. L., Johnston, D., Josephson, R., Marder, E., and Fields, R. D. (2005). The neuron doctrine, redux. Science, 310(5749):791-793.</li>\n</ul></li>\n</ol>\n"
}
] |
[
{
"answer_id": 29734,
"pm_score": 3,
"text": "<p>While action potentials are usually binary, you should note that <a href=\"http://en.wikipedia.org/wiki/Synapse\">synaptic communication</a> between neurons is generally not binary. Most synapses work by <a href=\"http://en.wikipedia.org/wiki/Neurotransmitter\">neurotransmittors</a>, and this is a chemically mediated <a href=\"http://en.wikipedia.org/wiki/Postsynaptic_potential\">graded response</a> that, for example, act on <a href=\"http://en.wikipedia.org/wiki/Voltage-gated_ion_channel\">voltage-gated ion channels</a>. So even though action potentials are often binary, communication between neurons are most often not, and action potential firing can involve the integration of synaptic information from many different neurons. Therefore, the brain as a whole cannot be reduced to a binary system.</p>\n\n<p>See this as a complement to @Memmings answer.</p>\n"
},
{
"answer_id": 29897,
"pm_score": 0,
"text": "<p>as far as I know the brain processes data in stages the neurons themselves are not purely binary as in a computer in that every action has a predetermined output. the neuron response tends to be goverened by sigmoid function output and hence the use of this function in artificial neural networks. further, the synapses have strengths that is depended on the amount of neurotransmitter in there which obviously varies from cell to cell and even in the same cell and hence one speaks of the probability of a neuron firing given a certain stimulus. additionally the neurons from sensory organs fire pulses at a frequency that increases with the strength of the stimulus. furthermore, the data from sensors is processed in layers of neurons lower layers have rapidly firing neurons whule higher layers fire at much lower rates.</p>\n\n<p>you also have to consider the fact that the brain is actually a complicated network of \"recurrent\" neurons meaning that the output is fedback as an input and this is different from simple computer gates such as AND gates or XOR gates it is similar to counters may be but obviously on a very bigger scale. one more point is that recurrent neural networks have built in memory that enables the pattern recall and recognition and so the study of the brain as a binary system is very complicated and will fail to explain how the brain works.</p>\n\n<p>on the macro scale the human brain operates as a bayesian inference engine more or less I mean when it comes to thinking and inference i.e. it relies on probabilities and knowledge gained from past experiences to deal with current problems and new data</p>\n"
},
{
"answer_id": 39041,
"pm_score": 2,
"text": "<p>John vonNeumann, the famous computer scientist, tackled this idea in his last book, 'The Computer and the Brain.' He personally landed on the side of the brain being a binary system, due to the behavior of neurons which either fire or do not fire.</p>\n\n<p>While that is an important observation, and will have significant consequences to people trying to create artificial brains within computer systems, I think a more important observation has to do with computational complexity. It is very easy to build systems which, at least theoretically, have the potential to be universal computers. From that fact, it is fairly trivial to see that whatever definitions you choose to work with in terms of brain input and output (sensory nerve cells feeding electrical impulses from organs of perception being a possible definition of 'input' and propagated impulses to muscles, or changes in the neural structure itself being possible definitions of 'output' for example), yes it is possible to construct a binary system which can perform the same calculations as a human brain.</p>\n\n<p>However, there is a catch. Because it is impossible to perfectly know the complete state of the brain, and because any degree of inaccuracy in the starting state of the binary system, no matter how small, will cause the behavior of the binary system to diverge completely from the behavior of the specific brain being modelled, it is reasonable to say that no particular individual brain can be reduced to a binary system.</p>\n"
},
{
"answer_id": 86471,
"pm_score": -1,
"text": "<p>human brain is strictly digital device using defined action potentials (0 volt as logical 0 and specified (fixed) voltage potential as logical 1). these two potentials work same way as complex logic gates systems. brain processes all types of analog-like variations (signal amplitude or response strength) as very short time based sums of logic gates operations. there is no other applicable description of brain functionality</p>\n"
},
{
"answer_id": 86476,
"pm_score": 0,
"text": "<p>It's theoretically possible, because all information can be well approximated/copied in binary, and it's\npractically impossible because of size, energy, and program size/depth.</p>\n\n<p>A fly brain is <1mm wide and an intel fly brain equivalent is >1000mm wide... much slower than the fruit fly. (Thats why flies see your hand coming in slow-mo). </p>\n\n<p>This intel chip has as many neurons as a slug, far less than a fly:\n<a href=\"https://www.cnet.com/google-amp/news/intel-packs-8-million-digital-neurons-onto-brain-like-pohoiki-beach-computer-loihi-chips/\" rel=\"nofollow noreferrer\">https://www.cnet.com/google-amp/news/intel-packs-8-million-digital-neurons-onto-brain-like-pohoiki-beach-computer-loihi-chips/</a></p>\n\n<p>he binary model has to include \"chemical modelling\" and \"physical modelling\" like a graphics card which models light and creatures as binary.</p>\n\n<p>Except that there is an added issue: processing speed. The brain can grow direct connections which are very fast. Silicon signals have to travel 1000 times further for every calculation.</p>\n\n<p>2d chips take as much space as a skyscraper and a small nuclear station for energy, and future mythical 3d transistors would take space and would be slower because they require direct chemical processing and flexible internal connection to be as fast. </p>\n\n<p>AI is very performant and is one of the future paradigm changes like \"internet/mobile phone / electric car / AI \"</p>\n"
}
] |
29,795 |
<p>How does a virus like HIV mutate into so many strains, and yet all of them are harmful to our immune system? What gives this virus the ability to mutate so efficiently?</p>
|
[
{
"answer_id": 29960,
"pm_score": 3,
"text": "<p>Others have already touched the important points. Consider this as a summary.</p>\n\n<blockquote>\n <p>What gives HIV the ability to mutate?</p>\n</blockquote>\n\n<p>All organisms mutate by two mechanisms:</p>\n\n<ol>\n<li>Replication errors</li>\n<li>Mutagenesis by physical/chemical agents that cause a chemical change\n(lesion) on DNA</li>\n</ol>\n\n<p>The main enzyme responsible for HIV replication is <strong>reverse transcriptase</strong> which makes a DNA copy of its RNA genome. All RNA and DNA polymerases make some amount of error but the error rate of reverse transcriptase is much higher than usual DNA-dependent DNA polymerases because it does not have a proofreading mechanism. </p>\n\n<blockquote>\n <p>How does a virus like HIV mutate into so many strains, and yet all of\n them are harmful to our immune system?</p>\n</blockquote>\n\n<p>As indicated in previous answers, the mutations will produce a virions with a spectrum of infectivity/pathogenicity (some can even be non-infective).\nHowever, the immune system acts as a selective barrier which selects only those mutants that can survive (similar to what happens in evolutionary process of natural selection). The selected strains expand their population and that is how these strains get established.</p>\n"
}
] |
[
{
"answer_id": 29796,
"pm_score": 2,
"text": "<p>Viral recombination produces genetic variation that contributes mostly to the evolution of the HIV-1 virus.</p>\n\n<p>HIV being an RNA Virus utilizes an enzyme called reverse transcriptase, which produces DNA from RNA. HIV also has <strong>two</strong> RNA genomes. After infection and then replication, which is catalyzed by reverse transcriptase, recombination between the two genomes can occur. specifically the single-strand (+)RNA genomes are reverse transcribed to form DNA. Then during this reverse transcription the nascent DNA can switch multiple times between the two copies of the viral RNA and multiple recombination occur throughout the genome. Furthermore, multiple events per genome may occur during each replication cycle, thus compounding the mutation. </p>\n"
},
{
"answer_id": 29799,
"pm_score": 1,
"text": "<p>Simple answer is that those mutations that create inactive virus, will never show up on screen, since it will be asymptomatic. In same fashion if virus loses its ability to infect new target (via sexual contact or blood directly) it will show up only in first victim, so that effectively be a non-problem for society.</p>\n\n<p>Addendum: I think I answered portion, starting with \"and yet...\", which seems to be most important in the question. I think that exact mechanism of mutagenesis must be covered in literature, if known. Also, it seems that since there are no vaccine for HIV, it's mutagenesis cannot be really \"efficient\", since it is not actively fighting anything.</p>\n"
},
{
"answer_id": 29800,
"pm_score": 2,
"text": "<p><strong>What gives HIV the ability to mutate?</strong></p>\n\n<p>HIV is a single standed RNA virus. DNA is much more stable than RNA as it has a stronger backbone and it is typically double stranded. But HIV mutates at a rate far higher than just being a RNA virus. That's because it uses an enzyme called reverse transcriptase (RT) to build it's RNA genome from RNA bases.</p>\n\n<p>RT is meant to copy the old HIV and make a new one but it does a rubbish job. Most the time it copies it well but every now and then (3 x 10<sup>−5</sup> per nucleotide base) it puts in a random base. That might seem like a small rate but that's HUGE if that was coding our genome we would die (if we ever even lived). And since HIV's replication rate is enormously high, there's always going to be a range of good and junk HIV (but it's mostly just junk - next answer for why that's not a bad thing).</p>\n\n<p>But that's not all, RT doesn't just use one old HIV to make a new one. It can use several different old HIVs to make a new one that's not only a combination of all the other ones but then add in the mutations from above, completely different. </p>\n\n<p><strong>So I get that there's lots of mutated strains all over the place. Surely that'd make them useless because the mutations are random?</strong></p>\n\n<p>Yeah they are random and yes that does mean some virus particles are useless. But it's very variable. There's ones which are greatly infectious, partly infectious, slightly infectious and basically junk. The body doesn't really know which ones are which and that's the beauty of it all. The body tries to fight all of them and has no clue which one to get. If it happens to target the greatly infectious one, the numbers of this go down but then the partly infectious one will become the most infectious one and the cycle continues. The junk HIV is basically just a sticky pool of most of the HIV particles that just gets the immune system going crazy and diverts it from the real threat.</p>\n"
},
{
"answer_id": 51886,
"pm_score": 0,
"text": "<p>First, you have to keep in mind that patients are not infected with a single strain. Because HIV is a chronic disease, and given its rapid mutation rate, it has enough time to evolve into a pool of enormous strains called \"quasi species\". So the virulence manifested is not virulence of individual strain, but the overall virulence of the quasi species.</p>\n\n<p>Actually, because of its high mutation rate, HIV produces many failure strains. These strains are even unable to replicate and account for around half of its progenies! So they're certainly avirulent. But these progenies will die out very soon. However, HIV makes billions of copies per day. So there will always be fully replication competent and fully virulent strains. That's how its virulence sustains. So patients will always develop AIDS if left untreated.</p>\n\n<p>Also, HIV may produce progenies with varying virulence. But the overall virulence is not determined by a single strain. And our immune system may serve as a natural selection. Only strains with good replication efficiency and immune evasion ability can survive. This may also explain how the virulence sustains.</p>\n\n<p>Actually, there're a few people infected with Nef deficient HIV mutants. Nef is an accessory gene. HIV without it can still replicate but cause much milder disease. However, Nef is crucial to the immune evasion mechanism of HIV. So HIV strains without it are more likely be out competed by fully virulent ones.</p>\n\n<p>I think influenza is another example. Influenza is also rapidly mutating, but its virulence varies greatly. From highly pathogenic avian flu to mild seasonal flu. I think the reason is that influenza don't cause chronic infection, so they don't generate quasi species, and there's no natural selection process. That's why the virulence of influenza fluctuates greater. Warning, this is just my guess.</p>\n"
}
] |
30,116 |
<p>Does DNA have anything like IF-statements, GOTO-jumps, or WHILE loops?</p>
<p>In software development, these constructs have the following functions:</p>
<ul>
<li><strong>IF-statements:</strong> An IF statement executes the code in a subsequent code block if some specific condition is met.</li>
<li><strong>WHILE-loops:</strong> The code in a subsequent code block is executes as many times as specified, or as long as a specific condition is met.</li>
<li><strong>Function calls:</strong> The code temporarily bypasses the subsequent code block, executing instead some other code block. After execution of the other code block the code returns (sometimes with some value) and continues the execution of the subsequent block.</li>
<li><strong>GOTO-statements:</strong> The code bypasses the subsequent code block, jumping instead directly to some other block.</li>
</ul>
<p>Are constructs similar to these present in DNA? If yes, how are they implemented and what are they called?</p>
|
[
{
"answer_id": 30120,
"pm_score": 8,
"text": "<p>Biological examples similar to programming statements:</p>\n\n<ul>\n<li><code>IF</code> : Transcriptional activator; when present a gene will be transcribed. In general there is no termination of events unless the signal is gone; the program ends only with the death of the cell. So the <code>IF</code> statement is always a part of a loop.</li>\n<li><code>WHILE</code> : Transcriptional repressor; gene will be transcribed until repressor is not present.</li>\n<li>There are no equivalents of <code>function</code> calls. All events happen is the\nsame space and there is always a likelihood of interference. One can\nargue that organelles can act as a compartment that may have a\n<code>function</code> like properties but they are highly complex and are\nnot just some kind of input-output devices.</li>\n<li><code>GOTO</code> is always dependent on a condition. This can happen in case of certain network connections such as feedforward loops and branched pathways. For example if there is a signalling pathway like this: <br> <strong>A → B → C</strong> and there is another connection <strong>D → C</strong> then if somehow <strong>D</strong> is activated it will directly affect <strong>C</strong>, making <strong>A</strong> and <strong>B</strong> dispensable. </li>\n</ul>\n\n<p>Logic gates have been constructed using synthetic biological circuits. See <a href=\"http://www.nature.com/nrg/journal/v16/n3/abs/nrg3885.html\" rel=\"noreferrer\">this</a> review for more information. </p>\n\n<hr>\n\n<h2>Note</h2>\n\n<p>Molecular biological processes cannot be directly compared to a computer code. It is the underlying logic that is important and not the statement construct itself and these examples should not be taken as absolute analogies. It is also to be noted that DNA is just a set of instructions and not really a fully functional entity (it is functional to some extent). However, even being just a code it is comparable to a HLL code that has to be compiled to execute its functions. See <a href=\"https://biology.stackexchange.com/questions/29663/can-dna-rna-be-considered-as-natures-programming-language\">this</a> post too.</p>\n\n<p>It is also important to note that the cell, like many other physical systems, is analog in nature. Therefore, in most situations there is no 0/1 (binary) value of variables. Consider gene expression. If a transcriptional activator is present, the gene will be transcribed. However, if you keep increasing the concentration of the activator, the expression of that gene will increase until it reaches a saturation point. So there is no digital logic here. Having said that, I would add that switching behaviour is possible in biological systems (including gene expression) and is also used in many cases. Certain kinds of regulatory network structures can give rise to such dynamics. Co-operativity with or without positive feedback is one of the mechanisms that can implement switching behaviour. For more details read about <a href=\"https://en.wikipedia.org/wiki/Ultrasensitivity\" rel=\"noreferrer\">ultrasensitivity</a>. Also check out \"<a href=\"https://biology.stackexchange.com/q/30588/3340\">Can molecular genetics make a boolean variable from a continuous variable?</a>\"</p>\n"
}
] |
[
{
"answer_id": 30117,
"pm_score": 4,
"text": "<p>There are certainly some comparisons that could be made between the way genes are expressed from DNA and logic functions, but they aren't great.</p>\n\n<p>But synthetic Biology is really a blossoming new field that is attempting to integrate logic functions into biology, see e.g. <a href=\"http://www.nature.com/nbt/journal/v31/n5/abs/nbt.2510.html\" rel=\"nofollow noreferrer\" title=\"Siuti et al. 2013. Synthetic circuits integrating logic and memory in living cells. Nature Biotechnology 31, 448–452. doi:10.1038/nbt.2510\">Siuti et al (2013)</a>.</p>\n\n<p>The above paper is a brilliant example of a group using bacteria to store information and assembling into biological circuits that can then be used to process logic functions. So its being done but not exactly in the way that you propose.</p>\n"
},
{
"answer_id": 30124,
"pm_score": 4,
"text": "<p>As WYSIWYG said there is no equivalent for function calls, as there will always be some interference. However one could argue that some modular pathways (eg. apoptosis signalling) can be seen as a \"code block\" where a certain input will (almost) certainly lead to a certain effect. The analogy with function calls is that, in describing many different mechanisms, it makes for shorter and more efficient \"code\" to consider everything between eg. caspase activation and cytochrome leakage as one block. Also, marking a protein with ubiquitin can maybe be seen as a function call for degradation.</p>\n\n<p>If you are interested in the building blocks for programming with biology, check out the biobricks.org program, which aims to define modular parts (bricks) which can be sensors, logic functions, effectors,...</p>\n"
},
{
"answer_id": 30126,
"pm_score": 4,
"text": "<p>Just to add to previous answers, but <strong>transcriptional interference</strong> (see e.g. <a href=\"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2941638/\">Shearwin et al., 2005</a>) can be seen as a form of IF-statement (or WHILE) in the sense that:</p>\n\n<pre><code>if(x transcribed){not y transcribed}\n</code></pre>\n\n<p>The interference does not have to be binary though, and more common are graded responses. Transcriptional interference can also take place at the RNA stage (see e.g. <a href=\"http://www.nature.com/nature/journal/v514/n7524/full/nature13671.html\">Xue et al, 2014</a>), using <a href=\"http://en.wikipedia.org/wiki/Antisense_RNA\"><em>antisense RNA</em></a> and often providing a negative feedback loop, but the interference is then removed from the DNA, and does not represent a direct IF-statement analog at the DNA stage.</p>\n\n<p>To me, GOTO mainly makes sense for sequential code execution, and this is not the case for DNA (lots of transcription is happening all the time in parallel). More generally, the parallel \"execution\" of DNA along with the continuous interactions and feedback loops between DNA, transcripts and proteins (among other things) also means that cellular processes are far less clear-cut and traceable than computer code, which means that computer code is a very poor metaphor for cellular processes and the functioning of DNA.</p>\n"
},
{
"answer_id": 30133,
"pm_score": 4,
"text": "<p>DNA is not analogous to computer code which renders your search for similar constructs in it meaningless. To give a couple of simple examples why this is:</p>\n\n<ul>\n<li><p>Computer code has a sequential order of execution; DNA acts in\nparallel and out of sequence, it is not \"executed\".</p></li>\n<li><p>Computer code has a strict and consistent meaning so the line <code>if x==4 : x=7</code> always does the same thing; coding DNA\ntranslates to amino acids and it's the complex chemical interactions\nbetween these acids which give proteins their function thus no piece\nof coding DNA can be understood outside of its protein.</p></li>\n</ul>\n\n<p>Biological systems do have some pathways that operate in a similar way to computers, but you should be looking for these at the protein level not the DNA level and, even then, you need to be extremely careful that your analogy does not impair your understanding of what is really happening.</p>\n"
},
{
"answer_id": 52674,
"pm_score": 2,
"text": "<p>Regarding function calls:</p>\n\n<blockquote>\n <p>There are no equivalents of function calls. All events happen is the same space and there is always a likelihood of interference. One can argue that organelles can act as a compartment that may have a function like properties but they are highly complex and are not just some kind of input-output devices.</p>\n</blockquote>\n\n<p>and</p>\n\n<blockquote>\n <p>As WYSIWYG said there is no equivalent for function calls, as there will always be some interference.</p>\n</blockquote>\n\n<p>I think that nuclear receptors are great examples of function calls. They hang out in the cytosol allowing normal programming to function in a normative fashion. Upon activation with their ligand, they translocate to the nucleus to activate subroutines of gene repression/activation and subsequent downstream processes. </p>\n\n<p>In this fashion one could even argue that most initial ligand interactions that kick off cellular signaling are function calls. </p>\n"
},
{
"answer_id": 60881,
"pm_score": 1,
"text": "<p>In addition to the excellent WYSIWYG answer, there are some programming-like constructs at the lower level:</p>\n\n<ul>\n<li>FUNCTION CALL - replacing a single sub-unit inside a complex protein, assembled from multiple sub-units, each encoded by separate genes. This can also be seen as COMPOSITION, another programming concept.</li>\n<li>IF - alternative splicing, a piece of DNA (exon) may be included or not included into transcript that encodes the final protein. </li>\n</ul>\n"
}
] |
30,468 |
<p>Why is the action of flexing the foot so that the toes move anteriorly/superiorly (i.e. in the direction opposite that which they move during plantar flexion) described as "dorsiflexion?" In the same vein, why is the top surface of the foot called the "dorsal surface?" </p>
<p>If anything, the action opposite to plantar flexion moves the foot in the ventral direction, doesn't it? And surely if you've ever seen a human in the anatomical position, you can see that there's nothing dorsal about the top surface of the foot - it's superior, perhaps, but by no means dorsal.</p>
|
[
{
"answer_id": 30470,
"pm_score": 5,
"text": "<p>Anatomical terms must be able to fit a wide variety of organisms, from insects to fish, dogs, horses, chimpanzees to humans. That's why the terms are sometimes confusing to people who are thinking only of bipedal humans.</p>\n\n<p>In anatomy, the dorsum is the <strong>upper side of animals that typically run fly, swim or crawl in a horizontal position</strong>. In vertebrates the dorsum contains the backbone. In such an animal the \"ground side\" is the ventrum. </p>\n\n<p>Due to varied orientation on quadrupedal mammals (where the term is more appropriately used) the \"back\"-side of the hand, the \"top\"-side of the foot and the upper surface of the tongue are referred to by the term dorsum.</p>\n\n<p><img src=\"https://i.stack.imgur.com/edn2U.jpg\" alt=\"enter image description here\"></p>\n\n<p>Does this picture help? Note the dorsal surfaces of the body, muzzle, feet.</p>\n\n<p>In anatomy, the sole of the foot is called the <em>plantar</em> surface. The top of the foot is called the <em>dorsum</em> of the foot. (Imagine us walking on all fours like apes.) Therefore when you extend your foot, it's called plantar flexion; when you flex your foot upwards towards your head, it's called dorsiflexion.</p>\n\n<p>Similarly, the arteries feeding the bottom of your foot form the plantar arch. Those feeding the top are the dorsal artery (or the dorsalis pedis).</p>\n\n<p>Because anatomy must describe other animals than ourselves with other orientations, it must be consistent. In a quadruped, the dorsum of the tongue and the feet <em>do</em> actually point to it's \"back\" surface. See the picture below:</p>\n\n<p><a href=\"https://i.stack.imgur.com/U3aAg.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/U3aAg.jpg\" alt=\"enter image description here\"></a></p>\n\n<p>Lynxes have big paws, so it's more obvious that the surface facing the backbone is appropriately called the dorsum of the paw/foot. This picture is particularly interesting because it shows three degrees of dorsiflexion and one paw in full plantar flexion.</p>\n\n<p>In humans, the \"back\" is actually the posterior surface, because we are not primarily in a horizontal orientation. The ventral surface is called \"anterior\". Thus we speak of the anterior chest wall and the posterior chest wall, not the dorsal and ventral surfaces, although those designations would still be entirely correct.</p>\n"
}
] |
[
{
"answer_id": 30469,
"pm_score": 2,
"text": "<p><em>Dors/dorsum</em> in Latin simply means \"back\", and it is rather normal and reasonable to use the equivalent term in English with regard to the extremities (hands and feet), see \"<a href=\"http://dictionary.cambridge.org/dictionary/british/know-sth-like-the-back-of-your-hand\" rel=\"nofollow\">back of my hand</a>\". </p>\n\n<p>It is medical convention to refer to the <a href=\"http://medical-dictionary.thefreedictionary.com/dorsal\" rel=\"nofollow\">non-gripping surfaces of the feet and hands</a>, as well as the upper (towards the brain) <a href=\"http://dictionary.reference.com/browse/dorsal\" rel=\"nofollow\">surface of the tongue</a> as \"dorsal\". </p>\n\n<p>My best guess for the etymology sequence is that all the terms were borrowed from Latin anatomical books written by Roman and Greek doctors (Dioscorides, Galen) which named the anatomical structures in normal language (back/dorsum, stomach/venter, sole/plantarum) and these terms were then fixed into modern medical terminology as jargon. </p>\n\n<p>Caveat: I could not find any citation for the etymological sequence, but it seems a rather reasonable explanation to me. </p>\n"
},
{
"answer_id": 55794,
"pm_score": 3,
"text": "<p>Although the other <a href=\"https://biology.stackexchange.com/a/30470/16866\">2</a> <a href=\"https://biology.stackexchange.com/a/30469/16866\">answers</a> are accurate and well thought out, I just wanted to answer this with a bit different focused response.</p>\n\n<p>Two things to note:</p>\n\n<ol>\n<li><p>In general, one should think of <strong>flexion</strong> as <strong>decreasing the angle of a joint</strong> (see <a href=\"https://www.med.umich.edu/lrc/Hypermuscle/Hyper.html#foot\" rel=\"nofollow noreferrer\">here</a>, <a href=\"http://droualb.faculty.mjc.edu/Course%20Materials/Elementary%20Anatomy%20and%20Physiology%2050/Lecture%20outlines/muscle_anatomy.htm\" rel=\"nofollow noreferrer\">here</a>, <a href=\"https://www.ttuhsc.edu/som/success/documents/introduction_to_anatomy.pdf\" rel=\"nofollow noreferrer\">here</a>, <a href=\"https://www.asu.edu/courses/kin335/documents/Movement%20Terminology.pdf\" rel=\"nofollow noreferrer\">here</a>, <a href=\"http://www.stolaf.edu/depts/dance/faculty/anthony/courses/Modern-Dance-Language.htm\" rel=\"nofollow noreferrer\">here</a>, <a href=\"http://www.mhhe.com/biosci/abio/glossary.mhtml\" rel=\"nofollow noreferrer\">here</a> or <a href=\"http://www.fundamentalsofanatomy.com/pdf/ch08_glossary.pdf\" rel=\"nofollow noreferrer\">here</a> for reference). From Saladin's 2015 Anatomy textbook<span class=\"math-container\">$^1$</span>:</p>\n\n<blockquote>\n <p><strong>Flexion</strong> = a joint movement that , in most cases, decreases the angle between two bones.</p>\n</blockquote>\n\n<p>Put <a href=\"http://teachmeanatomy.info/the-basics/anatomical-terminology/terms-of-movement/\" rel=\"nofollow noreferrer\">differently</a>, </p>\n\n<blockquote>\n <p><strong>Flexion</strong> refers to a movement that <em>decreases the angle between two body parts</em>. </p>\n</blockquote></li>\n<li><p>As the other linked answers have aptly described, the superior surface of the foot is referred to as the <strong>dorsal</strong> surface (<em>dorsum</em> meaning \"back\"), and the inferior surface is referred to as the <strong>plantar</strong> surface (from Latin <em>plantaris</em>, from <em>planta</em> meaning \"sole\"). </p>\n\n<p><a href=\"https://i.stack.imgur.com/7O07i.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/7O07i.png\" alt=\"foot anatomy\"></a></p></li>\n</ol>\n\n<p>Given these two pieces of information, we can understand why the terms <strong>dorsiflexion</strong> and <strong>plantarflexion</strong> are used:</p>\n\n<ul>\n<li><p><strong>Dorsiflexion</strong> = decreasing angle between <em>dorsal</em> surface of foot & anterior side of of the leg.</p></li>\n<li><p><strong>Plantarflexion</strong> = decreasing angle between <em>plantar</em> surface of foot & the posterior side of the leg (or, more realistically, between the plantar surface and coronal plane of the leg).</p></li>\n</ul>\n\n<p><a href=\"https://i.stack.imgur.com/MNtXV.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/MNtXV.jpg\" alt=\"Dorsiflexion and plantarflexion angle decreasing\"></a></p>\n\n<p>From <a href=\"https://www.med.umich.edu/lrc/Hypermuscle/Hyper.html#foot\" rel=\"nofollow noreferrer\">University of Michigan</a>:</p>\n\n<blockquote>\n <p>A transverse axis through the ankle joint allows a pair of actions similar to flexion and extension at the wrist joint.</p>\n \n <p>The analogous action to wrist flexion is one that would tip the sole of the foot downward, <strong>increasing the angle between foot and leg</strong>. The usual term for the increase in such an angle would be extension, but in order to emphasize the relation between foot and hand, this action is instead termed <strong>plantar flexion</strong> .</p>\n \n <p>The action similar to extension at the wrist would be a tipping of the upper surface (dorsum) of the foot toward the anterior surface of the leg. However, this would decrease the angle between the body segments, and action usually termed flexion. Since the term, plantar flexion, has been used for the opposite action, this is now referred to as <strong>dorsiflexion</strong>.</p>\n</blockquote>\n\n<hr>\n\n<p><span class=\"math-container\">$^1$</span> Saladin, K. S. 2015. Anatomy & Physiology: The Unity of Form and Function. Seventh ed., McGraw-Hill, New York, NY. 1248pp.</p>\n"
},
{
"answer_id": 70495,
"pm_score": 2,
"text": "<blockquote>\n <p>In the same vein, why is the top surface of the foot called the \"dorsal surface?\"</p>\n</blockquote>\n\n<p>I don't think the above answers are correct -- they do not really address the question of why the top of the foot is the dorsal surface, and why the surface of the hand opposite to the palmar surface is dorsal. </p>\n\n<p>The reason why the top of the foot is dorsal is due to how the body develops embryologically. See the below figure:</p>\n\n<p><a href=\"https://i.stack.imgur.com/kQYxA.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/kQYxA.png\" alt=\"Fig1\"></a></p>\n\n<p><em>Figure taken from Dr. Ann-Judith Silverman's human development notes, Columbia U.</em> See: <a href=\"http://www.columbia.edu/itc/hs/medical/humandev/2004/Chapt8-Limb.pdf\" rel=\"nofollow noreferrer\">Human Dev Notes</a></p>\n\n<p>The dorsal side of the upper and lower extremity begin on the dorsal/posterior surface of the body. However, during the 6-8th weeks of development, both the upper and lower extremity will turn medially, so that the originally dorsal surface is now anterior/ventral.</p>\n"
},
{
"answer_id": 73576,
"pm_score": 0,
"text": "<p>The position of the human foot by human anatomical convention dictates that the human foot is perpendicular to the human body in a standing position, such that the rest of the human body (including the hands with the palmar surface facing forward) , but except the foot, will conform to the anterior or ventral plane versus the posterior or dorsal plane. The foot, at conventional anatomical position will have its own plane, consistent with the same reasoning such that the top of the foot is the dorsum, while the underside is the plantar surface (more correct), or the ventral surface (less acceptable due its confusing orientation).</p>\n\n<p>The plane of reasoning for the entire human body at anatomical position above ends at the distal junction of the tibio-fibula with the tarsal bones, such that the human feet will have its own surface plane directly perpendicular at 90 degrees to have its own 'dorsal' and 'ventral' surface.</p>\n\n<p>The feet as such is in a special position compared to the rest of the human body's plane surfaces to warrant its own. Thus by convention, one may acceptably hear 'antero-flexion' or 'dorsi-flexion' of the foot, but not 'supero-flexion of the foot' which sounds sort of disagreeable.</p>\n\n<p>The same way, oppositely, it is customarily said the 'plantar-flexion of the foot' which is more accurate (rather than infero-flexion or ventro-flexion or postero-flexion of the foot which sounds quite confusing)</p>\n"
}
] |
31,546 |
<p>Does anyone know of sources for learning bioinformatics, focused on genomics? I would like to learn a lot of skills I could apply potently in the workforce if I ever became adept at the fields. My computer science knowledge is weak, and my biology knowledge is mediocre, but I find the topics to be interesting.</p>
<p>I have read "The dynamic Genome, A Darwinian Approach", by Fontdevila, and it was a bit rough for me. I have also read some of a introduction to genomics textbook, by Arthur M Lesk, and found it to be very "academic".</p>
|
[
{
"answer_id": 31558,
"pm_score": 4,
"text": "<p><a href=\"http://unixandperl.com/\" rel=\"nofollow\">Unix and Perl to the Rescue</a> by Keith Bradnam and Ian Korf is an excellent introductory book and guide for bioinformatics (Linux and Perl) in genomics. It includes exercises and starts with the very fundamentals. You will still need some basic understanding of genetics and biology though.</p>\n"
}
] |
[
{
"answer_id": 31552,
"pm_score": 3,
"text": "<p>Beginning Perl for Bioinformatics by Jim Tisdall <a href=\"http://shop.oreilly.com\">http://shop.oreilly.com</a> is quite good, in my opinion, and his sequel, Mastering Perl for Bioinformatics is also great. The focus is largely, but not exclusively genomics.</p>\n"
},
{
"answer_id": 31559,
"pm_score": 2,
"text": "<p>Elementary Sequence Analysis by Brian Golding and Dick Morton is a good starter. Online resources can be found here:<a href=\"http://helix.biology.mcmaster.ca/courses.html\" rel=\"nofollow\">http://helix.biology.mcmaster.ca/courses.html</a> \nHere's a great online tutorial for sequencing techniques, with introduction, examples and everything.\n<a href=\"http://bioinf.comav.upv.es/courses/sequence_analysis/sequencing_technologies.html\" rel=\"nofollow\">http://bioinf.comav.upv.es/courses/sequence_analysis/sequencing_technologies.html</a></p>\n"
},
{
"answer_id": 31562,
"pm_score": 2,
"text": "<p>While not a book per se, the edX Lifesciences course has been really useful for me, it does a great job of covering the entire pipeline of genome analysis that one would need to use. The link containing all 8 classes is here, scroll down a bit and you can see links to all of the classes in this module:</p>\n\n<p><a href=\"https://courses.edx.org/courses/HarvardX/PH525.3x/1T2015/dffde833663e4f71ab64246ebe5598d1/\" rel=\"nofollow\">https://courses.edx.org/courses/HarvardX/PH525.3x/1T2015/dffde833663e4f71ab64246ebe5598d1/</a></p>\n"
},
{
"answer_id": 31715,
"pm_score": 0,
"text": "<p>I strongly suggest you to take a free course on <a href=\"http://coursera.org\" rel=\"nofollow\">coursera</a>There are many valid courses focused on bioinformatics for beginners and they offers slides, notes and everything is necessary to start. If you are looking for a nice book to get started, then I suggest you <a href=\"http://www.onlamp.com/pub/a/python/2002/10/17/biopython.html\" rel=\"nofollow\">this one</a></p>\n"
},
{
"answer_id": 110392,
"pm_score": 0,
"text": "<p>This is a book being worked on by some people at biostars. It's being constantly updated</p>\n<p><a href=\"https://www.biostars.org/p/225812/\" rel=\"nofollow noreferrer\">https://www.biostars.org/p/225812/</a></p>\n<p>Perl is a good place to start if you don't know any coding, but when you want to use already written libraries, you'll want to know R or python, if not both.</p>\n"
},
{
"answer_id": 110393,
"pm_score": 1,
"text": "<p><a href=\"https://open.oregonstate.education/computationalbiology/\" rel=\"nofollow noreferrer\">A Primer for Computational Biology</a> is a great open-access book with intros to Unix, R, and Python. As the title says, it's focus is computational biology (e.g., applying a variety of methods and analyses) rather than strictly bioinformatics (the development of novel methods and analyses), but I've found very valuable both for myself and for teaching others.</p>\n"
}
] |
32,964 |
<p>I'm an engineer by training and teaching myself the basics of cell and developmental biology. I'm using Scott F. Gilbert's Developmental Biology and Alberts' Essential Cell Biology right now, and they are both great resources.</p>
<p>Can you recommend good books on similar topics that are written in a non-textbook format?</p>
<p>EDIT: For example, I found books like The Greatest Show on Earth, Extended Phenotype, and Nature via Nurture really useful to learn about the basics of evolution while I was reading Watson's Molecular Biology of the Gene. Are there similarly well-written books for cell biology, developmental biology, or biochemistry? I know this sounds broad, but I'm not asking for textbook recommendations. I'd like to read something that isn't a textbook alongside my current studies.</p>
<p>SECOND EDIT: I'd be like to extend this question to recommendations of broad review articles in Cell and Developmental Biology too. For example 'How do cells know where they are?' is an excellent article on different strategies cells may use to assess distance in a developing embryo.</p>
|
[
{
"answer_id": 52730,
"pm_score": 2,
"text": "<p>For Biochemistry:</p>\n\n<p><a href=\"https://i.stack.imgur.com/uvPKf.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/uvPKf.jpg\" alt=\"enter image description here\"></a></p>\n\n<p>For Molecular Genetics:</p>\n\n<p><a href=\"https://i.stack.imgur.com/xtq6o.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/xtq6o.jpg\" alt=\"enter image description here\"></a></p>\n\n<p>For Developmental Biology:</p>\n\n<p><a href=\"https://i.stack.imgur.com/sHgok.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/sHgok.jpg\" alt=\"enter image description here\"></a></p>\n\n<p>That last one, Life Unfolding, is really cool and I think exactly what you're looking for.</p>\n"
}
] |
[
{
"answer_id": 33010,
"pm_score": 0,
"text": "<p>Would you consider the New York Times a suitable level of detail (while admittedly not a book)? If so then you may want to peruse this collection:\n<a href=\"http://topics.nytimes.com/top/news/science/topics/biology_and_biochemistry/index.html\" rel=\"nofollow\">http://topics.nytimes.com/top/news/science/topics/biology_and_biochemistry/index.html</a></p>\n\n<p>You will have to be selective.</p>\n\n<p>This was my first hit in Google searching for 'lay articles on biochemistry.' I would recommend my own textbook but it is aimed at 3rd year undergraduates, and would probably contravene the Biology SE rules.</p>\n"
},
{
"answer_id": 34193,
"pm_score": 2,
"text": "<p><a href=\"http://books.google.com/books/about/Endless_Forms_Most_Beautiful_The_New_Sci.html?id=-SqwP8CLdIsC\" rel=\"nofollow\">Endless Form Most Beautiful: The New Science of Evo Devo</a> introduces the reader to several classic embryology experiments and some key principles too.</p>\n\n<p>I'll edit this answer when I find more books or reading material of this nature.</p>\n"
},
{
"answer_id": 40379,
"pm_score": 2,
"text": "<p>I recommend <a href=\"https://books.google.co.in/books/about/Lehninger_Principles_of_Biochemistry.html?id=7chAN0UY0LYC\" rel=\"nofollow\">Lehninger principles of biochemistry</a>.</p>\n\n<p>It is one of the best, most read, and referred books on Biochemistry.</p>\n"
},
{
"answer_id": 40384,
"pm_score": 1,
"text": "<p><a href=\"http://rads.stackoverflow.com/amzn/click/0387849246\" rel=\"nofollow noreferrer\">The Machinery of Life by David S Goodsell</a></p>\n\n<p><a href=\"https://i.stack.imgur.com/dfe4U.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/dfe4U.jpg\" alt=\"enter image description here\"></a></p>\n\n<p>I just picked this up and haven't actually read through it yet, but it looks amazing. Very well illustrated with drawings and molecular models. It's also not overly technical. I don't have much to say in the way of a review, but there's plenty on Amazon. It sort of seems exactly like the book you're looking for. </p>\n"
},
{
"answer_id": 56902,
"pm_score": 2,
"text": "<p>Please try reading 'Principles of development' by Lewi Wolpret. This book explains the general concepts in develpmental biology beautifully. Invertebrate models like dorsophilia and zebrafish are used as examples to simplify the concepts in developmental biology.</p>\n\n<p><a href=\"https://i.stack.imgur.com/J5cHc.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/J5cHc.jpg\" alt=\"enter image description here\"></a></p>\n"
}
] |
35,337 |
<p>Across the electromagnetic spectrum, 400-700 nm is a narrow spectrum of frequencies and focused in the region of short wavelengths. For example, radio waves cover a large range of frequencies unexploited by the visual system. So what biological reason is there that evolved us to use such a small frequency bandwidth for vision?</p>
|
[
{
"answer_id": 35353,
"pm_score": 6,
"text": "<p><strong>Short answer</strong><br>\nThe visible spectrum has the highest energy in sunlight at the earth's surface, explaining the gross location of the visible spectrum in life on earth. The specific frequency range varies across species and can be explained by species-specific survival strategies.</p>\n\n<p><strong>Background</strong><br>\nWhen you look at the solar light spectrum at the earth's surface the <strong>visible spectrum has the highest intensity</strong> (fig. 1).</p>\n\n<p><img src=\"https://i.stack.imgur.com/4BIlO.jpg\" alt=\"solar irradiation\"><br>\n<sup>Solar irradiation. Source: <a href=\"http://solarwiki.ucdavis.edu/The_Science_of_Solar/Solar_Basics/B._Basics_of_the_Sun/III._Solar_Radiation_Outside_the_Earth's_Atmosphere\" rel=\"noreferrer\">University of California</a>.</sup></p>\n\n<p>So it makes sense to use the range of frequencies that is represented most in sunlight as a starting point. </p>\n\n<p>Then the question becomes, why do <strong>humans utilize approximately 400 to 700 nm</strong>, and not infrared or UV? That can be explained because we do not need it. Our range has been hypothesized to be related to <strong>foraging behaviors</strong> and our visual system is particularly sensitive in the frequency range of the <strong>coloring of (ripe) fruits</strong>, which is thought to have been of great benefit to our hominid ancestors <a href=\"https://physics.stackexchange.com/questions/144936/is-there-a-physical-reason-for-colors-to-be-located-in-a-very-narrow-band-of-the\">(Osorio & Vorobyev, 1996)</a>.</p>\n\n<p>Why then do animals extend their vision into <strong>UV</strong>? Many fish, amphibian, reptilian, avian, and some mammalian species use UV vision. Many birds can identify UV-reflected <strong>nectar and berries</strong>, and UV-reflecting plumages in birds, and scales in fishes are used for <strong>recognition</strong> <a href=\"http://www.pnas.org/content/100/14/8308.full\" rel=\"noreferrer\">(Shi & Yokoyama, 2003)</a>. Moreover, some arthropod species are know to use UV vision to <strong>reduce light-reflection distortions</strong> under water, such as in the mantis shrimp that features 12 photoreceptor types (as opposed to four in humans) <a href=\"http://www.sciencemag.org/content/343/6169/411.short\" rel=\"noreferrer\">(Thoen <em>et al</em>., 2014)</a>.</p>\n\n<p>Why then do animals extend their dynamic range into the <strong>infrared</strong>? A notable beneficial effect of perceiving infrared is the detection of <strong>body heat</strong>. The generation of heat is accompanied by the generation of infrared light. The detection of this emitted light is highly useful for nocturnal predators, like the rattle snake <a href=\"http://www.scientificamerican.com/article/the-infrared-vision-of-snakes/\" rel=\"noreferrer\">(Hartline & Newman, 1982)</a>.</p>\n\n<p><sub><strong>References</strong><br>\n<strong>-</strong> <a href=\"http://www.scientificamerican.com/article/the-infrared-vision-of-snakes/\" rel=\"noreferrer\">Hartline & Newman, <em>Sci Am</em> (1982); <strong>246</strong>(3): 116-27</a><br>\n<strong>-</strong> <a href=\"https://physics.stackexchange.com/questions/144936/is-there-a-physical-reason-for-colors-to-be-located-in-a-very-narrow-band-of-the\">Osorio & Vorobyev, <em>Proc Roc Soc B</em> (1996); <strong>263</strong>(1370)</a><br>\n<strong>-</strong> <a href=\"http://www.pnas.org/content/100/14/8308.full\" rel=\"noreferrer\">Shi & Yokoyama, <em>PNAS</em> (2003); <strong>100</strong>(142003): 8308-13</a><br>\n<strong>-</strong> <a href=\"http://www.sciencemag.org/content/343/6169/411.short\" rel=\"noreferrer\">Thoen <em>et al., Science</em> (2014); <strong>343</strong>(6169): 411-3</a> </sub></p>\n\n<p><sub><strong>Further Reading</strong><br>\n<strong>1.</strong> <a href=\"https://biology.stackexchange.com/questions/24481/is-our-color-vision-calibrated-to-sky-vegetation-and-blood/24544#24544\">Is our color vision calibrated to sky, vegetation, and blood?</a><br>\n<strong>2.</strong> <a href=\"https://physics.stackexchange.com/questions/144936/is-there-a-physical-reason-for-colors-to-be-located-in-a-very-narrow-band-of-the\">Is there a physical reason for colors to be located in a very narrow band of the EM spectrum?</a></sub></p>\n"
}
] |
[
{
"answer_id": 35342,
"pm_score": -1,
"text": "<p>These wavelengths happen to satisfy two conditions.</p>\n\n<p>First, shorter wavelength photons (EM radiation) tend to be dangerous for biology. Even UV light (<350nm) is already can damage DNA. That is due to the fact that bond energies in biological molecules tend to have values close to energy of short-wavelength EM radiation. These is why high-energy particles called ionizing radiation. For reference, see <a href=\"http://pubs.acs.org/doi/abs/10.1021/jp049270k\" rel=\"nofollow noreferrer\">this paper</a>. ionization energy for DNA estimated in 4-5eV range, which is 300-250nm.</p>\n\n<p>Secondly, on low-energy hand of spectrum, water absorbs a lot of IR radiation:\n<img src=\"https://i.stack.imgur.com/KgufS.jpg\" alt=\"Water absorption spectrum\"></p>\n\n<p>So, as you can see, what we see <em>aka</em> visible spectrum is sitting nicely in valley of water absorption but does not extend to area of harsh UV light that will damage chemicals of your body.</p>\n\n<p>Now, why is that so? Because atoms have these masses and electrons around them have these energies. So bonds and molecular interactions have these values.</p>\n\n<p>(In radio range of frequencies you, opposite to UV, have not enough energy to elicit any significant molecular changes, which is why you can't perceive WiFi)</p>\n"
},
{
"answer_id": 35343,
"pm_score": -1,
"text": "<p>\"Visible light\" is the wavelength of the light that we can see, if human beings could see UV or IR, those wavelengths had been included in the \"visible light\" definition.\nNow, our Sun is brightest in yellow-green light, which (you guess?) is right in the midle of the \"visible light\" spectrum. So the only remaining question is: \"Why can we only see that short spectrum?\" The answer is EVOLUTION.\nThe same reason that made us to have only 5 fingers in our hands, only 2 eyes and only two kidneys.\nThe bandwith of the \"visible spectrum\" is enough to make the human beings (as specie) survive.</p>\n"
},
{
"answer_id": 35350,
"pm_score": -1,
"text": "<p>This is my speculation, but there are no or few organic chemicals which can absorb radio waves having longer wave lengths. Eyes sense lights by absorbing light with organic chemicals, but to sense longer wave length, eyes might need more sophisticated devices like tuners. </p>\n\n<p>In addition, less than 100nm radio waves from the outer space are absorbed by the atmosphere, so even if eyes could sense such radio waves, you don't see any signals on the earth.</p>\n"
},
{
"answer_id": 35352,
"pm_score": 3,
"text": "<p>Most of the light from the sun doesn't actually reach the earth's surface due to the atmosphere.</p>\n\n<p><img src=\"https://i.stack.imgur.com/CxDPY.jpg\" alt=\"enter image description here\"></p>\n\n<p>[<a href=\"http://imagine.gsfc.nasa.gov/science/toolbox/emspectrum1.html\" rel=\"noreferrer\">source</a>]</p>\n\n<p>So the light reaching earth includes near-UV, visible, near-IR and a band of radio waves. Seeing any other part of the spectrum would be impossible since it doesn't reach earth.</p>\n\n<p>You asked why we only see in the visible light range; this is due to evolution. <a href=\"http://www.sciencedirect.com/science/article/pii/004269899490149X\" rel=\"noreferrer\">Birds, among other animals, can see UV light</a>. In fact, <a href=\"http://onlinelibrary.wiley.com/doi/10.1034/j.1600-0706.2002.980315.x/abstract\" rel=\"noreferrer\">all vertebrates have the potential for near-UV vision</a>. <a href=\"http://www.sciencedirect.com/science/article/pii/0042698994901473?via%3Dihub\" rel=\"noreferrer\">Humans, as vertebrates, also have UV-sensitive photoreceptors</a>. However, our lens is opaque to UV light: </p>\n\n<p><img src=\"https://i.stack.imgur.com/fXN1C.jpg\" alt=\"enter image description here\"></p>\n\n<p>[from <em>Clinical Ocular Anatomy and Physiology</em> via <a href=\"http://www.clspectrum.com/articleviewer.aspx?articleID=103351\" rel=\"noreferrer\">this website</a>]</p>\n\n<p>Just speculating, it would seem that the ability to see near-UV is an ancestral condition which we lost at some point; either it provided no significant advantage (neutral regression) or there was some advantage provided by a UV-opaque lens, either directly (such as protection from UVB light) or indirectly (through pleiotropic antagonism). </p>\n\n<p>On the other hand, human photoreceptors cannot detect IR light. Again, this is a product of evolution. <a href=\"http://m.hopkinsmedicine.org/news/media/releases/why_animals_dont_have_infrared_vision\" rel=\"noreferrer\">These researchers hypothesize that the longer the wavelength of light detected, the more noise is produced.</a> This noise is due to activation of the pigment molecule by heat. Or, it could just be that never happened. An IR-sensitive photoreceptor might be possible, but evolution doesn't lead to perfect adaptation. In other words, there isn't necessarily a reason why.</p>\n\n<p>As for radio waves, they are too low energy to interact appreciably with matter, at least as far as vision is concerned. </p>\n"
},
{
"answer_id": 76066,
"pm_score": 2,
"text": "<p>Its not really</p>\n<p>That is only the <strong>human</strong> visible spectrum.</p>\n<p>Humans actually have a reduced spectrum compared to many animals. Mammals in particular have a reduced spectrum compared ot non-mammals. Reptiles and birds have 4 color sensitive cell types (cones) and can see into the ultraviolet. Many invertebrates can see an even wider spectrum. Mammals <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/20733295\" rel=\"nofollow noreferrer\">lost</a> two of these cells. Modern mammals are descended from early mammals who were nocturnal Thus color vision was less useful. <a href=\"https://www.ncbi.nlm.nih.gov/pubmed/15312027\" rel=\"nofollow noreferrer\">Primates evolved a third cone</a>, (a mutant variant of one of the two they had before) Primates did this because many are frugivores and color is excellent for determining when fruit is ripe.</p>\n<p><a href=\"https://i.stack.imgur.com/2ApNb.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/2ApNb.jpg\" alt=\"enter image description here\" /></a></p>\n"
}
] |
35,446 |
<p>There are plenty of different hand soaps out there, as well as hand sanitizers. Is there an advantage to soaps that claim that they're antibacterial vs soaps that just say soap?</p>
<p>In particular I'm looking at Softsoap who offers normal soap and antibacterial soap. </p>
<p><strong><em>Examples:</em></strong></p>
<p>Normal:</p>
<p><img src="https://i.stack.imgur.com/KICCXm.jpg" alt="Regular Softsoap"></p>
<p>Antibacterial: </p>
<p><img src="https://i.stack.imgur.com/jYnyam.jpg" alt="Antibacterial Softsoap"></p>
|
[
{
"answer_id": 35451,
"pm_score": 7,
"text": "<p>Short answer: There is no benefit for their use in households. </p>\n\n<p>Long answer: These soaps (see <a href=\"http://www.colgate.com/app/Softsoap/US/EN/Ingredients.cvsp\">here</a> for the complete list) contain the so called quaternary ammonium compounds <a href=\"https://en.wikipedia.org/wiki/Benzalkonium_chloride\">Benzalkonium chloride</a> and <a href=\"https://en.wikipedia.org/wiki/Cetrimonium_chloride\">Cetrimonium chloride</a> which indeed have antimicrobial properties.</p>\n\n<p>While they do not promote resistance to these compounds (see reference 1), their use is still not recommended, as their permanent use might dry out the skin, can cause contact allergies and the products released into the environment are also problematic.</p>\n\n<p>There are two studies, which compared the use of normal soap (which has some antibacterial properties on its own) to antibacterial soaps in household environments and found no differences. See article linked in reference 2 for a summary and references 3 and 4 for details on the studies.</p>\n\n<p>This doesn't mean that antibacterial soaps are useless at all, they simply make no sense in households. For hospitals or doctors they are an important tool to protect their patients before operations. But here detailed instructions for how long and how the hands have to be washed are provided. Hand washing is also followed by another disinfection step, which helps with efficiency. But this is very much different from the way people wash their hands at home. See reference 5 for some opinions here.</p>\n\n<p>References:</p>\n\n<ol>\n<li><a href=\"https://www.ncbi.nlm.nih.gov/pubmed/17006819\">Use of germicides in the home and the healthcare setting: is there a\nrelationship between germicide use and antibiotic resistance?</a></li>\n<li><a href=\"http://phys.org/news/2007-08-plain-soap-effective-antibacterial.html\">Plain soap as effective as antibacterial but without the risk</a></li>\n<li><a href=\"http://www.ncbi.nlm.nih.gov/pubmed/17683018\">Consumer antibacterial soaps: effective or just risky?</a></li>\n<li><a href=\"http://www.ncbi.nlm.nih.gov/pubmed/14996673\">Effect of antibacterial home cleaning and handwashing products on\ninfectious disease symptoms: a randomized, double-blind trial.</a></li>\n<li><a href=\"http://www.health.com/health/article/0,,20433634,00.html\">The Burning Question: Is It Safe to Use Antibacterial Soap?</a></li>\n</ol>\n"
}
] |
[
{
"answer_id": 35450,
"pm_score": 4,
"text": "<p>Chris has correctly identified the antibacterial agent in the hand soap depicted in the image in the question, and therefore his answer is superior as a direct answer. </p>\n\n<p>Nevertheless, other members of the Softsoap series of hand soap uses <a href=\"https://en.wikipedia.org/wiki/Triclosan\" rel=\"nofollow noreferrer\">triclosan, 0.15%</a> as their antibacterial agent, as seen in an image of their ingredient list on the reverse of the bottle. </p>\n\n<p>(click for enlarged image)</p>\n\n<p><a href=\"https://i.stack.imgur.com/sx2SZ.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/sx2SZs.jpg\" alt=\"enter image description here\"></a></p>\n\n<p>Triclosan has been shown to be effective by <a href=\"http://www.sciencedirect.com/science/article/pii/019567019290033I\" rel=\"nofollow noreferrer\">Webster et al (1992)</a> in reducing the incidence of MRSA infection as well as being milder to the skin as compared to chlorhexidine gluconate in a neonatal ward. </p>\n\n<blockquote>\n <p>The average number of new cases of MRSA per week was reduced from 3·4 to 0·14 (P < 0·0001) in the experimental ward whilst no significant changes occurred in the control ward. </p>\n</blockquote>\n\n<p>Triclosan has also been shown by <a href=\"http://www.sciencedirect.com/science/article/pii/S0196655300900270\" rel=\"nofollow noreferrer\">Jones et al (2000)</a> to be effective on a large variety of different bacterial, viral and fungal strains. </p>\n\n<p><img src=\"https://i.stack.imgur.com/DAOgE.png\" alt=\"enter image description here\"></p>\n\n<p><img src=\"https://i.stack.imgur.com/SzS9Q.png\" alt=\"enter image description here\"></p>\n\n<p><img src=\"https://i.stack.imgur.com/p1KuO.png\" alt=\"enter image description here\"></p>\n\n<p>Therefore, the usage of triclosan is effective as an antibacterial agent, and would likely result in less bacteria on the hands after washing. </p>\n"
},
{
"answer_id": 35467,
"pm_score": -1,
"text": "<p>Human immune defense response is primed by cell damage products as it does not have prior knowledge about bacterial or viral \"malware\".</p>\n\n<p>The whole purpose of disinfectant substances is damaging cells and potential organic disease carriers. As those substances are not discriminating, frequent use of them will prime your immune defense against benign organic matter as well. In combination with solvents that remove protective layers of fat and thus increase the permeation of this kind of cell waste into top skin layers, this sounds like a recipe for allergies and neurodermitic reactions in the long run.</p>\n\n<p>There is a high correlation of countries (and eras) with high standards of living including household hygiene and autoimmune response problems. Finding actual causations is work in progress.</p>\n\n<p>While that is still the case, it is my gut feeling that contact with disinfectants should be reserved to cases of tangible risk.</p>\n"
},
{
"answer_id": 35493,
"pm_score": 3,
"text": "<p>You may be interested to look into the <em>Old friends hypothesis</em>, since this is related to how the human immune system may respond to reduced biodiversity in the microbiota. The basic idea is that the human immune system is developed by exposture to the microbiota, and without exposture to organisms from our evolutionary past, immune system regulation might fail. This can then lead to poorly regulated inflammatory responses and \nmaybe allergies or other chronic inflammatory diseases. Since the exposture to our evolutionary <em>Old friends</em> is lower in developed countries and urban areas, this hypothesis might potentially (partially) explain the increased prevalence of allergies in developed countries. Even though it is somewhat tangential to your question, and does not directly answer the question of the pros and cons of antibacterial soap, it should still be relevant for a more general case.</p>\n\n<p>Two good starting points are <a href=\"http://www.pnas.org/content/110/46/18360\" rel=\"nofollow\">Rook (2013)</a> and <a href=\"http://www.pnas.org/content/109/21/8334\" rel=\"nofollow\">Hanski et al (2012)</a>. Rook (2013) is a general overview of the theory with many good references to empirical studies that relate to the hypothesis, by one of the main proponents of the theory. Hanski et al (2012) is an interesting epidemiological paper, where they relate the allergic disposition of individuals to both the general biodiversity in their larger living environment as well as the generic diversity of their skin microbiota. In the paper, they find a positive relationship in healthy individuals between immune responses and the abundance of the gammaproteobacterial genus Acinetobacter on the skin, but they do not find the same pattern in atopic individuals. The study also finds a negative relationship between the environmental biodiversity close to the homes of study subjects and the frequency of atopy (so high biodiversity -> lower levels of atopy).</p>\n\n<p>To be clear, this is still a hypothesis that needs further testing and support. However, there are many interesting case studies that can lend support to it, and indicate plausible mechanisms.</p>\n\n<p><strong>References:</strong></p>\n\n<ul>\n<li><a href=\"http://www.pnas.org/content/110/46/18360\" rel=\"nofollow\">Rook. 2013. <em>Regulation of the immune system by biodiversity from the natural environment: An ecosystem service essential to health</em>. PNAS 110(46)</a></li>\n<li><a href=\"http://www.pnas.org/content/109/21/8334\" rel=\"nofollow\">Hanski et al. 2012. <em>Environmental biodiversity, human microbiota, and allergy are interrelated</em>. PNAS 109(21)</a></li>\n<li><a href=\"http://emph.oxfordjournals.org/content/2013/1/46\" rel=\"nofollow\">Rook. 2013. <em>Microbial ‘Old Friends’, immunoregulation and stress resilience</em>. Evolution, Medicine, and Public Health\n2013(1)</a></li>\n</ul>\n"
},
{
"answer_id": 35582,
"pm_score": 2,
"text": "<p>Probably, it is worth to add some historic (and ironic) \"perspective\" to this question. It will probably explain that even without scientific research the answer to this question is probably \"no\" and that real use of bacterial soap should probably be reduced to hospital settings and not expanded to households as suggest promotions and commercials.</p>\n\n<p>The historic perspective I wanted to add relates to the book \"The Hermit in the Garden\" by Gordon Campbell. Here live hermits are described (there were non-alive as well, this is why I call these \"live\"). Campbell cites another book - \"Sir William Gell's A Tour in the Lakes Made in 1797\":</p>\n\n<p>\"the hermit is never to leave the place, or hold conversation with anyone for <strong>seven years</strong> during which he is <strong>neither to wash himself or cleanse himself in any way whatever</strong>, but is to let his hair and nails both on hands and feet, grow as long as nature will permit them.\" </p>\n\n<p>From this \"work\" description we can <em>speculate</em> that \"dangerous\" infections were not expected during such a long period of soapless live. This is why we could assume that any soap is probably of limited \"antibacterial\" value for otherwise healthy person. </p>\n\n<p>(Remark: This \"exclamation\" not trying to answer the question in a scientific way, but just to add some \"color\" to the question and the answers posted. I hope, it is worth to place it here instead of a comment). </p>\n"
}
] |
39,374 |
<p>It's easy to find information about the biggest animals at land / at sea / in the air. But what was the biggest underground-living animal that ever existed?</p>
<ul>
<li>No animals that were forced to live underground (e.g. pit ponies)</li>
<li>The animal should live at least 95% of its life under the earth (e.g. foxes)</li>
</ul>
<p>There are two possible answers:</p>
<ol>
<li>By length</li>
<li>By mass</li>
</ol>
<p>My first guess was a mole</p>
|
[
{
"answer_id": 57393,
"pm_score": 4,
"text": "<p><strong>Microchaetus rappi</strong>\nMicrochaetus rappi, the African giant earthworm, is a large earthworm in the Microchaetidae family, the largest of the segmented worms (commonly called earthworms). It averages about 1.36 m (4.5 ft) in length, but can reach a length of as much as 6.7 m (22 ft) and can weigh over 1.5 kg (3.3 lb).(<a href=\"https://en.wikipedia.org/wiki/Microchaetus_rappi\" rel=\"noreferrer\">https://en.wikipedia.org/wiki/Microchaetus_rappi</a>)</p>\n\n<p><strong>Giant Gippsland earthworm</strong>\nThese giant earthworms average 1 metre (3.3 ft) long and 2 centimetres (0.79 in) in diameter and can reach 3 metres (9.8 ft) in length; however, their body is able to expand and contract making them appear much larger. On average they weigh about 200 grams (0.44 lb). They have a dark purple head and a blue-grey body, and about 300 to 400 body segments.(<a href=\"https://en.wikipedia.org/wiki/Giant_Gippsland_earthworm\" rel=\"noreferrer\">https://en.wikipedia.org/wiki/Giant_Gippsland_earthworm</a>)</p>\n"
}
] |
[
{
"answer_id": 39375,
"pm_score": 3,
"text": "<p>I don't know if there is a bigger animal, but the biggest <strong>mole</strong> is the <a href=\"https://en.wikipedia.org/wiki/Russian_desman\" rel=\"noreferrer\">Russian desman</a> with 400-520g and a length of \n18-21 cm (35-41cm including the tail)</p>\n"
},
{
"answer_id": 57391,
"pm_score": 2,
"text": "<p>Can badgers qualify? They shelter underground and get a significant proportion of their food underground as well, I don't know if they stay there 95% of the time though. Wikipedia gives them as going up to 17kg and 90cm in length.</p>\n\n<p>I thought a snake might get the record for length but there don't seem to be many burrowing snakes and they seem to be small. Given the sizes of other non-mammalian tetrapods and how few of them are burrowers whichever the largest underground animal is may well be a mammal.</p>\n"
},
{
"answer_id": 57392,
"pm_score": 2,
"text": "<p>If you accept far-fetched argument, I've got an individual that weight more than a ton! But let's start with a simple example of a large troglodyte.</p>\n\n<p><strong>Blind cave eel</strong></p>\n\n<p>The <a href=\"https://en.wikipedia.org/wiki/Blind_cave_eel\" rel=\"nofollow noreferrer\">blind cave eel (<em>Ophisternon candidum</em>)</a> is a troglodite. It is a pure white fish growing to 40 cm, with an eel-like body, no eyes, and a thin rayless membrane around the tip of the tail. I could not find its weight but it probably does not weight much! Just like many troglodite species, its distribution range is very restricted. It only occurs in a single location in Western Australia.</p>\n\n<p><a href=\"https://i.stack.imgur.com/fmZdq.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/fmZdq.png\" alt=\"enter image description here\"></a></p>\n\n<p><strong>Fungus</strong></p>\n\n<p>Well a fungus is not an animal (but is closely related), so it does not answer your question but I still wanted to mention it. There's an individual fungus that covers 965 hectares. See this <a href=\"https://www.scientificamerican.com/article/strange-but-true-largest-organism-is-fungus/\" rel=\"nofollow noreferrer\">popular article</a>.</p>\n\n<p><strong>Ant supercolonial individual</strong></p>\n\n<p>The individual ant is of course not that big but it is not uncommon to consider a colony as a superorganism. You might want to have a look at <a href=\"https://www.amazon.ca/Major-Transitions-Evolution-Revisited/dp/0262015242/ref=sr_1_1?ie=UTF8&qid=1489766434&sr=8-1&keywords=major%20transitions%20in%20evolution%3A%20revisited\" rel=\"nofollow noreferrer\">major transitions in evolution: revisited</a> for a discussion about the concept of individual for social species. Note also that most ant casts spend most of their time underground in the nest.</p>\n\n<p>From <a href=\"https://en.wikipedia.org/wiki/Ant_colony#Supercolonies\" rel=\"nofollow noreferrer\">wikipedia</a></p>\n\n<blockquote>\n <p>Until 2000, the largest known ant supercolony was on the Ishikari coast of Hokkaidō, Japan. The colony was estimated to contain 306 million worker ants and one million queen ants living in 45,000 nests interconnected by underground passages over an area of 2.7 km2 (670 acres). In 2000, an enormous supercolony of Argentine ants was found in Southern Europe (report published in 2002). Of 33 ant populations tested along the 6,004-kilometre (3,731 mi) stretch along the Mediterranean and Atlantic coasts in Southern Europe, 30 belonged to one supercolony with estimated millions of nests and billions of workers, interspersed with three populations of another supercolony. The researchers claim that this case of unicoloniality cannot be explained by loss of their genetic diversity due to the genetic bottleneck of the imported ants.[citation needed] In 2009, it was demonstrated that the largest Japanese, Californian and European Argentine ant supercolonies were in fact part of a single global \"megacolony\".</p>\n</blockquote>\n\n<p>Considering a weight of 3.5 mg per individual, a colony of 306 millions ant weight more than a ton (1071 kg exactly) and of course this excludes their constructed habitat which could arguably be considered as part of the individual. </p>\n"
},
{
"answer_id": 57398,
"pm_score": 3,
"text": "<p><strong>Key Words</strong>:</p>\n\n<p>To aid in your search, you might want to try searching the term \"<a href=\"https://en.wikipedia.org/wiki/Fossorial\" rel=\"noreferrer\"><strong>Fossorial</strong></a>.\"</p>\n\n<ul>\n<li><p>Fossorial animals are animals that are adapted to digging and life underground.</p>\n\n<ul>\n<li>Though note: <a href=\"https://www.researchgate.net/profile/Matias_Mora/publication/229878464_Evolution_of_morphological_adaptations_for_digging_in_living_and_extinct_ctenomyid_and_octodontid_rodents_ADAPTATIONS_FOR_DIGGING_IN_CTENOMYIDS_AND_OCTODONTIDS/links/0046351b9fee74a47c000000.pdf\" rel=\"noreferrer\">Lessa et al (2008)</a> use <strong>fossorial</strong> to describe species that spend a substantial fraction of their lives outside their burrows, while they use <strong><em>subterranean</em></strong> to describe species that perform most activities underground. </li>\n</ul></li>\n</ul>\n\n<p>You might also want to examine a list of <a href=\"https://en.wikipedia.org/wiki/List_of_troglobites\" rel=\"noreferrer\">troglobites</a>.</p>\n\n<ul>\n<li>Troglobites are animals that live entirely in the dark parts of caves.</li>\n</ul>\n\n<hr>\n\n<p><strong>Big Species</strong></p>\n\n<p>I think large specimens of @JayCkat's suggested species (<a href=\"https://en.wikipedia.org/wiki/Microchaetus_rappi\" rel=\"noreferrer\"><strong><em>Microchaetus rappi</em></strong></a>) will be tough to \"beat\", with large specimens reaching 6.7 m and 1.5 kg. </p>\n\n<p>However, here's a list of other species anyways:</p>\n\n<p>Some <strong>extant large species of fossorial animals</strong>:</p>\n\n<ul>\n<li><p><a href=\"https://en.wikipedia.org/wiki/Cape_dune_mole-rat\" rel=\"noreferrer\"><strong>Cape dune mole-rat</strong></a> (<em>Bathyergus suillus</em>): 27-35 cm (up to 39cm including tail); 570-1350 g</p>\n\n<ul>\n<li>Supposedly, some <a href=\"https://en.wikipedia.org/wiki/Blesmol\" rel=\"noreferrer\">blesmols</a> can reach a weight of 1800 g. </li>\n</ul></li>\n<li><p><a href=\"https://en.wikipedia.org/wiki/Russian_desman\" rel=\"noreferrer\"><strong>Russian Desman</strong></a> (<em>Desmana moschata</em>): 18-21 cm (up to 41 cm including the tail); 400-520 g</p></li>\n<li><p><a href=\"https://en.wikipedia.org/wiki/Giant_armadillo\" rel=\"noreferrer\"><strong>Giant Armadillo</strong></a> (<em>Priodontes maximus</em>): up to 1.5 m; up to 50 kg</p>\n\n<ul>\n<li>It spends all day in underground burrows though it hunts above ground at night. </li>\n</ul></li>\n<li><p><a href=\"https://en.wikipedia.org/wiki/Olm\" rel=\"noreferrer\"><strong>Olm</strong></a> (<em>Proteus anguinus</em>): up to 40 cm long. </p></li>\n</ul>\n\n<p><a href=\"https://i.stack.imgur.com/Tch1u.jpg\" rel=\"noreferrer\"><img src=\"https://i.stack.imgur.com/Tch1u.jpg\" alt=\"Cape dune mole-rat\"></a></p>\n\n<p><sup> <a href=\"http://www.ispotnature.org/node/837957\" rel=\"noreferrer\">Cape dune mole-rat</a> </sup></p>\n\n<p><a href=\"https://i.stack.imgur.com/3OPSH.jpg\" rel=\"noreferrer\"><img src=\"https://i.stack.imgur.com/3OPSH.jpg\" alt=\"Giant Armadillo\"></a></p>\n\n<p><sup> <a href=\"https://www.youtube.com/watch?v=zM2o4XYlBzM\" rel=\"noreferrer\">Giant Armadillo</a> </sup></p>\n\n<hr>\n\n<p>The only info I could find via a quick search for <strong>prehistoric fossorial animals</strong>:</p>\n\n<ul>\n<li><p>A series of 240 million year old underground tunnels/chambers suggest some burrowing species lived there. [Source: <a href=\"http://www.seeker.com/pre-dino-subterranean-world-discovered-1765411287.html\" rel=\"noreferrer\">Seeker</a>].</p>\n\n<blockquote>\n <p>\"You should imagine the tracemaker as a stout, short-bodied, four-legged animal with a short tail and short neck...The trunk was about 20-25 centimeters (8-10 inches) in length.</p>\n</blockquote></li>\n</ul>\n\n<hr>\n\n<p><strong>Bonus</strong>: \nHow about the <strong><em>deepest</em></strong> living animal?</p>\n\n<ul>\n<li><p>That award goes to the <a href=\"http://news.nationalgeographic.com/news/2011/06/110601-deepest-worm-earth-devil-science-animals-life/\" rel=\"noreferrer\">\"<strong>Devil Worm</strong>\"</a> (<em>Halicephalobus mephisto</em>), a nematode that has been found living at 3.6 km below the surface!! ...(tied w/ <em>Plectus aquatilis</em>).</p>\n\n<ul>\n<li>Though at 0.5 mm, it's definitely not winning the <em>largest</em> trophy :p.</li>\n</ul></li>\n</ul>\n\n<hr>\n\n<p><sup> <em>Citations</em>: </sup></p>\n\n<p><sup>- Lessa, E. P., Vassallo, A. I., Verzi, D. H., & Mora, M. S. (2008). Evolution of morphological adaptations for digging in living and extinct ctenomyid and octodontid rodents. Biological Journal of the Linnean Society, 95(2), 267-283. </sup></p>\n"
}
] |
39,664 |
<p>To be clear, I'm not doubting that <em>Homo sapiens</em> and <em>Homo neanderthalensis</em> did interbreed: of that much I'm convinced.</p>
<p>Within the past few years I've seen an upcropping of pop-sci articles discussing the interbreeding between pre-historic species of humans. In everything that I see in these articles, as well as in scientific literature (my college Bio textbook, among others), I see these different human groups being referred to as separate species.</p>
<p>This conflicts with my understanding of a species. Given the following definition, wouldn't <em>Homo sapiens</em> and <em>Homo neanderthalensis</em> be the same species?</p>
<blockquote>
<p>A species is often defined as the largest group of organisms where
two hybrids are capable of reproducing fertile offspring, typically
using sexual reproduction. <a href="https://en.wikipedia.org/wiki/Species" rel="nofollow noreferrer">~Wikipedia</a></p>
</blockquote>
<ul>
<li>Is this definition incorrect?</li>
<li>Are the publications using "species" colloquially, as opposed to scientifically?</li>
<li>Is "species" still a poorly defined concept? (see <a href="https://en.wikipedia.org/wiki/Ring_species" rel="nofollow noreferrer">Ring Species</a>)</li>
</ul>
<p>Thanks!</p>
|
[
{
"answer_id": 39669,
"pm_score": 8,
"text": "<h1>Short answer</h1>\n<p>The concept of species is poorly defined and is often misleading. The concepts of <a href=\"https://en.wikipedia.org/wiki/Lineage_(evolution)\" rel=\"noreferrer\">lineage</a> and <a href=\"https://en.wikipedia.org/wiki/Monophyly\" rel=\"noreferrer\">clade / monophyletic group</a> are much more helpful. IMO, the only usefulness of this poorly defined concept that is the "species" is to have a common vocabulary for naming lineages.</p>\n<p>Note that <em>Homo neanderthalis</em> is sometimes (although it is rare) called <em>H. sapiens neanderthalis</em> though highlighting that some would consider neanderthals and modern humans as being part of the same species.</p>\n<h1>Long answer</h1>\n<p><strong>Are neanderthals and modern humans really considered different species?</strong></p>\n<p>Often, yes they are considered as different species, neanderthals being called <em>Homo neanderthalis</em> and modern humans are being called <em>Homo sapiens</em>. However, some authors prefer to call neanderthals <em>Homo sapiens neanderthalis</em> and modern humans <em>Homo sapiens sapiens</em>, putting both lineages in the same species (but different subspecies).</p>\n<p><strong>How common were interbreeding between <em>H. sapiens</em> and <em>H. neanderthalis</em></strong></p>\n<p>Please, have a look at <a href=\"https://biology.stackexchange.com/questions/39664/how-could-humans-have-interbred-with-neanderthals-if-were-a-different-species/40690#40690\">@iayork's answer</a>.</p>\n<p>The rest of the post is here to highlight that whether you consider <em>H. sapiens</em> and <em>H. neanderthalis</em> to be the same species or not is mainly a matter of personal preference given that the concept of species is mainly arbitrary.</p>\n<p><strong>Short history of the concept of species</strong></p>\n<p>To my knowledge, the concept of species has first been used in the antiquity. At this time, most people viewed species as fixed entities, unable to change through time and without within-population variance (see <a href=\"http://amazingdiscoveries.org/C-deception-evolution_Plato_Darwin\" rel=\"noreferrer\">Aristotle and Plato's thoughts</a>). For some reason, we stuck to this concept even though it sometimes appears to not be very useful.</p>\n<p><a href=\"https://en.wikipedia.org/wiki/Charles_Darwin\" rel=\"noreferrer\">Charles Darwin</a> already understood that as he says in <a href=\"https://en.wikipedia.org/wiki/On_the_Origin_of_Species\" rel=\"noreferrer\">On the Origin of Species</a> (see <a href=\"http://darwin-online.org.uk/Variorum/1860/1860-51-c-1869.html\" rel=\"noreferrer\">here</a>)</p>\n<blockquote>\n<p>Certainly no clear line of demarcation has as yet been drawn between species and sub-species- that is, the forms which in the opinion of some naturalists come very near to, but do not quite arrive at the rank of species; or, again, between sub-species and well-marked varieties, or between lesser varieties and individual differences. These differences blend into each other in an insensible series; and a series impresses the mind with the idea of an actual passage.</p>\n</blockquote>\n<p>You might also want to have a look at the post <a href=\"https://biology.stackexchange.com/questions/19762/why-are-there-species-instead-of-a-continuum-of-various-animals\">Why are there species instead of a continuum of various animals?</a></p>\n<p><strong>Several definitions of species</strong></p>\n<p>There are several definitions of species that yield me once again to argue that we should rather forget about this concept and just use the term lineage and use an accurate description of the reproductive barriers or genetic/functional divergence between lineage rather than using this made-up word that is "species".</p>\n<p>I will below discuss the most commonly used definition (the one you cite) that is called the <a href=\"http://evolution.berkeley.edu/evolibrary/article/side_0_0/biospecies_01\" rel=\"noreferrer\">Biological species concept</a>.</p>\n<p><strong>Problems with the definition you cite</strong></p>\n<blockquote>\n<p>A species is often defined as the largest group of organisms where two hybrids are capable of reproducing fertile offspring, typically using sexual reproduction.</p>\n</blockquote>\n<p><em>Only applies to species that reproduce sexually</em></p>\n<p>Of course, this definition only applies to lineages that use sexual reproduction. If we were to use this definition for asexual lineages, then every single individual would be its own species.</p>\n<p><em>In practice</em></p>\n<p>In general, everybody refers to this definition when talking about sexual lineages but IMO few people are correctly applying for practical reasons of communicating effectively.</p>\n<p><em>How low the fitness of the hybrids need to be?</em></p>\n<p>One has to arbitrarily define a limit of the minimal fitness (or maximal outbreeding depression) to get an accurate definition. Such boundary can be defined in absolute terms or in relative terms (relative to the fitness of the "parent lineages"). If, the hybrid has a fitness that is 100 times lower than any of the two parent lineages, then would you consider the two parent lineages to belong to the same species?</p>\n<p><em>Type of reproductive isolation</em></p>\n<p>We generally categorize the types of reproductive isolation into post-zygotic and pre-zygotic reproductive isolation (see <a href=\"https://en.wikipedia.org/wiki/Reproductive_isolation\" rel=\"noreferrer\">wiki</a>). There is a lot to say on this subject but let's just focus on two interesting hypothetical cases:</p>\n<ul>\n<li><p>Let's consider two lineages of birds. One lineage has blue feathers while the other has red feathers. They absolutely never interbreed because the blue birds don't like the red and the red birds don't like the blue. But if you artificially fuse their gametes, then you get a viable and fertile offspring. Are they of the same species?</p>\n</li>\n<li><p>Let's imagine we have two lineages of mosquitoes living in the same geographic region. One flying between 6 pm and 8 pm while the other is flying between 1 am and 3 am. They never see each other. But if they were to meet while flying they would mate together and have viable and fertile offsprings. Are they of the same species?</p>\n</li>\n</ul>\n<p><em>Under what condition is the hybrids survival and fertility measured</em></p>\n<p>Modern biology can do great stuff! Does it count if the hybrid can't develop in the mother's uterus (let's assume we are talking about mammals) but can develop in some other environment and then become a healthy adult?</p>\n<p><em>Ring species in space</em></p>\n<p>As you said in your question, ring species is another good example as to why the concept of species is not very helpful (see the post <a href=\"https://biology.stackexchange.com/questions/11240/transitivity-of-species-definitions\">Transitivity of Species Definitions</a>). <em>Ensatina eschscholtzii</em> (a salamander; see <a href=\"https://en.wikipedia.org/wiki/Reproductive_isolation\" rel=\"noreferrer\">DeVitt et al. 2011</a> and other articles from the same group) is a classic example of ring species.</p>\n<p><em>Species transition through time</em></p>\n<p>Many modern lineages cannot interbreed with their ancestors. So, then people might be asking, when exactly did the species change occurred? What generation of parent where part of species A and offspring where part of species B. Of course, there is no such clearly defined time in which transition occurred. It is more a smooth transition from being clearly reproductively isolated (if they were placed to each other) from being clearly the same species.</p>\n<p><em>Practical issue - Renaming lineages</em></p>\n<p>How boring it would be if every time we discover the two species can in some circumstances interbreed, we had to rename them! That would be a mess.</p>\n<p><em>Time</em></p>\n<p>Of course, when we talk about a species we refer to a group of individuals at a given time. However, we don't want to rename the group of individuals of interest every time a single individual die and get born. This notion yield to the question of how long in time can a single species exist. Consider a lineage that has not split for 60,000 years. Was the population 60,000 years ago the same species as the one today? The two groups may differ a lot phenotypically and may actually be reproductively isolated if they were to exist at the same time.</p>\n<p><em>Special cases</em></p>\n<p>When considering a few special cases, the concept of species become even harder to apply.</p>\n<p>The <strong>Amazon molly</strong> (a fish) is a "species" that have "sexual intercourse" without having "sexual reproduction" and there are no males in the species! How is it possible? The females have to seek for sperm in a sister species in order to activate the development of the eggs but the genes of the father from the sister species are not used (<a href=\"http://classic.rspb.royalsocietypublishing.org/content/275/1636/817.short\" rel=\"noreferrer\">Kokko et al. (2008)</a>).</p>\n<p>In an ant "species", males and females can both reproduce by <a href=\"https://en.wikipedia.org/wiki/Parthenogenesis\" rel=\"noreferrer\">parthenogenesis</a> (some kind of cloning but with meiosis and cross-over) and don't need each other to reproduce. In this respect, males could actually be called females. But they still meet to reproduce together. The offsprings of a male and a female (via sexual reproduction) are sterile workers. So males and females are just like two sister species that reproduce sexually to create a sterile army to protect and feed them (<a href=\"http://www.nature.com/nature/journal/v435/n7046/abs/nature03705.html\" rel=\"noreferrer\">Fournier et al. (2005)</a>).</p>\n<p><em>Bias</em></p>\n<p>It often brings fame to discover a large new species. In consequence, scientists might tend to apply a definition of species that allow them to tell that their species is a new one. A typical example of such eventual bias concern dinosaurs where many new fossils are abusively called a new species while they sometimes are just the same species but at a different stage of development (according to this <a href=\"https://www.ted.com/talks/jack_horner_shape_shifting_dinosaurs?language=en\" rel=\"noreferrer\">TED</a>).</p>\n<p><strong>So why do we still use the concept of species?</strong></p>\n<p><em>Naming</em></p>\n<p>IMO, its only usefulness is that it allows us to name lineages. And it is very important that we have the appropriate vocabulary to name different lineages even if this brings us to make a few mistakes and use some bad definitions.</p>\n<p><em>The alternative use of the concept of lineage</em></p>\n<p>It is important though that we are aware that the concept of species is poorly defined and that if we need to be accurate that we can talk in terms of lineages. The main issue with the term lineage is not semantic and comes about the fact that gene lineages may well differ considerably from what one would consider being the "species lineage" as defined by the "lineages of most sequences"... but this is a story for another time.</p>\n<p><strong>In consequence</strong></p>\n<p>In consequence to the above issues, we often call two lineages that can interbreed to some extent by different species names. On the other hand, two lineages that can hardly interbreed are sometimes called by the same species name but I would expect this case to be rarer (as discussed by @DarrelHoffman and @AMR in the comments).</p>\n<p><strong>Homo lineages</strong></p>\n<p>I hope it makes sense from the above that the question is really not related to the special case of the interbreeding between the <em>Homo sapiens</em> and the <em>Homo neanderthalis</em> lineages. The issue is a matter of the definition of species.</p>\n<h1>Video and podcast</h1>\n<p>SciShow made a video on the subject: <a href=\"https://www.youtube.com/watch?v=dnfaiJJnzdE\" rel=\"noreferrer\">What Makes a Species a Species?</a></p>\n<p>For the French speakers, you will find an interesting (one hour long) podcast on the consequence of the false belief that the concept of species is an objective concept on conservation science at <a href=\"http://podcast.unil.ch/\" rel=\"noreferrer\">podcast.unil.ch</a> > La biodiversité - plus qu'une simple question de conservation > Pierre-Henry Gouyon</p>\n<hr />\n<p><a href=\"https://biology.stackexchange.com/questions/34953/are-there-examples-of-now-living-species-where-one-is-descended-from-the-other/34956#34956\">Here is a related answer</a></p>\n"
}
] |
[
{
"answer_id": 39668,
"pm_score": 4,
"text": "<p>The definition of species is open for debate, and this is especially the case when you try to define it from a paleontology perspective. </p>\n\n<p><a href=\"https://en.wikipedia.org/wiki/Neanderthal\">Homo neanderthalensis</a> was first discovered and defined in the 1860's, long before we were able to sequence their genome, which was published in 2010. There genome was different enough that most scientists would still say that they are distinct from modern humans, but that doesn't necessarily mean that those distinctions were enough that it affected the ability to produce fertile offspring between sapiens/neanderthalensis matings. </p>\n\n<p>In fact on the wikipedia article I linked to the alternative Homo sapiens neanderthalensis is suggested as a synonym making us Homo sapiens sapiens for <a href=\"https://en.wikipedia.org/wiki/Anatomically_modern_human\">anatomically modern humans</a>. This is similar to distinctions made in the wolf lineages where you have Canis lupus for grey wolves, Canis lupus familiaris for Domestic dogs, Canis lupus dingo for the wild dogs of Australia, and on and on for many other sub species of Canis lupus. Wolf/Dog hybrids are known to be fertile.</p>\n\n<p>Female Horses and Male Donkeys can breed to create sterile offspring, <a href=\"https://en.wikipedia.org/wiki/Mule\">Mules</a>. The sterility is likely due to the fact that there is a greater phylogenetic distance between Horses and Donkey than there is for sapiens/neanderthalensis and also due to the fact that Horses have a different number of chromosomes to Donkey's , where as sapiens/neanderthalensis have the same number.</p>\n\n<p>Another thing you have to remember is that the discovery of Homo neanderthalensis occurred about 5 years after Darwin created an uproar about Humans being evolved primates. Now you were faced with a skeleton that clearly was different from modern human but was clearly hominid. The closely held view that humans were special and therefore held dominion over all other creatures made it difficult to accept the fact that we may actually have evolved.</p>\n"
},
{
"answer_id": 40690,
"pm_score": 4,
"text": "<p>In addition to @Remi.b's answer on the species concept, and the perils of using human definitions to try to encompass biological reality, you need to understand what \"interbreeding\" meant to humans and neanderthals. Fertile crosses between sapiens and neandertalis were very rare, probably less than one successful cross per generation, and there's some evidence that male hybrids were almost all sterile (or that this was a fatal condition). This is probably less successful interbreeding than horse-donkey crosses, where the two partners are unambiguously different species by just about any definition (they have different chromosome numbers!). So it's not like sapiens and neandertalis could effortlessly hybridize; it was very rare and generally unsuccessful.</p>\n\n<p>References:</p>\n\n<blockquote>\n <p>We find that observed low levels of Neanderthal ancestry in Eurasians are compatible with a very low rate of interbreeding (<2%), potentially attributable to a very strong avoidance of interspecific matings, a low fitness of hybrids, or both. These results suggesting the presence of very effective barriers to gene flow between the two species are robust to uncertainties about the exact demography of the Paleolithic populations, and they are also found to be compatible with the observed lack of mtDNA introgression. Our model additionally suggests that similarly low levels of introgression in Europe and Asia may result from distinct admixture events having occurred beyond the Middle East, after the split of Europeans and Asians.</p>\n</blockquote>\n\n<p>--<a href=\"http://www.pnas.org/content/108/37/15129.abstract\" rel=\"noreferrer\">Strong reproductive isolation between humans and Neanderthals inferred from observed patterns of introgression.</a> Currat M, Excoffier L. Proc Natl Acad Sci U S A. 2011 Sep 13;108(37):15129-34 </p>\n\n<blockquote>\n <p>Our results indicate that the amount of Neanderthal DNA in living non-Africans can be explained with maximum probability by the exchange of a single pair of individuals between the subpopulations at each 77 generations, but larger exchange frequencies are also allowed with sizeable probability.</p>\n</blockquote>\n\n<p>--<a href=\"http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0047076\" rel=\"noreferrer\">Extremely Rare Interbreeding Events Can Explain Neanderthal DNA in Living Humans.</a> Neves AGM, Serva M PLoS ONE 2012 7(10): e47076</p>\n\n<blockquote>\n <p>These results suggest that part of the explanation for genomic regions of reduced Neanderthal ancestry is Neanderthal alleles that caused decreased fertility in males when moved to a modern human genetic background.</p>\n</blockquote>\n\n<p>--<a href=\"http://www.nature.com/nature/journal/v507/n7492/full/nature12961.html\" rel=\"noreferrer\">The genomic landscape of Neanderthal ancestry in present-day humans</a> Sankararaman et al Nature 2014 507:354–357</p>\n"
},
{
"answer_id": 54434,
"pm_score": 1,
"text": "<p>The same way lions and tiger are different species but can interbreed. They do so poorly, not very often, and the male hybrids are infertile, although the female hybrids retain some fertility. Gene flow between the two species is possible but very limited. We call lions and tigers two species because gene flow between the two is limited. Free flow of genes between the two species is not possible. </p>\n\n<p>If we look at the papers coming out it is obvious that the flow of genes between <em>Homo Sapiens</em> and Neanderthals was limited. It was so limited that we can say that two species were on the verge of cutting all ties between each other. </p>\n\n<p>Firstly, there are no Neanderthal mitochrondria, meaning successful mating involving Neanderthals was mainly between human females and male Neanderthals. Next there are no Neanderthal Y chromosomes, meaning male hybrids were sterile. </p>\n\n<p>Although there are Neanderthal gene in autosomes, there are no Neanderthal genes on X chromosomes, which house many of the genes regulating intelligence and fertility. So natural selection has selectively weeded out Neanderthal genes in those two areas, probably because they don't play well with their human counterparts (i.e. they cause a fitness disadvantage).</p>\n\n<p>Also, the Neanderthal gene segments, although found in all non-Africans, are in small pieces. Individual have less than 2% (although as much as 35-60% of the Neanderthal genome remains in the non-African human population). So it means that the hybridization event occurred rarely and far in the past — probably when the first <em>Homo sapiens</em> left Africa.</p>\n"
},
{
"answer_id": 107157,
"pm_score": -1,
"text": "<p>A microbiology professor once told us "The Russians have about 14 times more species than the English"</p>\n<p>The word species (Greek εἶδος¹) begins in greece. According to St. Thomas Aquinas (Summa Theologica, ca. 1265-1274 A.D.), used as the scientific way of referring to different types of living things.</p>\n<p>It's a notable buzzword in english owing to it's rhyming syllables, it focuses attention, and my... It isn't more precise than referring to colours... <em>Espèces</em> in French doesn't warrant the same obsessive buzz. Genetics is a spectrum and we divide them as best we can a bit like we divide colours of the rainbow.</p>\n<p>Neanderthals came about only half a million years ago, and we diverge from them perhaps a million years ago.</p>\n<p>Dinosaur species usually live for about 3 to 10 million years before changing two new species according to scientists, and their generations are closer together than humans...</p>\n<p>So they are closer than bonobos and classical chimpanzees, perhaps something like the northern and the southern white rhino.</p>\n"
},
{
"answer_id": 107159,
"pm_score": 0,
"text": "<p>I'm not really educated into the scientific community's mindset very much, but as a person who is interested in taxonomy to one degree or another, as well as plant breeding, I can give you some perspective to help you decide on an answer.</p>\n<p>Lots of different species can hybridize (interspecies hybrids): e.g. some different pepper species, some different tomato species, some different toad species, cows and bison, lions and tigers, different species of strawberries, etc. Interspecies hybrids sometimes even become invasive species. For instance, collared doves invaded my area years ago, and hybridized with the native doves (which native doves were quite a bit different: much smaller, much different behavior; they made different sounds, and had no collars); we've had the hybrids ever since (although they took some years to stabilize much--which was a fascinating process to observe), and the other two species appear to be gone, for the most part. In my personal opinion, interspecies hybrids (perhaps^ driven by changes in habitat: for instance, if the magnetic fields of the earth change, maybe because of a disturbance caused by a solar storm, animals might migrate different places than they used to, because some animals migrate via their ability to detect magnetic fields; if they migrate different places than usual, they might find new animals to hybridize with) are a very significant driver of new forms of life, which often gets overlooked.</p>\n<p>^That's a hypothesis of mine, anyway. I don't claim it's a proven fact.</p>\n<p>There are even hybrids between different genera, although they're pretty rare (sheep and goats have been known to cross, for instance; hybrids can also supposedly be made between goji and tomatoes--although I have yet to see plants or seeds of the hybrid for sale).</p>\n<p>My impression from things I've studied isn't that species differentiate sexually <em><strong>in</strong></em>compatible groups, but rather that they differentiate sexually compatible groups that tend to stick together. (You're probably not going to see llamas and camels hanging out very often, or horses and zebras, or donkeys and zebras, but that doesn't mean they can't reproduce. They are not the same species, however, and some--not all--interspecies hybrids have infertile offspring^.) It seems that other traits are also important for defining species: such as structure and lifestyle, but it's a work in progress (and they move things around taxonomically sometimes).</p>\n<p>^It should be noted that you can have diploids and tetraploids (or greater) of the same species of plant (thanks, in part, to chromosome doubling chemicals), and their offspring aren't fertile (but if you doubled the chromosomes of the offspring, they would be).</p>\n<p>None of the higher ranks guarantee sexual compatibility (even if it sometimes can happen). However, chromosome doubling and such aside, you can generally expect members of a species to be compatible with confidence.</p>\n<p>In summary, it sounds like members of the same species tend to reproduce with each other over another species when given the chance (but there's no guarantee they can't and won't breed with other species, generally speaking; you can evaluate that on a case-by-case basis, however). Each species tends to have a certain set of traits (and habits) that set it apart. But, we're still figuring everything out.</p>\n<p>That's what I gather, anyway.</p>\n"
}
] |
40,156 |
<p>Let me explain... A friend and I read some articles, part of a Biology book, and watched a video on evolution. We then tried to explain what Evolution is to each other.</p>
<p>My friend said that Natural Selection is a mechanism inside the organism that mutates the DNA to make its offspring survive in an environment; that natural selection mutates the DNA beneficially and that random mutations are not useful (like blue eyes). But I disagree and think that it is closer to Lamarkian theory.</p>
<p>I told him that DNA from male and female recombines and randomly mutates making a new "recipe" for the offspring (adding a new characteristic(s)). If the offspring is well suited for the environment, then it survives and passes on its characteristics to its offspring. If it does not have fitness for its environment, it dies. So, Natural Selection is were nature "selects" who survives and reproduces a lot.</p>
<p>So is the DNA mutation process random or is mutation directed to make an organism that is suited to survive its environment?</p>
<p>None of my friends are Biology students, so I can't ask then which explanation is correct (or at least more valid).</p>
<p>I'd prefer you don't answer: "None of these explanations are correct," but to say which one is more valid and correct misconceptions or add more that is missing (of course these are only summaries of our discussion). But of course, you can answer that neither of our explanations is correct...</p>
|
[
{
"answer_id": 40165,
"pm_score": 5,
"text": "<p>I accidentally wrote a lot!</p>\n\n<p>I first discuss the term <em>Darwinian evolution</em>. I then describe the main evolutionary processes insisting on the two elements of interest in your question, that is <em>mutations</em> and <em>natural selection</em>. In the end, I directly address your two statements and bring a few more complications into the subjects.</p>\n\n<p><strong>Did you say Darwinian evolution?</strong></p>\n\n<p><em>Evolution is more than Darwinian evolution</em></p>\n\n<p>The expression \"Darwinian evolution\" easily yield to misunderstandings. Darwin was probably the most important scientist and one of the first (if not the first) to develop the theory of evolution but evolutionary biology today is so much more than Darwin's theory of evolution.</p>\n\n<p><em>Examples of very basic things Darwin did not know</em></p>\n\n<ul>\n<li><p>We discovered the structure of DNA in the 1950s-1960s only with Miesher, Chargaff and most renowned Watson and Crick (<a href=\"http://www.nature.com/scitable/topicpage/discovery-of-dna-structure-and-function-watson-397\" rel=\"nofollow noreferrer\">history of the discovery</a>). Darwin had no idea of the existence of DNA and had not even hypothesized about the existence of such a molecule (which came first by Erwin Schrödinger).</p></li>\n<li><p>Darwin was not aware either that inheritance was through the transmission of \"particles/atomic\" and not through the inheritance of some kind of \"fluid/continuum\". In other words, Darwin did not know the <a href=\"https://www.dnalc.org/view/16151-Biography-1-Gregor-Mendel-1822-1884-.html\" rel=\"nofollow noreferrer\">Law of Segregation by Gregor Mendel</a> (even if they lived in the same epoch).</p></li>\n<li><p>Darwin had no idea about Evo-Devo, that is he had no idea about the similitudes in developmental processes among related (even distantly related) organisms.</p></li>\n<li><p>Globally speaking, while Darwin managed to touch a little bit about many of the subjects of modern evolutionary biology (which is very impressive), he only manages to mention them and failed to provide any prediction. This is a large part because no one had no concept in genetics at that time.</p></li>\n</ul>\n\n<p><em>Evolution is more than natural selection and mutations</em></p>\n\n<p>Evolution is not only about natural selection. Even C. Darwin knew that evolution is way more than natural selection. It is for example very important to consider random events. One of them is <em>mutation</em>, another is <em>genetic drift</em> (I am not trying to list every process that influence evolution but only to give you a sense of why natural selection is different than evolution with a goal of explaining why a trait that is needed do not necessarily appear). Both mutations and genetic drift explain why a species will not necessarily be perfectly adapted to its environment. Evolutionary biology is a big field of knowledge and there is a lot to know about evolutionary processes.</p>\n\n<p><strong>Natural Selection and Mutations explained by the Lewontin Recipe</strong></p>\n\n<p>The Lewontin's recipe is a good way in order to understand what is natural selection and when it occurs. The Lewontin's recipe says that natural selection occurs whenever:</p>\n\n<ol>\n<li>Individuals in a population vary in terms of a given trait</li>\n<li>This trait has some (additive) heritability. <a href=\"http://evolution.berkeley.edu/evolibrary/home.php\" rel=\"nofollow noreferrer\">Here</a> is one of the several posts that explain the concept of heritability. It might be slightly a post that is a bit advanced for you though but shortly speaking it means that offspring are more similar to their parents more than they are to other non-kin individuals in the population.</li>\n<li>The fitness varies (not necessarily linearly) as the trait varies.</li>\n</ol>\n\n<p>Simple example:</p>\n\n<ol>\n<li>In a population, there are blue pens and red pens</li>\n<li>Reproduction is asexual and blue pens create other blue pens while red pens create other red pens.</li>\n<li>blue pens make more offspring than red pens.</li>\n</ol>\n\n<p>In such a situation, natural selection occurs yielding the frequency of the blue pens to increase in the population while the frequency of red pens will decrease.</p>\n\n<p><strong>Natural Selection</strong></p>\n\n<p>Natural Selection is the process by which variants of genes called alleles are selected and therefore increase in frequency. This selection result from a differential reproductive success.</p>\n\n<p><strong>Mutations</strong></p>\n\n<p>In the broad sense mutation is any change in the DNA sequence. Some changes are more likely to happen than other but in any case, the likeliness of these changes to happen is not dependent on the consequence they will have on the phenotype (shortly speaking, a phenotype is how an individual looks like) and on the reproductive success. So mutations occur randomly and the specific mutation that would be needed in the population may not occur. Therefore saying, if a trait is needed (in the sense of \"if a trait would be beneficial\"), then a mutation will occur to make this trait existing is wrong. Note that most mutations are deleterious (decrease the reproductive success) while few of them are beneficial (increase the reproductive success) and those that are beneficial are more likely to rise in frequency in the population.</p>\n\n<p><strong>Genetic drift</strong></p>\n\n<p>If the change in frequency of mutations would depend exclusively on natural selection, then I would not have said before that a beneficial mutation is more likely to raise in frequency but I would have said that a beneficial mutation will raise in frequency deterministically. An intuitive explanation of what is genetic drift can be found on <a href=\"https://biology.stackexchange.com/questions/14543/why-is-the-strength-of-genetic-drift-inversely-proportional-to-the-population-si\">this post</a>. It will also allow you to understand why small population undergo a more random change in frequency of their genes than are big population.</p>\n\n<hr>\n\n<p><strong>Considering your opposing statements</strong></p>\n\n<p>Hopefully, the following is clear from the above discussion but I would like to directly address your statements.</p>\n\n<blockquote>\n <p>My friend said that Natural Selection is a mechanism inside the organism that mutates the DNA to make its offspring survive in an environment; that natural selection mutates the DNA beneficially and that random mutations are not useful (like blue eyes). But I disagree and think that it is closer to Lamarkian theory.</p>\n</blockquote>\n\n<p><em>You are right that your friend is wrong!</em></p>\n\n<p>It indeed sounds more or less Lamarkian. In any case, it is very wrong, as you said. Mutations are not caused deterministically under the pressure of natural selection to do specific things.</p>\n\n<p><em>Are mutations completely random?</em></p>\n\n<p>See <a href=\"https://biology.stackexchange.com/questions/66183/are-mutations-random\"><strong>Are mutations random?</strong></a>.</p>\n\n<p>I do not want to go into too many complications. The sentence \"mutations are random\" is unclear. Does it mean that the mutation rate is random? Does it mean that the effect of a new mutation is random? And also the concept of randomness only make sense if we consider a set of a priori knowledge. So it is a little hard to fully answer this question and the easy, close-enough approximation for a starter in evolutionary biology is just to say that mutations are random (whatever that means). A slightly better approximation of reality is that mutation rate is an adaptive trait and can vary depending on the environment where the individual is found (adaptively or not). However, the effect of new mutations is really not deterministic. </p>\n\n<p>The mutation rate varies with the type of sequence considered. For example, a <a href=\"https://en.wikipedia.org/wiki/Microsatellite\" rel=\"nofollow noreferrer\">microsatellite sequence</a> is a sequence or repeated DNA. For example <code>AATAATAATAATAATAATAAT</code> etc.. (note that the genetic code is written with 4 letters, A, T, C and G). Such sequences are highly mutable. So a mutation is more likely to occur in this region than in the middle of a coding region. And it is more likely for a mutation occurring in a coding region to affect fitness than for a mutation occurring in a microsatellite (it is possible that a mutation occurring in a microsatellite will affect fitness). </p>\n\n<p>Depending on the level of stress some organisms (plants mostly to my knowledge) can change their mutation rate. Consider for example an individual that is maladapted to its environment. If it mutates little, then the offspring will likely be as maladapted and in the long run, the lineage will disappear. If the individual is mutating a lot then, most offspring will have a very low fitness but eventually one will receive a beneficial mutation that will make it very strong and by itself, this offspring may save the lineage. This is what is called a <a href=\"http://rspb.royalsocietypublishing.org/content/277/1685/1153\" rel=\"nofollow noreferrer\">bet-hedging strategy</a>. The concept of bet-hedging can be summarized with the expression \"Don't put all your eggs in the same basket\".</p>\n\n<p>You will note that the mutation rate is an evolving feature of an organism. This yield observation such as what is now called Drake's rule (<a href=\"http://www.pnas.org/content/88/16/7160.full.pdf\" rel=\"nofollow noreferrer\">original paper</a>). Drake's rule indicates that the genome-wide mutation rate is always at the order of 1 (there is quite a bit of variation but it is a good approximation). </p>\n\n<blockquote>\n <p>I told him that DNA from male and female recombines and randomly mutates making a new \"recipe\" for the offspring (adding a new characteristic(s)). If the offspring is well suited for the environment, then it survives and passes on its characteristics to its offspring. If it does not have fitness for its environment, it dies. So, Natural Selection is were nature \"selects\" who survives and reproduces a lot.</p>\n</blockquote>\n\n<p><em>Sounds quite right!</em></p>\n\n<p>You pretty much nailed it. Mutation adds genetic variation and natural selection selects from the available genetic variation. Your wording is a little uncommon though :). For example, an individual, it is incorrect to say that an individual has fitness or not. Each individual has a fitness, that is some value that encompasses both its fertility and survival probability. In a simple model, fitness is simply the expected number of offspring.</p>\n\n<p>Note also, that the majority of mutations that affect the fitness of the individuals are not so much dependent on the details of the environment. Many mutations are just bad wherever you are. Think about a mutation that would reduce the efficiency of energy production (ATP in mitochondria). Such a mutation will be deleterious regardless of whether the weather is hot or cold for example.</p>\n\n<hr>\n\n<p><strong>Introductory course to evolutionary biology</strong></p>\n\n<p>You probably want to have a look at an introductory course to evolutionary biology such as <a href=\"http://evolution.berkeley.edu/evolibrary/home.php\" rel=\"nofollow noreferrer\">Understanding Evolution</a>.</p>\n"
}
] |
[
{
"answer_id": 40158,
"pm_score": 1,
"text": "<p>Your description of Evolution seems more accurate than your friends. DNA cannot mutate with a particular goal in mind, mutations are random. Most mutations have no effect on an organism's survival, but some will be detrimental, and a few will helpful. Helpful mutations will improve an organisms odds of surviving and passing on its DNA, so those traits will eventually spread through a population.</p>\n\n<p>However, if we wanted to talk about \"goals\" for evolution, then the goal of every piece of DNA is to be copied and passed on. (of course it cannot think about achieving that goal, it's just a chemical.) DNA mutations that make an organism more suited for a particular environment will be selected for, and those that are detrimental will be selected against. This competition between different copies of DNA eventually optimizes the species for that environment.</p>\n\n<p>So at the molecular level, mutation is a totally random process, but if we zoom out to the ecosystem and population levels, then evolution \"designs\" a species to better survive in its environment. But this design is a result of random mutations and trial and error.</p>\n"
},
{
"answer_id": 40160,
"pm_score": 1,
"text": "<p>Mutation is a random process that mainly happens when a cell's DNA is replicated (= <em>copied</em>) before the cell's division, because the enzyme responsible for this replication sometimes makes mistakes. It's a rare process, as for eukaryotic cells (the ones with a nucleus, so animals and plant cells), it happens once every <span class=\"math-container\">$10^9$</span> nucleotide. </p>\n\n<p>Now, let's say we consider an organism that has sexual reproduction.</p>\n\n<p>To be transmitted to the descendants of the organism, the mutation must appear in a cell of the germline (spermatozoid or ovule for example).\nIf transmitted, this mutation can have several effects :</p>\n\n<ul>\n<li>It can be lethal, the organism cannot survive because the mutation makes a vital protein inoperative</li>\n<li>It can give the organism a disadvantage in his environment (e.g. living in a snowy environment, the pigmentation of the organism's skin becomes glowing red)</li>\n<li>It can be neutral, something is modified, but it keeps working (e.g. a certain protein has a different amino acid sequence but keeps working)</li>\n<li>It can give the organism an evolutive advantage, the protein works better, in a way that favorises the organism vs. its fellows' organisms in surviving in their environment (e.g. in the snowy environment, the pigmentation of the organism's skin becomes perfectly white, whereas one of its fellows is greyish)</li>\n</ul>\n\n<p>In the fourth case, this organism has more chances to reproduce (because he is less likely to be killed, or more likely to access a resource), and hence, to transmit this mutation. This is where natural selection applies: the \"fitness\" of the organism <em>in his environment</em> is greater than the one of the other organisms of his species. </p>\n\n<p>Now, it's important to note that the evolution (= <em>the change in a specie</em>) is driven by the natural selection (= <em>the process of selection</em>), and that those changes, in <strong>nature</strong>, are random and take a long time and aren't easily noticeable at the scale of a human life.</p>\n"
},
{
"answer_id": 40177,
"pm_score": 1,
"text": "<p>Great answers have been given already. But one phenomenon that is mostly not explicitly mentioned that can and should be regarded a part of the process of Evolution is <strong>symbiosis</strong>.</p>\n\n<p><strong>symbiosis</strong></p>\n\n<p>The probably most fundamental example for symbiosis is <a href=\"https://en.wikipedia.org/wiki/Symbiogenesis\" rel=\"nofollow\">endosymbiotic theory</a>. This theory in strongly simplified terms says that eukaryotic cells are the result of a symbiotic relationship between prokaryotes and early bacteria: both evolved separately with the prokaryotes probably being predators of some bacterial species. These species then are proposed to have evolved towards mutually beneficial, symbiotic relationship which essentially created a new form of life, eukaryotes. </p>\n\n<p>From a more abstract point of view, symbiosis can be regarded a further mechanism of evolution: while mutation and recombination act on a molecular level, symbiosis acts on a similar level to selection. It is basically a macro-level recombination of not just genes, but whole or partial organisms into new life forms.</p>\n\n<p>Some random examples:</p>\n\n<ul>\n<li>eukaryotes: mitochondria from proteobacteria, chloroplasts from cyanobacteria.</li>\n<li>bioluminescence in \"fireflies\" by vibrio bacteria</li>\n<li>microbiome inside \"guts\" of more complex organisms</li>\n<li>mycorrhizae (phosphor fixing) at the roots of some plants</li>\n</ul>\n"
},
{
"answer_id": 61135,
"pm_score": -1,
"text": "<p>Short Answer: As far as we know, it doesn't.</p>\n\n<h2><strong>Mutations at Conception</strong></h2>\n\n<p>The mutations you describe as occurring during conception which generate new information have never been observed to take place. Instead, we have observed mutations which <em>reduce</em> existing information. In humans, approximately 100 such mutations take place every generation.</p>\n\n<p>Necessarily if information-additive mutations existed, they'd need to produce a lot more information to make up for the loss. Necessarily, descendants would have a larger and more complex genome than their ancestors. The opposite has been observed, where descendants have smaller genomes than their ancestors.</p>\n\n<h2>Abiogenesis</h2>\n\n<p>Before Darwin had written <em>On the Origin of Species by Means of Natural Selection, or the Preservation of Favoured Races in the Struggle for Life</em>, Pasteur was disproving the idea of abiogenesis, as the theory had gone around that germs could spontaneously appear. Despite this, Darwin took abiogenesis as part of the theory of evolution, which has consistently proved impossible in tests with no observable data to the contrary.</p>\n\n<p>Genetic information is fragile and is quickly destroyed over time if it doesn't have enzymes to continually maintain it. There is no gradual process of accumulated information that can result in life able to reproduce, as far as we have found from study and observation. The very difficult process of creating amino acids to bond and form the nucleotides (necessary to form DNA chains) is complicated by the chirality problem, where artificial tests have resulted in both left-handed (L) and right-handed (D) optical isomers were created in a racemic mixture. In biological systems, almost all of the compounds are non-racemic, or homochiral, and biological creatures only use left-handed amino acids in the construction of DNA and RNA. All subsequent have tests run into the same problem.</p>\n\n<h2>Theory</h2>\n\n<p>As for the theory itself, you and Remi.b have described it accurately. As genetics was an unknown field at that time, it was the mistaken idea that natural selection changed a creature through the creation of information, rather than the reformation, sharing, and loss of existing information.</p>\n\n<p><strong>Sources:</strong> <em>Genetic Entropy and the Mystery of the Genome</em> by John Sanford. <em>The Miller–Urey experiment</em>.</p>\n"
}
] |
40,964 |
<p>I'm trying to find out how many molecules of nucleoside triphosphates (ATP, GTP, UTP and/or CTP) it takes to release enough energy to link two amino acid monomers together with a peptide bond, specifically during the process of mRNA translation.</p>
<p>I've tried to do some research online, but I could not find a reputable source that will say definitely how much energy is consumed in the process. The best answer I could find is formulated based on <em>'Molecular Biology of the Cell'</em> 4th edition by Alberts B, Johnson A, Lewis J, et al., which is that at least one molecule of ATP is consumed for every peptide linkage. Is this correct?</p>
<p>I've also read on a science forum that the amount of ATP consumed during translation is different for every amino acid, but I could not find a reliable source to back up that claim. Is this true?</p>
|
[
{
"answer_id": 65168,
"pm_score": 4,
"text": "<p>Although the question shows considerable effort to achieve clarity, the way it is phrased as:</p>\n\n<blockquote>\n <p>How many molecules of nucleoside triphosphate… [does] it take <em>to release enough energy</em></p>\n</blockquote>\n\n<p>still allows ambiguity, as I would not really regard the NTPs involved in protein synthesis “releasing energy”. So let us consider two reformulations of the question, as the explanation of the answers is of more scientific interest than the actual answers.</p>\n\n<p><strong>1. How many molecules of NTP are hydrolysed in the reactions causing the formation of one peptide bond on the ribosome?</strong></p>\n\n<blockquote>\n <p>Answer = 3</p>\n</blockquote>\n\n<p>Formation of each peptide bond involves a cycle consisting of the introduction of a single new aminoacyl-tRNA to the A site of a ribosome carrying a growing polypeptide chain (or initiator tRNA for the first peptide bond), the peptidyl transferase reaction, and than translocation of the extended peptidyl-tRNA from A- to P-site. (<em>See</em>, e.g. Berg <em>et al.</em> online — <a href=\"https://www.ncbi.nlm.nih.gov/books/NBK22425/\" rel=\"noreferrer\">Ch. 29</a>)</p>\n\n<p><em>1 ATP</em> is hydrolysed in the aminoacylation reaction:</p>\n\n<pre><code> Amino Acid + tRNA + ATP → Aminoacyl-tRNA + AMP + PPi\n</code></pre>\n\n<p><em>1 GTP</em> is hydrolysed in the aatRNA binding reaction catalysed by EF-Tu/EF1.</p>\n\n<p><em>1 GTP</em> is hydrolysed in the translocation reaction catalysed by EF-G/EF2</p>\n\n<p><em>No</em> NTP is consumed directly in the peptidyl transferase reaction — the energy for bond formation comes from the ‘activated’ aminoacyl-tRNA.</p>\n\n<p><a href=\"https://i.stack.imgur.com/Zsxg0.png\" rel=\"noreferrer\"><img src=\"https://i.stack.imgur.com/Zsxg0.png\" alt=\"Elongation and GTP hydrolysis\"></a></p>\n\n<p><strong>2. What is the total energetic cost in molecules of ATP for the formation of one peptide bond?</strong></p>\n\n<p>Here one might argue that: </p>\n\n<blockquote>\n <p>Answer = 4+</p>\n</blockquote>\n\n<p>The additional ATP occurs if one considers the total energetic cost of the aminoacylation reaction as 2 ATP, not 1 ATP. This arises from the fact that the ATP is hydrolysed to AMP (+PPi) and not ADP. Recycling of the AMP involves first the use of 1 molecule of ATP in the <a href=\"https://en.wikipedia.org/wiki/Adenylate_kinase\" rel=\"noreferrer\">adenylate kinase</a> reaction to produce ADP:</p>\n\n<pre><code> ATP + AMP ⇄ 2ADP\n</code></pre>\n\n<p>followed by the energy (from membrane <a href=\"https://en.wikipedia.org/wiki/ATP_synthase\" rel=\"noreferrer\">ATP synthase</a>) to regenerate ATP from ADP:</p>\n\n<pre><code> ADP + Pi ⇾ ATP\n</code></pre>\n\n<p>Why 4+? Certain amino acids (e.g. val and ile) are sufficiently similar to one another that the aminoacyl-tRNA synthetases have evolved a <a href=\"https://www.ncbi.nlm.nih.gov/books/NBK22356/#_A4151_\" rel=\"noreferrer\">proof reading</a> capacity, in which any incorrectly aminoacylated tRNA is hydrolysed. This only occurs for certain amino acids and at a rate that is difficult to determine, so the wastage of the ATP in this manner cannot be calculated precisely.</p>\n"
}
] |
[
{
"answer_id": 40973,
"pm_score": -1,
"text": "<p>First, during the initiation of translation, a small ribosomal subunit binds to a molecule of mRNA. In a bacterial cell, the mRNA binding site on this subunit recognizes a specific nucleotide sequence on the mRNA just upstream of the start codon. An initiator tRNA, with the anticodon UAC, base-pairs with the start codon, AUG. This tRNA carries the amino acid methionine. And then, this process need one molecular GTP, and GTP--->GDP+Pi, which can provide energy for the assembly.\nYou can find more details in the book Campbell Biology, by Reece, Urry, et.al..</p>\n"
},
{
"answer_id": 41105,
"pm_score": -1,
"text": "<p>About 5 ATP molecules are required for the addition of a single amino aid to a growing peptide chain.</p>\n\n<p>I found this answer in <em>Ribosome and transcript copy numbers, polysome occupancy and enzyme dynamics in Arabidopsis</em> by Piques et al.:</p>\n\n<blockquote>\n <p>The addition of an amino acid to a growing peptide chain requires two ATP molecules for amino acid activation and another two ATP for peptide bond formation and ribosome translation, plus additional costs of about another ATP, for error correction and the synthesis of sequences that are removed during protein maturation.</p>\n</blockquote>\n"
},
{
"answer_id": 51530,
"pm_score": -1,
"text": "<p>Actually it depends on the question. Whether you mean to say: How many amino acids are required? Or proteins?\nThere is a characteristic difference between amino acids and proteins.\nHence the number. Of amino acids can be determined by the following-\nIf we consider a protein composed of \"n\" number of amino acids,\nit takes (4n)-1 number of ATP for the translation process.</p>\n"
},
{
"answer_id": 65162,
"pm_score": -1,
"text": "<p>4 ATP :\n2 for activation amino acids to bind with specific tRNA.\n1 for initiation \n1 for elongation to push tRNA to the p site of ribosome</p>\n"
}
] |
42,050 |
<p>In my <a href="https://biology.stackexchange.com/questions/42033/what-are-we-missing-about-the-real-workings-of-the-evolutionary-process">last question</a> I asked why we don't see increased complexity in artificial life simulations of evolution. It seems I had fallen for a common misconception, that evolution was about <em>improvement by increasing complexity</em>. One comment discussing that post read</p>
<blockquote>
<p>"... he [David Deutsch] is falling for one of the biggest
misconceptions about evolution that you can, that evolution is about
<em>improvement</em>. Evolution has simply only ever been about change..." </p>
</blockquote>
<p>However, when you look at the history of life you see increases in complexity. You see this increasing complexity evolving over billions of years, suggesting that it requires an explanation.</p>
<p><strong>My question</strong><br>
If evolution is not about increasing complexity then how does so much complexity evolve?</p>
|
[
{
"answer_id": 42053,
"pm_score": 7,
"text": "<p>I think possibly the problem here is the way you're approaching the issue.</p>\n\n<p>You're considering <em>improvement</em> as anything that increases the abilities or complexity of the organism—that isn't necessarily what an <em>improvement</em> is though. The outcome of natural selection is that the organism best equipped to survive/reproduce in a certain environment is the <a href=\"https://en.wikipedia.org/wiki/Natural_selection#Mechanism\" rel=\"nofollow noreferrer\">most successful</a>. So, for example, thermophillic archaea do much better in 60°C-plus pools of water than humans do. Our capacity to process information, use tools, etc. doesn't actually confer much advantage in that situation. And there can be downsides to that kind of complexity as well, <a href=\"http://www.nature.com/nature/journal/v467/n7318/full/nature09486.html?foxtrotcallback=true\" rel=\"nofollow noreferrer\">requiring more energy</a> and <a href=\"https://books.google.com.au/books?id=XDoZSBPj_tQC&lpg=PT18&ots=GLltT9R3UX&dq=complex%20organism%20gestation%20time&pg=PT18#v=onepage&q=complex%20organism%20gestation%20time&f=false\" rel=\"nofollow noreferrer\">longer developmental periods</a>. So, natural selection in 60°C-plus pools of water gives you archaea, and in (presumably) the plains of East Africa, it gives you humans.</p>\n\n<p>The comment you quote mentions sickle-cell anaemia, which is a different example. While there is little benefit to having the sickle-cell anaemia allele in a temperate region, in those regions where malaria is endemic, heterozygosity can provide a survival advantage, and so the allele is maintained in the population. If you're someone living in a malaria-endemic region, and you don't have access to antimalarials, heterozygosity for the sickle-cell anaemia allele is arguably an <a href=\"https://www.cdc.gov/malaria/about/biology/sickle_cell.html\" rel=\"nofollow noreferrer\"><em>improvement</em></a>. It depends entirely on how you define the word.</p>\n\n<p>The <a href=\"https://en.wikipedia.org/wiki/Evolution#Natural_selection\" rel=\"nofollow noreferrer\">fundamental principal</a> of natural selection is that it favours the organism most suited to a particular environment. But, that <a href=\"https://en.wikipedia.org/wiki/Evolution_of_biological_complexity#Selection_for_simplicity_and_complexity\" rel=\"nofollow noreferrer\">isn't always</a> the <a href=\"https://www.newscientist.com/article/dn13617-evolution-myths-natural-selection-leads-to-ever-greater-complexity/\" rel=\"nofollow noreferrer\">most complex</a> organism. It's important not to confuse <em>human-like</em> with <em>better</em>. It isn't the universal endpoint of evolution to produce an organism similar to us, just the organism most suited to the environment in question.</p>\n\n<p>Also, to briefly address the previous question you asked—you asserted that we must be missing something from the process of evolution because we were unable to simulate it. You also pointed out that (in your opinion) we have sufficient computing power to simulate the kinds of organisms you're referring to. But natural selection is intrinsically linked to the environment it occurs in, so the simulation wouldn't just have to accurately simulate the biological processes of the organism, but also <strong>all</strong> of the external pressures the organism faces. I'd imagine that, in simulating evolution, <em>that</em> would be the real obstacle.</p>\n"
}
] |
[
{
"answer_id": 42063,
"pm_score": 4,
"text": "<p><strong>Evolution is simply a process of change.</strong> It is a change in trait values of populations over time. It results from four mechanisms: mutation, migration, drift, and selection. The first three lead to random change from one generation to the next, which may increase or decrease fitness, while selection will <em>generally</em> lead to adaptation (relatively increased fitness in subsequent generations).</p>\n\n<blockquote>\n <p>\"Evolution means change, change in the form and behaviour of organisms\n between generations. ... When members of a population breed and\n produce the next generation we can imagine a lineage of populations,\n made up of a series of populations through time. Each population is\n ancestral to the descendant population in the next generation: a\n lineage is an ancestor-descendent series of populations. Evolution is\n then change between generations within a population lineage.\" - <a href=\"https://www.blackwellpublishing.com/ridley/\" rel=\"nofollow noreferrer\">Ridley,\n Evolution, Page 4.</a></p>\n</blockquote>\n\n<p>This is what Darwin termed \"<a href=\"http://www.fossilmuseum.net/Evolution/DarwinsFinches.htm\" rel=\"nofollow noreferrer\">descent with modification</a>\". Later in Ridley's book he goes on to say something which is important to for evolutionary biology; <em>why is there so much adaptation?</em></p>\n\n<blockquote>\n <p>\".. not every detail of an organism's form and behaviour is\n necessarily adaptive. Adaptations are, however, so common that they\n have to be explained. Darwin regarded adaptation as the key problem\n that any theory of evolution had to solve. In Darwin's theory - as in\n modern evolutionary biology - the problem is solved by natural\n selection.\" - Ridley</p>\n</blockquote>\n\n<p>Another good clue as to what evolution really is comes from the Charlesworth & Charlesworth book:</p>\n\n<blockquote>\n <p>\"Evolution means cumulative change over time in the characteristics of\n a population of living organisms. ... All evolutionary changes require\n initially rare genetic variants to spread among the members of a\n population, rising to high frequency...\" <a href=\"http://rads.stackoverflow.com/amzn/click/0981519423\" rel=\"nofollow noreferrer\">Charlesworth & Charlesworth,\n Elements of Evolutionary Genetics</a>, page XXV</p>\n</blockquote>\n\n<p>Basically the random mechanisms of evolution (mutation, migration, drift) are not as good at making rare beneficial alleles spread through a population as selection is. Selection is the major mechanism that should, as a general rule, <a href=\"https://en.wikipedia.org/wiki/Fixed_allele\" rel=\"nofollow noreferrer\">fix</a> beneficial alleles in a population. Drift, mutation, and migration will rarely cause the beneficial (adaptive) alleles to fix. Furthermore, mutation will generally have deleterious (maladaptive) effects <a href=\"http://www.nature.com/nrg/journal/v6/n2/full/nrg1523.html\" rel=\"nofollow noreferrer\">according to Fisher's geometric model of adaptation</a>.</p>\n\n<p>You can read more about the process of adaptation and why selection doesn't guarantee adaptive evolution in <a href=\"https://biology.stackexchange.com/questions/41813/why-even-if-all-requirements-for-natural-selection-are-met-it-may-not-happen/41843#41843\">my answer here</a>. Briefly, selection will lead to adaptation if there is sufficient genetic variance in fitness, selection is a constant from one generation to the next, and genetic correlations do not impede the response to selection. Furthermore, the other evolutionary mechanisms can counteract selection, preventing adaptation. These are some of the reasons that simulating evolution accurately is so difficult.</p>\n\n<p><strong>The reason that we can't say complexity increases by evolution is that none of these mechanisms give a consistent increase in complexity.</strong> While mutation, migration, and drift will have random effects on organismal complexity, fitness (thus selection) may have some relation to complexity. <strong>To evolve, some degree of complexity is required such that the minimum conditions for evolution can be met.</strong> However, selection should favour the most fit genes over time, which depends on the niche/adaptive landscape and genetic variation available. Selection in the <em>real</em> world (as opposed to alife<sup>*</sup> world) would, as an <em>approximate</em> rule of thumb, favour an intermediate level of complexity where fitness is optimised (individuals are good at producing offspring in their niche) with minimal wasteful complexity (complex structures that do not increase fitness).</p>\n\n<p>In summary, to answer your question, we see so much improvement because of selection, which leads to the process of adaptation, but adaptation does not equate to increasing complexity. The key to understanding your problem is an understanding of the difference between <strong>the process of evolution (change) and the process of adaptation (improvement), and the difference between optimality and complexity.</strong> In the world of alife simulation complexity $\\equiv$ adaptedness, in the real word complexity $\\neq$ adaptedness. </p>\n\n<hr>\n\n<p>Good reading can be found in <a href=\"http://evolution.berkeley.edu/evolibrary/misconceptions_faq.php#a3\" rel=\"nofollow noreferrer\">a link</a> that AMR posted in a comment to another answer.</p>\n\n<hr>\n\n<p><sup>*</sup> <em>Artificial life (alife) simulations of evolution generally use complexity as a proxy for fitness such that selection will be directional for increased complexity</em></p>\n\n<hr>\n\n<p>Just as a response to a comment you made under your question, as to why simulations don't produce \"stylized facts found in real evolution\": Scientists understand quite well how evolution works (as explained in my answer, is a result of selection, genetic (co)variation, and population demographics), however, simulation to produce \"stylized facts found in real evolution\" would require a complete and precise history of the selection, genetic (co)variation, and population demographics that have existed since the origins of life. That is why simulation does not work like you think it should.</p>\n"
},
{
"answer_id": 42064,
"pm_score": 4,
"text": "<p>It might help to not think about evolution as a process at all - it tends to imply some sort of planning or goals or something like that. That's not what evolution is - evolution is simply a fact. When we talk about \"the evolution of humans\", we're describing the <em>history</em> of various human precursors. Evolution is basically a historical record of <em>things that worked in the past in a given environment</em>.</p>\n\n<p>Most people tend to antropomorphize evolution, give it goals. There's no such thing, and it just makes you even more confused. There's nothing paradoxical about \"evolving to extinction\" - evolution is not a path from a base organism to an improved organism. It's simply a history of the changes that survived and thrived in a population. Sometimes that's because those changes gave the individuals and populations a better chance of surviving in their environment, so those traits became more and more prevalent in a population - for example, skin turning to hardened skin, turning to armour plates or weapons, or a better beak allowing it to reach into a food source that isn't available to others. Sometimes, it's simply dumb luck - don't forget that there was a point where the whole (pre-)human population was reduced to a ridiculously low number (I think it was something like 10 000 individuals or maybe even less). It would only take one local catastrophe to kill off the whole human species, no matter how \"improved\" and \"advanced\" we might consider ourselves to be.</p>\n\n<p>Another rather brutal example would be the evolution of photosynthesis - when the atmosphere started filling up with free oxygen, it killed off almost all life on the Earth. Sounds like an improvement? Getting rid of your competiton? Well, it also fueled a massive growth of new species that were not only <em>adapted</em> to an oxygen atmosphere, they used it as a source of energy! Not only would they thrive on the \"waste products\" of the photosynthesers, they even consumed them.</p>\n\n<p>Even if you wanted to describe evolution as a process that improves fitness, you must not forget that a change that improves your reproduction rates in one kind of environment can hinder (or kill) you in another.</p>\n\n<p>When pre-Koala bears drifted to be exclusive Eucalyptus-vores, it gave them an advantage - they had a food source noöne else can use. But it also made them 100% dependent on Eucalyptus. When Eucalyptus dies, they will as well. Something that was arguably an improvement can easily be the thing that kills of your entire species. It only \"improved\" their ability to survive and thrive in one specific environment - it also entirely locked them in their niche.</p>\n\n<p>In summary:</p>\n\n<ul>\n<li>Evolution doesn't have goals, so it's weird to say \"evolution is about improvement\". Random changes have a tiny chance of becoming (locally) useful traits, and useful traits have a tiny chance of becoming entrenched in the population, and thus forming a new species over time. It's a history of changes, not a prediction of the future. The great thing about Darwin's Theory of Evolution is that it predicts what <em>kinds</em> of changes are possible (and which are impossible!) - for example, that complex systems can't arise out of the blue, or that different branches of history (\"evolutionary tree\") cannot exchange traits.</li>\n<li>Almost all changes also have their drawbacks - it's a balancing act. There's some great examples of changes that are almost universally good - sexual reproduction and human-level intelligence are a great example of something that works in almost any environment. But even so, there's still examples of where they didn't \"win\" yet. There's still asexual reproduction on Earth, and most of Earthly life doesn't have human-level intelligence yet. Lions do not rule the world, even though they're apex predators in some environments.</li>\n</ul>\n"
},
{
"answer_id": 42071,
"pm_score": 3,
"text": "<p>I'm going to chime in here. As both a scientist and a software engineer.</p>\n\n<p>Firstly, evolution is not about improvement at all. It is about survival and random change. There are as many if not more mutations that are disadvantageous. But they tend not to survive.</p>\n\n<p>On the other hand, genetic algorithms are an attempt to use a similar process of mutation and survival of the fittest.</p>\n\n<p>But the first step in a genetic algorithm is to define a fitness function. This function will cull the weakest algorithms, just like an environment kills life in the real world.</p>\n\n<p>A good primer on Genetic Algo can be found on <a href=\"https://www.youtube.com/watch?v=qv6UVOQ0F44\" rel=\"nofollow\">https://www.youtube.com/watch?v=qv6UVOQ0F44</a></p>\n\n<p>However that fitness function will only optimise for certain goals. For example, a badly tuned fitness function will end life on earth either by the <a href=\"https://wiki.lesswrong.com/wiki/Paperclip_maximizer\" rel=\"nofollow\">paperclip apocalypse</a>, or giving rise to skynet.</p>\n\n<p>In these cases the algo is not improving towards the goals you want. But never the less it improves.</p>\n\n<p>Another complexity is that, genetics is a very greedy optimisation strategy. Mutations tend to be small, because large mutations tend to more often move away from optimal solutions. This means that evolution can only find local maximas and will often miss the global maxima.</p>\n\n<p>Hence improvements can only occur when there is a small tunneling cost to the new maxima.</p>\n\n<p>An example of this can be found in mammalian eyes. Our optic nerve passes through retina and connects to the front of our retina, and physically blocking the retina from doing an optimal job. If evolution were able to find a global maxima, then mammals would have been able to evolve to have squid like eyes, which route from behind.</p>\n\n<p>Moreover, had evolution been about pure improvement, then we should have evolved away our blind spot many many generations ago.</p>\n\n<p>However, human ancestors have rarely been attacked by circles and crosses that are precisely spaced apart in the African continent.</p>\n\n<p>Saying that evolution is about improvements is like setting up a school where there is no teaching, and every year you expell the bottom 10% of the students.</p>\n"
},
{
"answer_id": 62898,
"pm_score": 0,
"text": "<p>Evolution produces branching trees, and branching is multiplicity.</p>\n\n<p>Fitness is associated with complexity, and, with radiation into more or less challenging environments. Fitness increases with versatility and added functions, in equilibrium within one niche, and for change across niches. Are cold blooded animals simpler than warm blooded ones? the consensus is that they are simpler, less apt and globally superseded. Even if a lizard has as many genes as a human (40,000) it is less complex than a human.</p>\n\n<p>Take Motility for example. Locomotion is complex, compared to passive or sedentary displacement. Most prokariotes have evolved some kind of motility, cilia and flagella. The simpler procariotes were eaten out of existence, as the motile ones grew to dominate and pervade. There is a predator prey issue which has resulted in the extinction of simpler, slower species and in the promotion of more complex ones. The ones that survived did so by adding defense functions. </p>\n\n<p>Life is thought to have started in simpler environments with less biochemical and physical fluctuations than it later evolved into. Eukaryotes have not evolved back into prokaryotes, even though they could, and eukaryotes have more scope for complexity, same as lego blocks in multiple numbers are not as simple as single blocks. </p>\n\n<p>Evolution is also about the blind use of an initially small but potentially much larger memory bank of many gigabytes.\"Gene Duplication is believed to play a major role in Evolution.\"</p>\n\n<p>Unless life began in greater quantity than it now exists, evolution requires that natural processes have, over time, increased the total quantity of genetic material (DNA) present on our planet.</p>\n\n<p>I'm going out on a pirate's plank of logic here. sorry about that.</p>\n\n<p>Survival fitness is about increased complexity when the environment is increasingly complex. Evolution Causes complexity to occur... </p>\n\n<p>Change is an additive process, and the more change is provoked, the more added functions tend to result along.</p>\n\n<p>The more complex the path has been to arrive at the current stage of the species, the additive complexity rises. (Also the DNA keeps on record the genes from old environments to not lose many precious years spent finding useful genes/biochemistries, while adding new ones). However evolution can be about the conquest of less complex environments:</p>\n\n<p>Put a fish into a cave with no lights, constant temperature, and simple tasks, it will lose some of it's complex genes and may, over time become genetically simpler, than a fish living in a river. It requires less senses, less thermal adaptations, less locomotion pressure and less species competition. It is rare for species to retrograde generally, they tend to extend their range, but in deep sea and caves, locomotive and biochemical retrograde can happen. </p>\n\n<p>Increased size gives increased fitness in most settings: larger metabolic reserves, less sensitivity to change, bigger predator pray advantage... and bigger size means more cells, different locomotion pressure, which means different metabilic resource distribution(lymph, digestion, blood), and That is that's the essence of your complex topic: Do environments encourage complexity? if so, how \"complex\" are environments in the universes land/sea biomes? Geology, climate and hydrology are of incredible complexity... So... can we say evolution is not about the conquest of new environments? It requires a good philospher to shed light on this question.</p>\n\n<p>The <em>pressure</em> is more often on increased performance in a complex environment using highly complex foods and locomotions. </p>\n\n<p>Increased complexity is an inevitable ramification of the evolutionary process through time and space, rather than a direct and inevitable requirement of it.</p>\n\n<p>Because species evolve into <em>new</em> niches, The most logical and efficient way to do that, is to keep the genes for <em>old</em> niches, in the DNA library, and to add new ones next to it. If the organism did not keep genes from old niches, and use them for a proportion of it's mutations, it would be less apt. Useful genes are costly, they can cost millions of years to find them, for example The more of a toolbox of biochemistry and morphology.</p>\n\n<p>For Biochemistry, life \"discovers\" new materials and proteins, and puts them to use, and it keeps a record of those materials after they are not needed. </p>\n\n<p>A sea slug can evolve into a vertebrate fish, but a fish can't evolve back to a slug, because complexity enhances fitness, so perhaps we can say that fitness and complexity are not disassociable.</p>\n\n<p>Change is complex thing, and evolution is about changing, so for me, evolution adds complexity every time it changes. </p>\n"
},
{
"answer_id": 88589,
"pm_score": 0,
"text": "<p><strong>The simplest way to look at it is there is a near infinite number of ways to be more complex but a very limited number of ways to be simpler.</strong> There is even fewer ways of being simple. So even with just pure random variation, over time all things being equal you will end up with more complex organisms. </p>\n\n<p>This becomes even more true when you take competitor into account, competition, go too simple and you lose the ability to do things that you really need to compete with the rest of life around you, go too simple and you can't reproduce fast enough to keep up with all the things eating you. While on the other hand the cost of complexity can be offset by better capabilities. On top of this imagine a ruler with as simple as life can be and still function on one side and as complex as life can get and still function on the other. the first life is going to be pretty close to the simplest possible life, so most of the ways of being alive that are possible are going to be more complex, so again even if you ignore selective pressures either way, just random variation is going to create more complex life than simple life. There is more complex phase space to occupy than simple phase space. </p>\n\n<p>imagine I stand with my back to a cliff and throw a ball randomly in the air, now after I throw a thousand balls the vast number of balls I find are going to be in front of me, not becasue I am actively trying to throw them there but because most of the balls that fall behind be get lost, (go extinct for our analogy)</p>\n"
}
] |
42,273 |
<p>On <a href="http://ericturkheimer.blogspot.com/2015/05/the-heritability-of-everything.html">his blog</a>, Eric Turkheimer writes:</p>
<blockquote>
<p>[T]aken as a number, a unit of analysis, heritability coefficients are
funny things to aggregate on such a massive level. What exactly are
we supposed to make of the fact that twins studies in the
ophthalmology domain produced the highest heritabilities? Should eye
doctors, as opposed to say dermatologists, be rushing to the genetics
lab because their trait turns out to be more heritable? No. Whatever
else a heritability may be, it is not an index of how "genetic"
something is. It is not, for example, a useful indicator of how
successful gene-finding efforts are likely to be. If nothing else,
differences in reliability of measurement are confounded every
heritability tallied here. My point is this-- although it's nice to
know that on average everything is 50% heritable, it's hard to attach
much meaning to the number itself, or especially to deviations from
that number, to the fact that eye conditions have heritabilities
around .7 and attitudes around .3. Having two arms has a heritability
of 0.</p>
</blockquote>
<p>As I understand this, one reason Turkheimer believes heritability coefficients are not an index of how genetic a trait is is that they are confounded by varying levels of measurement error. So, for example, maybe the relatively low heritabilities in skin conditions compared to eye conditions are because there is more measurement error in relation to skin conditions.</p>
<p>Turkheimer implies that there are other reasons why it's not appropriate to say a heritability coefficient is an index of "how genetic" something is. What are those other reasons?</p>
|
[
{
"answer_id": 42280,
"pm_score": 6,
"text": "<p>Rather than discussing what heritability is not through wordy sentences, let's just talk about what heritability <strong>is</strong>. There are two \"types of heritability\":</p>\n\n<ul>\n<li><em>Heritability in the broad sense</em></li>\n<li><em>Heritability in the narrow sense</em>.</li>\n</ul>\n\n<p>I will discuss a few concepts and slowly introduce the concept of heritability in both senses.</p>\n\n<p><strong>Phenotypic trait</strong></p>\n\n<p>The phenotype is the consequence of the genotype on the world. In brief, a phenotypic trait is any trait that an individual is made of! </p>\n\n<p><strong>Quantitative trait</strong></p>\n\n<p>A quantitative trait is any trait that you can measure and ordinate, that is any trait that you can measure with numbers. For example, height is a quantitative trait as you can say that individual <code>A</code> is taller than individual <code>B</code> which is itself taller that individual <code>C</code>.</p>\n\n<p><strong>Variance of a quantitative trait</strong></p>\n\n<p>In a population, different individuals can have different values for a given phenotypic trait <span class=\"math-container\">$x$</span>. Because we are talking about quantitative traits we can calculate the variance of the trait in the population. Let's call this variance <span class=\"math-container\">$V_P$</span> such as</p>\n\n<p><span class=\"math-container\">$$V_P=\\frac{1}{N}\\sum_i (x_i - \\bar x)^2$$</span></p>\n\n<p>In the above equation, <span class=\"math-container\">$x_i$</span> is the value of the phenotypic trait <span class=\"math-container\">$x$</span> of individual <span class=\"math-container\">$i$</span>. <span class=\"math-container\">$N$</span> is the population size (there are <span class=\"math-container\">$N$</span> individuals in the population) and <span class=\"math-container\">$\\bar x$</span> is the average phenotypic trait <span class=\"math-container\">$x$</span> in the population.</p>\n\n<p><span class=\"math-container\">$$\\bar x = \\frac{1}{N}\\sum_i x_i$$</span></p>\n\n<p><strong>What is causing phenotypic variance</strong></p>\n\n<p>Why would a population display any phenotypic variance? Why wouldn't we just look exactly the same? What explains these differences?</p>\n\n<p>For some traits, we see very little variance. To consider the example the OP gave in the post, the number of arms in the human population shows very little variance. However, there is quite a bit of variance in terms of the number of IQ, in terms of height or of weight.</p>\n\n<p>There are two (main) sources of variance that are underlying this phenotypic variance. The first one is the genetic variance and the second one is the environmental variance. We will call the genetic variance <span class=\"math-container\">$V_G$</span> and the environment variance <span class=\"math-container\">$V_E$</span>.</p>\n\n<p>If in a population, people vary a lot in terms of how many hamburgers they eat, then there is a non-negligible <span class=\"math-container\">$V_E$</span> underlying the phenotypic variance <span class=\"math-container\">$V_P$</span> for weight. If in a population, there is a lot of variation of genes affecting weight, then there is a non-negligible <span class=\"math-container\">$V_G$</span> underlying the phenotypic variance <span class=\"math-container\">$V_P$</span> for weight.</p>\n\n<p>By the way, a gene (or another non-coding sequence) that is polymorphic (i.e. has more than 1 allele in the population) and which explains some of the variance in the phenotypic quantitative trait is called a Quantitative Trait Locus (QTL). A locus is a sequence (of any length) on the genome. </p>\n\n<p><strong>Math reminder</strong></p>\n\n<p>Variances of uncorrelated variables can simply be added! For simplicity, we will assume for the moment that we are considering uncorrelated variables. As a consequence, we can express the phenotypic variance <span class=\"math-container\">$V_P$</span> as a sum of the phenotypic variance that is due to environmental variance <span class=\"math-container\">$V_E$</span> and the phenotypic variance that is due to genetic variance <span class=\"math-container\">$V_G$</span></p>\n\n<p><span class=\"math-container\">$$V_P=V_E+V_G$$</span></p>\n\n<p>This equation is slightly simplified and this will affect the below calculations. See the section <em>Other sources of phenotypic variance</em> for more info.</p>\n\n<p>We can now talk about heritability!</p>\n\n<p><strong>Heritability in the broad sense</strong></p>\n\n<p>Heritability in the broad sense <span class=\"math-container\">$h_B$</span> is defined as the fraction of phenotypic variance <span class=\"math-container\">$V_P$</span> that is explained by genetic variance <span class=\"math-container\">$V_G$</span>. In the equation, it gives:</p>\n\n<p><span class=\"math-container\">$$h_B=\\frac{V_G}{V_P} = \\frac{V_G}{V_E+V_G}$$</span></p>\n\n<p><strong>Heritability in the narrow sense</strong></p>\n\n<p>Heritability in the narrow sense <span class=\"math-container\">$h_N$</span> makes one further trick. We have to consider that the genetic variance <span class=\"math-container\">$V_G$</span> that is underlying the phenotypic variance can itself be decomposed into a sum of variances. The variances that we like to consider the <em>additive genetic variance</em> <span class=\"math-container\">$V_{G,A}$</span> and the <em>dominance genetic variance</em> <span class=\"math-container\">$V_{G,D}$</span>.</p>\n\n<p>The additive genetic variance is the genetic variance that is due to additive interaction between alleles. The dominance of genetic variance is due to non-additive interactions between allele.</p>\n\n<p>We can now define the heritability in the narrow sense <span class=\"math-container\">$h_N$</span> as the is defined as the fraction of phenotypic variance <span class=\"math-container\">$V_P$</span> that is explained by the additive genetic variance <span class=\"math-container\">$V_{G,A}$</span>. In the equation, it gives:</p>\n\n<p><span class=\"math-container\">$$h_N=\\frac{V_{G,A}}{V_P} = \\frac{V_{G,A}}{V_E+V_G} = \\frac{V_{G,A}}{V_E+V_{G,A}+V_{G,D}}$$</span></p>\n\n<p>In the special case, when all the genetic variance <span class=\"math-container\">$V_G$</span> is exclusively done through additive interactions, then <span class=\"math-container\">$V_{G,D} = 0$</span> and <span class=\"math-container\">$V_{G,A}=V_G$</span> and therefore <span class=\"math-container\">$h_N=h_B$</span></p>\n\n<p><strong>Interpretation of the heritability</strong></p>\n\n<p>If all of the phenotypic variance is due to genetic causes (and regardless of whether there is a lot or a little variance), then <span class=\"math-container\">$h_B=1$</span>. If all of the phenotypic variance is due to environmental variance, then <span class=\"math-container\">$h_B=0$</span>.</p>\n\n<p><em>So what does a <span class=\"math-container\">$h_B=0.3$</span> means?</em></p>\n\n<p>It means that 30% of the phenotypic variance is explained by genetic variance and that 70% of the phenotypic variance is due to environmental variance.</p>\n\n<p>So, what if there is no phenotypic variance in the population? if <span class=\"math-container\">$V_P=0$</span>, then the heritability is undefined (as dividing by zero is undefined). However, in general, we tend to think that there is always a tiny bit of environmental variance and most people would just go on saying that heritability is 0 when <span class=\"math-container\">$V_P=0$</span>.</p>\n\n<p><strong>What will affect the heritability?</strong></p>\n\n<p>A measure of heritability is true for one population, in one environment.</p>\n\n<p>If you change the population, add a few mutations for example, you might well create a polymorphic locus that is causing some phenotypic variance. If you put the same population in another environment, you could suddenly have more or less phenotypic variation due to environmental variance. Typically, if you measure heritability in the lab in a controlled and constant environment, then you will likely overestimate the heritability (as you underestimate <span class=\"math-container\">$V_e$</span>) compared to the same population that is living in a very heterogeneous environment.</p>\n\n<p><strong>What heritability is not!</strong></p>\n\n<p>If a trait has low heritability, it does NOT mean that it is (or is not) an adaptation. It only means that there is no genetic variance that explains the phenotypic variance.</p>\n\n<p><strong>Why do we care about heritability?</strong></p>\n\n<p>If there is no genetic variance for a trait, it means that the only way this trait can change through time is by changing the environment (or by creating a non-zero genetic variance through mutations). If there is a non-zero genetic variance and if there is a difference in fitness between individuals having different trait value then, the trait is under natural selection.</p>\n\n<p>The most commonly used index of heritability in the heritability in the narrow sense <span class=\"math-container\">$h_N. $</span>Why do we care about <span class=\"math-container\">$h_N$</span>?</p>\n\n<p>Let <span class=\"math-container\">$\\bar x_t$</span> be the mean phenotypic value of the trait <span class=\"math-container\">$x$</span> at time <span class=\"math-container\">$t$</span>. One generation later, that is at time <span class=\"math-container\">$t+1$</span>, the mean phenotypic value is <span class=\"math-container\">$\\bar x_{t+1}$</span>. Let's define the response of selection <span class=\"math-container\">$R$</span> as the expected difference between these two quantities, that <span class=\"math-container\">$R=E[\\bar x_{t+1} - \\bar x_t]$</span>. Let's define the strength of selection <span class=\"math-container\">$S$</span> and the heritability in the narrow sense <span class=\"math-container\">$h_N$</span>, then </p>\n\n<p><span class=\"math-container\">$$R=h_N \\cdot S$$</span></p>\n\n<p>As a consequence knowing <span class=\"math-container\">$h_N$</span> allows us to predict the effect of selection on a given trait.</p>\n\n<p>This equation is called the breeder's equation (see <a href=\"https://biology.stackexchange.com/questions/16806/how-to-interpret-the-breeders-equation\">this post</a> about its interpretation).</p>\n\n<p><strong>Other sources of phenotypic variance</strong></p>\n\n<p>Saying <span class=\"math-container\">$V_P=V_G+V_E$</span> is a little too simplistic. In reality, there are other sources of phenotypic variation such as variance due to epigenetic changes <span class=\"math-container\">$V_I$</span> and variance due to developmental noise <span class=\"math-container\">$V_{DN}$</span> for example. It is also sometimes very important to consider the covariance between any pair of such variance. So, the equation would more correct if stated as</p>\n\n<p><span class=\"math-container\">$$V_P = V_G + V_E + V_I + V_{DN} + COV(V_G, V_E) + COV(V_G, V_I) + COV(V_G, V_{DN}) + COV(V_E, V_I) + COV(V_E, V_{DN}) + COV(V_I, V_{DN})$$</span></p>\n\n<p>Note that everyone is free to further decompose any of the above variance into a sum of variances as we did above for the genetic variance. For example, the environmental variance <span class=\"math-container\">$V_E$</span> could be decomposed into the sum of the phenotypic variance due to variance in temperature <span class=\"math-container\">$V_T$</span> and the phenotypic variance due to variance in precipitation <span class=\"math-container\">$V_{\\text{precipitation}}$</span> assuming the other types of environmental variances are negligible.</p>\n"
}
] |
[
{
"answer_id": 42445,
"pm_score": 3,
"text": "<p>Briefly, because remi.b gives a lot of good detail about this in his answer, (narrow sense) heritability is essentially a measure of how much of the phenotypic variance is explained by (additive) genetic variance. Phenotype (P) in an individual is the result of genetic (G) and environmental effects (E). </p>\n\n<p>$P = G + E$</p>\n\n<p>Thus the within-population variance in phenotype is</p>\n\n<p>$V_P = V_G + V_E$</p>\n\n<p>Genetic variance further decomposes in to additive (A), dominance (D), and interaction/epistatic variance (I).</p>\n\n<p>$V_G = V_A + V_D + V_I$</p>\n\n<p>Narrow sense heritability ($h^2$) is then</p>\n\n<p>$h^2 = \\frac{V_A}{V_P}$</p>\n\n<p><strong>Additive genetic variance and, as a result, the narrow sense heritability can be zero for two reasons.</strong> </p>\n\n<p>Firstly, <strong>if no genes have an effect on your trait</strong>, then additive genetic variance will be zero. </p>\n\n<p>Secondly, <strong>if the alleles at the loci affecting the trait are fixed within the population</strong>, additive genetic variance will be zero. </p>\n\n<p>Therefore, Eric Turkheimer is correct to say that heritability is not a measure of how genetic something is. However, a heritability of zero <em>does not mean</em> that something is not genetically controlled, just that there is no variance in the effects of genes. </p>\n\n<p>To follow from the example of having two arms, clearly having arms is genetically controlled, its a heritable trait, but the number of arms has very little/no genetic variance. Very few people have >2 or <2 arms, thus any allele for that seems to be exceptionally rare (the alleles determining that two arms are produced are more or less fixed, $p \\approx 1$, where p is the frequency of the allele coding for two arms).</p>\n\n<p>The following graph shows the effect of allele frequency on additive genetic variance, additive genetic variance is zero when the locus has a fixed allele, and maximised when the frequency of both alleles (a two allele model) 0.5. In practical terms, when p = 0.5, half of the population are heterozygotes, one quarter are homozygotes for allele 1, and one quarter are homozygotes for allele 2.</p>\n\n<p><a href=\"https://i.stack.imgur.com/qswUh.jpg\" rel=\"noreferrer\"><img src=\"https://i.stack.imgur.com/qswUh.jpg\" alt=\"enter image description here\"></a></p>\n\n<p>For example, <a href=\"http://www.ncbi.nlm.nih.gov/pubmed/26230387\" rel=\"noreferrer\">in this study</a>, we showed that genetic variance on the Y chromosome explained only ~0.4% of the variation in lifespan, which could be because very few of the genes affecting lifespan are on the Y (likely, because the Y contains very few genes, while lifespan is highly polygenic) and/or the genes on the Y affecting lifespan have low polymorphism (likely, because the Y is subject to various processes that greatly reduce within population molecular variation, compared to other chromosomes).</p>\n\n<p><strong>Heritability and additive genetic variance are important to understand because they determine the rate at which adaptation (evolution as a response to selection) can occur.</strong> <a href=\"http://onlinelibrary.wiley.com/doi/10.1111/j.1469-1809.1972.tb00764.x/abstract\" rel=\"noreferrer\">Following Fisher's fundamental theorem</a>, and as shown in the breeders equation ($r = h^2s$ where r is the response and s is selection), when $V_A = 0$ the $r = 0$.</p>\n"
},
{
"answer_id": 51961,
"pm_score": 3,
"text": "<p>Heritability is not a measure of how genetic a trait is. It's a measure of how much of the <em>variation</em> in the trait is due to <em>variation</em> in genetics.</p>\n\n<p>I'll try to make this clear with a story, to supplement the answers that rely more heavily on mathematics.</p>\n\n<blockquote>\n <p>For reference: technically it's the fraction of <em>phenotypic variance</em>\n which is due to variance in genetic effects: <span class=\"math-container\">$H^2=\\frac{V_G}{V_P}$</span> (if\n you're talking about heritability in the broad sense); or, it's the\n fraction of phenotypic variance which is due to variance in\n <em>breeding values</em>: <span class=\"math-container\">$h^2 = \\frac{V_A}{V_P}$</span> (if you're talking about heritability in the narrow sense). <span class=\"math-container\">$V_A$</span> is also often called\n <em>additive genetic variance</em>.</p>\n</blockquote>\n\n<hr>\n\n<p>Suppose we have two islands, side by side. On both of the islands, some people are taller than others. </p>\n\n<p>It so happens that we know (God told us) that there is a particular gene which can make a difference to your height: all else being equal, <em>A</em>s are a foot taller than <em>a</em>s. It also so happens that we know (God told us) that coffee stunts your growth; all else being equal, people who drink tea are a foot taller than people who drink coffee.</p>\n\n<p>(We also happen to know that, at this moment, there aren't any other factors contributing to variation in height. Convenient!)</p>\n\n<p>Now to our islands.</p>\n\n<p><strong>On the Blue island</strong>, we see that some people are taller than others. We do some testing, and we find out that on this island some people are <em>A</em> and others are <em>a</em>. In contrast, we also find that <em>everybody</em> on this island drinks tea and nobody drinks coffee.</p>\n\n<p>There is variation in height: <em>all</em> of it is due to variation in genes, and <em>none</em> of it is due to variation in choice of beverage. Heritability = 1.</p>\n\n<p>But that doesn't mean that the environment isn't relevant to height in this case. On the contrary, we happen to know (God told us) that if they'd all drunk coffee instead, they'd all be a foot shorter.</p>\n\n<p><strong>On the Red island</strong>, we see that some people are taller than others. We do some testing and find out that <em>all</em> of them are <em>a</em>'s; <em>none</em> of them are <em>A</em>s. In contrast, some of them drink coffee and some of them drink tea.</p>\n\n<p>There is variation in height: <em>none</em> of it is due to variation in genes, and <em>all</em> of it is due to variation in choice of beverage. Heritability = 0.</p>\n\n<p>But that doesn't mean that genetics is irrelevant to height in this case. On the contrary, we know (God told us) that if they'd all been <em>A</em>s instead, then they'd all be a foot taller.</p>\n\n<hr>\n\n<p>The most convincing way to remind yourself why heritability isn't about \"how genetic a trait is\", I find, is to remember that if <em>everyone</em> has the gene, then the gene doesn't vary, and won't contribute to variation; but that doesn't mean the gene isn't relevant!</p>\n\n<p>For example, as far as I know, there is no genetic variation for \"having a heart\". <em>Everyone</em> is born with a heart. People without hearts are missing hearts because of environmental factors such as this:</p>\n\n<p><a href=\"https://i.stack.imgur.com/OGN77.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/OGN77.jpg\" alt=\"enter image description here\"></a></p>\n\n<p>So having a heart has a low heritability, but that doesn't mean genes aren't involved in building hearts!</p>\n\n<p>Likewise, a high heritability doesn't mean that environmental effects aren't important to the trait; it just means that <em>differences</em> in the environment aren't currently contributing to <em>differences</em> in the trait.</p>\n\n<p>It also doesn't mean that <em>future</em> environmental factors might not become important. For example, the heritability of eyesight was presumably somewhat high. But that didn't stop whoever did it from <em>inventing glasses</em>!</p>\n\n<p>So that's another lesson. Heritability is not a constant. Natural selection actually tends to push heritabilities down (since it gets rid of the worse genes); and if the environment changes, then the heritability can go up down or all over the place.</p>\n"
},
{
"answer_id": 70122,
"pm_score": 0,
"text": "<p>\"If all of the phenotypic variance is due to genetic causes (and regardless of whether there is a lot or a little variance), then hB=1hB=1. If all of the phenotypic variance if due to environment variance, then hB=0hB=0.</p>\n\n<p>So what does a hB=0.3hB=0.3 means?</p>\n\n<p>It means that 30% of the phenotypic variance is explained by genetic variance and that 70% of the phenotypic variance is due to environmental variance.</p>\n\n<p>So, what if there is no phenotypic variance in the population? if VP=0VP=0, then the heritability is undefined (as dividing by zero is undefined). However, in general, we tend to think that there is always a tiny bit of environmental variance and most people would just go on saying that heritability is 0 when VP=0VP=0.\"</p>\n\n<p>So, the environmental factors being listed in conjunction with the genetic factors is an attempt to explain heritable factors that do not result from modifications in the DNA sequence, or epigenetic factors. I think that this is why heritability coefficients used in the sense of only being the only useful variable to demonstrate heredity is a problem. The current statistical models that are used to try to delineate environmental variance do not take into account (such as the ones shown above) and although these are the best models we have right now, they do not incorporate variables that could potentially affect epigenetic factors such as DNA repair, cell cycles or DNA methylation. </p>\n"
},
{
"answer_id": 97348,
"pm_score": 1,
"text": "<p>Very good reviews of the overall concept have been posted, but I would like to focus in on the soft question of in what ways heritability does not reflect "how genetic" something is. Of course, that's not really a technically defined statement and in some ways it <em>does</em>, but let's stick to the question:</p>\n<ul>\n<li><em>Environmental contributions vary</em>. Consider pulmonary fibrosis. A certain low rate of familial pulmonary fibrosis will always be present due to genetics. But in a town built around a coal mine, you expect to see a much higher level of idiopathic pulmonary fibrosis. You could argue the semantics, but probably traits related to this condition are not "more genetic" in the towns without coal mines.</li>\n<li><em>Genetic contributions depend on environment</em>. The correlation of cognitive deficits with phenylketonuria alleles is quite high under some conditions, but with appropriate diet and supplements these genes have much less influence - "reduced penetrance", you might say. Is PKU "less genetic" depending on nutrition? Perhaps eye-tracking software will lead to a new sort of gaming next year, and as "eyethletes" suffer misfortunes the heritability of some ophthalmic traits will plummet, but does that mean the genes are weaker?</li>\n<li><em>Not all genetic contributions are known</em>. Before the HIV pandemic, delta32 CCR5 would not have been recognized to have an effect on immunosuppression (at least, not by that means). So we may not truly understand the genetic component that <em>potentially</em> exists even after thorough study of the trait under present conditions.</li>\n</ul>\n"
}
] |
43,095 |
<p>For me it seems reasonable that if I kept my gaze on a fixed point in a room with low light, a progressively brighter and better picture would appear before my eyes, just like a camera can see in the dark if the shutter speed is really slow, e.g. 4 seconds exposure. Why can't our brain do this trick as well (accumulate visual information over time)? Or is it a limitation of the eyes?</p>
<p><em>edit:</em></p>
<p>To further clarify what I'm after; I will show a concrete example from the world of photography (images taken from <a href="http://www.media-division.com/photoshop-tricks-solving-common-photography-problems-using-image-stacks/" rel="noreferrer">this website</a>).</p>
<p>Here is an example where we have a series of underexposed images - this would be what the brain receives:
<a href="https://i.stack.imgur.com/QaCQy.jpg" rel="noreferrer"><img src="https://i.stack.imgur.com/QaCQy.jpg" alt="Series of under exposed images"></a></p>
<p>Now, combining all of them with a simple add-operation reveals one image that has normal exposure.
<a href="https://i.stack.imgur.com/AH0yj.jpg" rel="noreferrer"><img src="https://i.stack.imgur.com/AH0yj.jpg" alt="Sum of all images equals one normal exposed image"></a></p>
<p>This seems like a simple trick for our powerful brain - surely it can add incoming signals?</p>
|
[
{
"answer_id": 43100,
"pm_score": 7,
"text": "<p>For simplicity's sake, let's really reduce this to something like photography.</p>\n\n<p>A camera's aperture can stay open indefinitely, allowing the plate (or whatever is receiving and recording light) to \"collect and save the effect of photons\" over time, if you want to phrase it that way. That allows a camera to make images that our eyes never can, for example, of \"star trails\".</p>\n\n<p><a href=\"https://i.stack.imgur.com/f2p2d.jpg\" rel=\"noreferrer\"><img src=\"https://i.stack.imgur.com/f2p2d.jpg\" alt=\"enter image description here\"></a></p>\n\n<p>The retina isn't like a photographic plate or a digital sensor's <em>photosites</em> (or pixels). It can't \"collect and save\" like a camera can. There is a \"refresh rate\", if you will, that disallows a collection and saving of light that doesn't apply to cameras, because cameras don't care if something in their vicinity is sneaking up on them and presenting a danger to their lives. Not being able to detect <strong>change</strong> rapidly is something that would be most inconvenient to survival.</p>\n\n<blockquote>\n <p>It is the time sampling with long exposures that really makes the magic of digital astrophotography possible. A digital sensor's true power comes from its ability to integrate, or collect, photons over much longer time periods than the eye. This is why we can record details in long exposures that are invisible to the eye, even through a large telescope.</p>\n</blockquote>\n\n<p><sub><a href=\"http://www.astropix.com/HTML/I_ASTROP/HOW.HTM\" rel=\"noreferrer\">How Digital Cameras Work</a></sub></p>\n"
}
] |
[
{
"answer_id": 43097,
"pm_score": 2,
"text": "<p>What I believe you are referring to, is the phenomenon by which the camera adjusts light exposure by adjusting aperture. We can also do this, but it happens very fast. Go from a dark room to a brighter room and you will be blinded, but that effect soon subsides, and vice-versa.</p>\n\n<p>The pupil opens up in a dark room and production of visual purple or Rhodopsin takes place in the Retina, a pigment responsible for visibility in low light. When you enter a bright area, the pupil contracts and Rhodopsin is photobleached, with production of Iodopsin taking place.</p>\n\n<p><a href=\"https://en.wikipedia.org/wiki/Adaptation_(eye)\" rel=\"nofollow\">https://en.wikipedia.org/wiki/Adaptation_(eye)</a></p>\n\n<p>^\nCheck out the Dark adaptaion and Light adaptation sections</p>\n\n<p>(Sorry I don't have more sources, I had done this from my highschool bio textbook, and I can't find it)</p>\n"
},
{
"answer_id": 43101,
"pm_score": 4,
"text": "<p>The simple answer is, that eye is not constructed such way.</p>\n\n<p>The eye have much more \"pixels\" than \"links\" to the brain and sends in \"preprocessed\" image. Moreover the the eye is constantly moving and scanning the \"area of vision\" and the body and head are supposedly also moving (willingly or not - nobody can freeze totally) so longer accumulation of data would lead to big blur. </p>\n\n<p>And the main purpose of eye is to spot danger - something changing, or moving victim - as we human are not nocturnal animals, we are constructed/optimized to work in mode active on light, passive and sleeping in dark. As there is real need for sleep anyway, there is not good reason to develope secondary system for night vision - meaning duplicate the main vision system completely with totally different mode of work (long time collecting data) which would be used only in very little split of time - when predator find us in night sleeping and we survive the first attack. </p>\n\n<p>So only the main system was slightly modified with other kind of pixels more sensitive to light, but less to color, which allows us work to relatively last night and from really early morning when only split of light is accessible. At the price of color and details. But it is much cheaper, then mainly unused secondary system. And covers more time, than we usually use to move in.</p>\n"
},
{
"answer_id": 43102,
"pm_score": 4,
"text": "<p>There's probably a theoretical capacity to do so. The brain is amazingly good at signal processing, and could probably pull off such a summation. However, there is a limit. You have to hold very very still for it to work.</p>\n\n<p>Go take one of the time lapse pictures, like anongoodnurse's answer posted. The shutter is open for quite some time (her picture looks like a 30 minute or 1 hour exposure to me). <strong>During that exposure, the camera holds perfectly still.</strong> All motion you see is motion due to the objects in the scene moving (or, if you prefer the technicality, the stars are holding still, and the camera is rotating... really really really smoothly).</p>\n\n<p>The body does not have such an ability to lock itself down. Try taking one of those pictures while holding the camera in your hands, and you'll see its particularly difficult. Now consider that your eyes are even more twitchy than the rest of your body, capable of darting this way and that. We have good control over our eyes, but nothing close to what you need to create an effect similar to that of a tripod.</p>\n\n<p>Thus, if you were to try to use your eyes in this way, almost all of what you would see is your own motion. Presumably a <em>very</em> well controlled individual might be able to sense that movement and account for it, but there's little reason for the brain to have that ability in \"hardware.\"</p>\n\n<p>Of course we can lock our eyes on to see with incredible accuracy, right? We can read words on an eye chart at 20 paces. Those activities are being done in a scene which permits visual feedback. If its too dark, we don't get enough visual feedback to see where our eyes are pointing and compensate.</p>\n"
},
{
"answer_id": 43118,
"pm_score": 4,
"text": "<p>The differences at the photoreceptor level have been addressed by others. The mechanical restrictions of the visual system were shortly hinted at by @gilhad <em>et al.</em>, but deserve more attention in my opinion.</p>\n\n<p>First off, in darkness we cannot focus on an object and our eyes will move. And even when we focus on a specific point there is always movement of the eyes due to due to <a href=\"http://www.diku.dk/~panic/eyegaze/node16.html\" rel=\"noreferrer\">tremor, drift and microsaccades</a>. <strong>Microsaccades</strong> are involuntary small movements of the eye (Fig. 1) that have received quite some attention lately. It is estimated they occur 1 - 2 times per second and they can reach amplitudes of up to 1 degrees of field of view <a href=\"http://www.nature.com/nrn/journal/v14/n2/full/nrn3405.html\" rel=\"noreferrer\">(Martinez-Conde <em>et al</em>., 2013)</a> and last for about 15 ms <a href=\"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3427003/\" rel=\"noreferrer\">(Cui <em>et al</em>., 2009)</a>. It is thought that these movements prevent adaptation at the retinal level, and prevent image fading. Hence, <strong>images on the retina</strong> are constantly mechanically <strong>refreshed</strong>. The brain in turn stabilizes the image by correcting the image at the perceptual level through oculomotor feedback <a href=\"http://www.nature.com/nrn/journal/v14/n2/full/nrn3405.html\" rel=\"noreferrer\">(Martinez-Conde <em>et al</em>., 2013)</a>.</p>\n\n<p><a href=\"https://i.stack.imgur.com/hHZTr.jpg\" rel=\"noreferrer\"><img src=\"https://i.stack.imgur.com/hHZTr.jpg\" alt=\"Microsaccades\"></a><br>\n<sup>Fig. 1. Microsaccades recorded by an eye tracker. Source: <a href=\"http://www.nature.com/nrn/journal/v14/n2/full/nrn3405.html\" rel=\"noreferrer\">Martinez-Conde <em>et al</em>. (2013)</a></sup></p>\n\n<p>While a <strong>camera must be fixated</strong> on a tripod stand to allow for overexposure, our <strong>eyes cannot be fixated to the same extent</strong>, even when we try. Hence, combining exposures as indicated in the question is impossible and results in image blur. Instead, retinal images are constantly refreshed and when lighting conditions are too dim we cannot integrate photon input in the temporal domain. </p>\n\n<p>Note, however, that photoreceptors do integrate photon input to some extent, given that higher luminance results in brighter perceptions. However, this operates only in the order of milliseconds and doesn't allow for long-term exposures as necessary to obtain images like the one shown in the great answer from @anongoodnurse.</p>\n\n<p><sub><strong>References</strong><br>\n<strong>-</strong> <a href=\"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3427003/\" rel=\"noreferrer\">Cui <em>et al</em>., <em>Vis Res</em> (2009); <strong>49</strong>(2): 228–36</a><br>\n<strong>-</strong> <a href=\"http://www.nature.com/nrn/journal/v14/n2/full/nrn3405.html\" rel=\"noreferrer\">Martinez-Conde <em>et al</em>., <em>Nature Reviews Neurosci</em> (2013); <strong>14</strong>: 83-96</a></sub></p>\n"
},
{
"answer_id": 43140,
"pm_score": 2,
"text": "<p>Pretty much all answers which focus on movement of the eye causing blur (something a digital camera does not have to deal with) are wrong. The brain has absolutely no problem processing images in low-light at speed.</p>\n\n<p>The answer is all to do with the fact that the eye is not a camera. Much of the old-school theories which where based on the fact that the eye works like a camera, such as persistence of vision, etc, have been proven demonstrably wrong. The eye does not have a shutter speed - information is constantly being sent back to the brain with no interval delay.\n(<a href=\"https://en.wikipedia.org/wiki/Persistence_of_vision\" rel=\"nofollow\">https://en.wikipedia.org/wiki/Persistence_of_vision</a>)</p>\n\n<p>This means that resolving blur/etc is done in the brain, not by the eye. Think of digital image stabilization that actually works, and works in real-time.\nHowever, the brain does appear to work on chunks of eye-input, at roughly 16-24 chunks a second. Why this speed? Well, liking the brain to a computer, it probably has something to do with the amount of memory the brain can store for unprocessed eye-data. Long-exposure photos require a lot of RAM to store the raw data, then a lot of time to compile it into a single image. The brain could do no doubt do the compilation from raw data to image, but it very likely cannot store more than 1/24th of a second's worth of data in \"memory\" before it has to compile.</p>\n\n<p>More importantly, doing so would reduce our reaction time significantly. This is important because you do not want an organism that can see a branch clearly at night, but when they try to grab it, miss by 5-10 seconds.</p>\n"
},
{
"answer_id": 43307,
"pm_score": 2,
"text": "<p>I wish my computer as capable of sending an illustration of the arrangement of the human eye, versus the hypothetical \"camera lens\" idea, <strong><em>as organic eyes and camera optics are in NO WAY SIMILAR!</em></strong> Most of you have been in gross error by doing such, in your discussions. </p>\n\n<p>The eye uses a combination of organic optical cells called \"rods,\" and \"cones,\" in order to manifest an image. In addition, there is a \"dead spot\" on the image perceived by an eye, owing to the insertion-point of the optical nerve. Any discussion of organic vision has to take these facts into account.</p>\n\n<p>Organic eyes MUST go through a variable period of \"dark-adaptation\" in order to be able to perceive an image,as well. <strong>The minimum period is between 50-120 minutes;</strong> and even then, even an instant's exposure to \"brighter\" light will erase all of this adaptation, necessitating \"restarting the clock\" to dark-adapt the eye, again. </p>\n\n<p>There's an anecdotal tale purporting that pirates had worn eye patches so that they achieved and kept dark-adaptation in one eye. There are many advantages to keeping one eye dark-adapted--- one is going from a brightly-lit deck, down into the very dim below-decks areas of a victim's ship. This is a case where being able to pull off the patch and being able to immediately see the enemy crewman coming in with a cutlass would be very valuable!</p>\n\n<p>Another factor is that the distribution of rods and cones is not uniform, across the eye. <strong>Cones deal with colour-perception</strong>, and are concentrated at the centre of of the visual field. The concentration of cones rapidly declines, going outward. </p>\n\n<p>Densities of rods in the same eye rapidly increases, going out from about five degrees from dead centre to a maximum of approximately 25 degrees from dead centre. <strong>Rods are responsible for our peripheral vision, our \"sensitivity\" to even seemingly-microscopic motion, AND OUR NIGHT VISION.</strong></p>\n\n<p>Because of the lack of rod-cells at the centre of our eyes' visual field, we are unable to see anything dead-ahead of us, under low-light conditions!</p>\n\n<p>In order to be able to bring the maximum number of rod-cells to bear on an \"item of interest\" in our visual field, <strong>we have to use our peripheral vision and \"cheat\" off to one side of our visual field by about 25 degrees.</strong> This is like watching the front door in the centre of a building by looking \"straight\" at the middle of the left or right facade.</p>\n\n<p>One would also be able to detect motion far easier than exact shape by looking in such a way. By continually \"looking to one side,\" and by altering our location so as to change the background, it is entirely possible for an astute woodsman (a Native American or a Hillbilly, for example!) to be able to not only spot a raccoon in the top of an oak tree, but also to make out the form of the opossum looking up at him, from a lower limb!</p>\n\n<p>Many animals far better able to operate at night have eyes that are not only better-equipped with rod-cells, but are in fact, <strong>much larger than ours!</strong> We would see as well as any owl, <strong>had only we been born with eyes the diameters of \"jumbo\" grapefruit!</strong></p>\n\n<p>Plus, watching and closely emulating the owl, with the head-bobbing, the weaving from side to side, and the peering-ahead, we would naturally improve the peripheral-sensitivity and the \"looking to one side\" conjuring of sharper images of those objects of interest to us!</p>\n\n<p>I am sorry to be critical, as many comments showed great understanding of non-organic optics, as well as great imagination, but it is simply not possible to be able to blythly interchange the principles of non-organic optics and organic optics.</p>\n"
}
] |
45,942 |
<p>A human encountering a tiger or a malaria plasmodium is likely to suffer, and the tiger/plasmodium is likely to gain from the transaction. Not necessarily a good example, and I am aware that a successful parasite avoids prematurely killing its host, but I can't see any fundamental difference.</p>
<p>Of course it's like pornography: "we know it when we see it". But is there a formal, generally-accepted distinction? </p>
|
[
{
"answer_id": 45964,
"pm_score": 4,
"text": "<p>Good question.</p>\n\n<p>There is no fundamental difference between parasites and predators.</p>\n\n<p><strong>Ecological Interaction</strong></p>\n\n<p>In terms of <a href=\"https://en.wikipedia.org/wiki/Ecological_relationship\" rel=\"nofollow noreferrer\">ecological interaction</a>, they are both defined as an interaction where one species benefits and the other suffers from the interaction. </p>\n\n<p><strong>Intuition parasite vs predator</strong></p>\n\n<p><a href=\"https://i.stack.imgur.com/9pK3l.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/9pK3l.png\" alt=\"enter image description here\"></a></p>\n\n<p>In general predation is viewed as a big individual eating a smaller one while parasitism is when a small individual eats a bigger one. These general intuition however fails to consider a number of cases. Here some cases I can think of</p>\n\n<p><strong>Examples when intuition don't match the above picture</strong></p>\n\n<p>Generally considered as predation but does not fit the above picture-based definition:</p>\n\n<ul>\n<li>social animals attacking in groups preys that are much larger than themselves - non-social animal attacking prey larger than themselves</li>\n<li>herbivores browsing on large trees</li>\n</ul>\n\n<p>Generally considered as parasitism but does not fit the above picture-based definition:</p>\n\n<ul>\n<li>indirect effect of habitat modification that would rather be considered as parasitism.</li>\n<li>Species that take advantage of parental care of another species by mimicking babies (but being larger)</li>\n<li>Individuals of large species stealing the habitat built by a smaller species</li>\n<li>Batesian mimicry (see <a href=\"https://biology.stackexchange.com/questions/15526/parasitism-and-mimicry\">this post</a>; Thank you @WYSIWYG and @NL_Derek for the comments)</li>\n</ul>\n\n<p><strong>Population culture vs science literature</strong></p>\n\n<p>In the popular culture, some people call parasites only endoparasites. This concept is also misleading and not so much in accordance with the general literature in biology.</p>\n"
}
] |
[
{
"answer_id": 45946,
"pm_score": -1,
"text": "<p>A parasite may or may not kill the host. It's basic motive is to constantly derive nutrition from the host. More a sort of one time investment and as an interest you keep getting the nutrition.\nWhereas a predator's motive is to kill the host to satisfy it's hunger. One kill and eat can be a taken as a case of consideration here.</p>\n"
},
{
"answer_id": 45949,
"pm_score": 3,
"text": "<p><strong>Parasitism</strong> – a parasite that lives on or in an host, obtaining food from the host and harming it. </p>\n\n<p><em>Example</em>: Ixodes ticks use white tailed deer as a host </p>\n\n<ul>\n<li>Parasite is smaller and weaker than the host</li>\n<li>Parasite may feed over the host from outside or inside</li>\n<li>In parasite-host relationship a weaker organism is benefitted</li>\n<li>Host specificity is more common </li>\n<li>The host is most likely alive when nourished on </li>\n</ul>\n\n<hr>\n\n<p><strong>Predation</strong> – predators benefit as they feed on prey; predation affects numbers and behaviour of prey </p>\n\n<p><em>Example</em>: Coyotes are predators of white tailed deer </p>\n\n<ul>\n<li>Predators are generally larger than their prey </li>\n<li>There is progressive development of characters or evolution</li>\n<li>In predator-prey relationship the stronger organism is benefitted</li>\n<li>Prey specificity is not very common </li>\n<li>Predator usually feeds on prey from the \"outside\"</li>\n<li>The prey is usually dead when consumed </li>\n</ul>\n"
},
{
"answer_id": 68536,
"pm_score": 1,
"text": "<p>Previous answers to the question seem to originate from one misunderstanding. Of course, the large-small distinction between predators and parasites is easily observed by anyone, like the fact that predators kill their prey while parasites only sap the strength of their hosts. </p>\n\n<p>But parasites do not actually attack a host. Parasites attack only a TINY component of the host. The parasite and that tiny component then develop what is fundamentally a predator-prey relationship. Whether the host is significantly affected or not depends upon the role of the component in the host’s overall health, and the size of the infection or wound. Exactly the same could be said about an attack by a predator on its prey. The actual significance of the attack comes down to the size of the wound and the significance of the wounded body part to the health of the prey. </p>\n\n<p>To sum this up in a few words, the methods and logic of a parasite are the same as those of a predator. Their size difference is not critical; not all parasites are small, and not all predators are large. The size of the host or prey is not the critical issue, either. </p>\n\n<p>I think the biggest PRACTICAL difference between predators and parasites are the methods used to defeat them. Weapons like spears and guns for predators; nutrition, soap and science for parasites. Avoidance — aided by brainpower— is the best defense of all</p>\n"
},
{
"answer_id": 68545,
"pm_score": 1,
"text": "<p>Most definitions of predator/parasite rely on quite subjective (or not exactly precise) characteristics. That being said, I like Ricklefs' definition (Ricklefs, 2009), which is simple and straightforward:</p>\n\n<p>It can be summarised like this:</p>\n\n<ul>\n<li><strong>Predatism</strong>: a consumer-resource interaction in which the consumer (predator) removes the resource from the resource population.</li>\n<li><strong>Parasitism</strong>: a consumer-resource interaction in which the consumer (parasite) does not remove the resource from the resource population.</li>\n</ul>\n\n<p>Of course not everything is black or white, and there are situations in which applying the above definition is quite complicated, such as parasitoids or cases of parasitism that end up killing the host. However, it can be used for most of interactions.</p>\n\n<p>Let's see some (counter-intuitive) examples:</p>\n\n<h3>This is a parasite:</h3>\n\n<p><a href=\"https://i.stack.imgur.com/gXPIo.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/gXPIo.jpg\" alt=\"enter image description here\"></a></p>\n\n<p>A cow grazing doesn't kill the grass plant: it only eats parts of the leaves, not the whole plant. Therefore, the resource (plant) is not removed from the resource population.</p>\n\n<p>This example is interesting because we, normally, tend to imagine the parasite smaller than the host. However, as you can see, a cow (the parasite) is some orders of magnitude heavier/bigger than the grass plant (the host).</p>\n\n<h3>This is a predator:</h3> \n\n<p><a href=\"https://i.stack.imgur.com/pXIUXm.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/pXIUXm.jpg\" alt=\"enter image description here\"></a></p>\n\n<p>Pigs (sometimes, not always) like to pull up the root, eating the whole plant and, therefore, killing it. Thus, the resource (plant) is removed from the resource population, that changes from <em><code>N</code></em> to <em><code>N - 1</code></em>. </p>\n\n<hr>\n\n<p>Source: Ricklefs, R. (2009). The economy of nature. Vancouver, B.C.: Langara College.</p>\n"
}
] |
46,016 |
<p>I'm trying to establish if it's required to add a NLS to Cas9 when expressed (or transfected) in a Eukaryotic cell. Several papers report using a viral NLS, but is it absolutely necessary? Could Cas9 be trafficked to nucleus without addition of a NLS?</p>
|
[
{
"answer_id": 45964,
"pm_score": 4,
"text": "<p>Good question.</p>\n\n<p>There is no fundamental difference between parasites and predators.</p>\n\n<p><strong>Ecological Interaction</strong></p>\n\n<p>In terms of <a href=\"https://en.wikipedia.org/wiki/Ecological_relationship\" rel=\"nofollow noreferrer\">ecological interaction</a>, they are both defined as an interaction where one species benefits and the other suffers from the interaction. </p>\n\n<p><strong>Intuition parasite vs predator</strong></p>\n\n<p><a href=\"https://i.stack.imgur.com/9pK3l.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/9pK3l.png\" alt=\"enter image description here\"></a></p>\n\n<p>In general predation is viewed as a big individual eating a smaller one while parasitism is when a small individual eats a bigger one. These general intuition however fails to consider a number of cases. Here some cases I can think of</p>\n\n<p><strong>Examples when intuition don't match the above picture</strong></p>\n\n<p>Generally considered as predation but does not fit the above picture-based definition:</p>\n\n<ul>\n<li>social animals attacking in groups preys that are much larger than themselves - non-social animal attacking prey larger than themselves</li>\n<li>herbivores browsing on large trees</li>\n</ul>\n\n<p>Generally considered as parasitism but does not fit the above picture-based definition:</p>\n\n<ul>\n<li>indirect effect of habitat modification that would rather be considered as parasitism.</li>\n<li>Species that take advantage of parental care of another species by mimicking babies (but being larger)</li>\n<li>Individuals of large species stealing the habitat built by a smaller species</li>\n<li>Batesian mimicry (see <a href=\"https://biology.stackexchange.com/questions/15526/parasitism-and-mimicry\">this post</a>; Thank you @WYSIWYG and @NL_Derek for the comments)</li>\n</ul>\n\n<p><strong>Population culture vs science literature</strong></p>\n\n<p>In the popular culture, some people call parasites only endoparasites. This concept is also misleading and not so much in accordance with the general literature in biology.</p>\n"
}
] |
[
{
"answer_id": 45946,
"pm_score": -1,
"text": "<p>A parasite may or may not kill the host. It's basic motive is to constantly derive nutrition from the host. More a sort of one time investment and as an interest you keep getting the nutrition.\nWhereas a predator's motive is to kill the host to satisfy it's hunger. One kill and eat can be a taken as a case of consideration here.</p>\n"
},
{
"answer_id": 45949,
"pm_score": 3,
"text": "<p><strong>Parasitism</strong> – a parasite that lives on or in an host, obtaining food from the host and harming it. </p>\n\n<p><em>Example</em>: Ixodes ticks use white tailed deer as a host </p>\n\n<ul>\n<li>Parasite is smaller and weaker than the host</li>\n<li>Parasite may feed over the host from outside or inside</li>\n<li>In parasite-host relationship a weaker organism is benefitted</li>\n<li>Host specificity is more common </li>\n<li>The host is most likely alive when nourished on </li>\n</ul>\n\n<hr>\n\n<p><strong>Predation</strong> – predators benefit as they feed on prey; predation affects numbers and behaviour of prey </p>\n\n<p><em>Example</em>: Coyotes are predators of white tailed deer </p>\n\n<ul>\n<li>Predators are generally larger than their prey </li>\n<li>There is progressive development of characters or evolution</li>\n<li>In predator-prey relationship the stronger organism is benefitted</li>\n<li>Prey specificity is not very common </li>\n<li>Predator usually feeds on prey from the \"outside\"</li>\n<li>The prey is usually dead when consumed </li>\n</ul>\n"
},
{
"answer_id": 68536,
"pm_score": 1,
"text": "<p>Previous answers to the question seem to originate from one misunderstanding. Of course, the large-small distinction between predators and parasites is easily observed by anyone, like the fact that predators kill their prey while parasites only sap the strength of their hosts. </p>\n\n<p>But parasites do not actually attack a host. Parasites attack only a TINY component of the host. The parasite and that tiny component then develop what is fundamentally a predator-prey relationship. Whether the host is significantly affected or not depends upon the role of the component in the host’s overall health, and the size of the infection or wound. Exactly the same could be said about an attack by a predator on its prey. The actual significance of the attack comes down to the size of the wound and the significance of the wounded body part to the health of the prey. </p>\n\n<p>To sum this up in a few words, the methods and logic of a parasite are the same as those of a predator. Their size difference is not critical; not all parasites are small, and not all predators are large. The size of the host or prey is not the critical issue, either. </p>\n\n<p>I think the biggest PRACTICAL difference between predators and parasites are the methods used to defeat them. Weapons like spears and guns for predators; nutrition, soap and science for parasites. Avoidance — aided by brainpower— is the best defense of all</p>\n"
},
{
"answer_id": 68545,
"pm_score": 1,
"text": "<p>Most definitions of predator/parasite rely on quite subjective (or not exactly precise) characteristics. That being said, I like Ricklefs' definition (Ricklefs, 2009), which is simple and straightforward:</p>\n\n<p>It can be summarised like this:</p>\n\n<ul>\n<li><strong>Predatism</strong>: a consumer-resource interaction in which the consumer (predator) removes the resource from the resource population.</li>\n<li><strong>Parasitism</strong>: a consumer-resource interaction in which the consumer (parasite) does not remove the resource from the resource population.</li>\n</ul>\n\n<p>Of course not everything is black or white, and there are situations in which applying the above definition is quite complicated, such as parasitoids or cases of parasitism that end up killing the host. However, it can be used for most of interactions.</p>\n\n<p>Let's see some (counter-intuitive) examples:</p>\n\n<h3>This is a parasite:</h3>\n\n<p><a href=\"https://i.stack.imgur.com/gXPIo.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/gXPIo.jpg\" alt=\"enter image description here\"></a></p>\n\n<p>A cow grazing doesn't kill the grass plant: it only eats parts of the leaves, not the whole plant. Therefore, the resource (plant) is not removed from the resource population.</p>\n\n<p>This example is interesting because we, normally, tend to imagine the parasite smaller than the host. However, as you can see, a cow (the parasite) is some orders of magnitude heavier/bigger than the grass plant (the host).</p>\n\n<h3>This is a predator:</h3> \n\n<p><a href=\"https://i.stack.imgur.com/pXIUXm.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/pXIUXm.jpg\" alt=\"enter image description here\"></a></p>\n\n<p>Pigs (sometimes, not always) like to pull up the root, eating the whole plant and, therefore, killing it. Thus, the resource (plant) is removed from the resource population, that changes from <em><code>N</code></em> to <em><code>N - 1</code></em>. </p>\n\n<hr>\n\n<p>Source: Ricklefs, R. (2009). The economy of nature. Vancouver, B.C.: Langara College.</p>\n"
}
] |
49,209 |
<p>How has evolution created our blood, lungs and the heart?</p>
<p>We can't exist without blood, which transports the oxygen to all areas of our body. However, the blood needs a lung, which gives it the oxygen to transport. The blood also needs something which lets it flow through the whole body, which are our veins. And in order to allow the blood to flow through our veins, an organ is needed to pump the blood, which is our heart. We also need a brain which controls all that, and the brain in turn needs the blood in order to function right.</p>
<p>Evolution makes very slow steps....."it just doesn't jump". So, How did evolution manage to create all that?</p>
|
[
{
"answer_id": 49218,
"pm_score": 6,
"text": "<p>While others have addressed the big picture aspects of your question, I think it would be useful to look at the specifics. </p>\n\n<p>Have a look at the heart (or more accurately, the <em>hearts</em>) of the earthworm: <a href=\"https://i.stack.imgur.com/VD1up.jpg\" rel=\"noreferrer\"><img src=\"https://i.stack.imgur.com/VD1up.jpg\" alt=\"enter image description here\"></a> </p>\n\n<p>They're nothing more than veins with some pumping muscles wrapped around them. It seems almost a stretch to call them hearts, they are shaped so different from what we think of as a heart proper.</p>\n\n<p>Also, note the earthworm's lungs, or rather, lack of them. It doesn't have any! Why not? It doesn't need them. It gets enough oxygen through its skin via osmosis. It's only larger organisms that need dedicated systems to concentrate oxygen from the surrounding environment.</p>\n\n<p>So, the worm has a simpler system (no chambered heart, no lungs) that works.</p>\n\n<p>All vertebrates descended from a common ancestor that was very similar to this earthworm. It had simple hearts, and no lungs. You can follow the evolution of the human heart through fish heart: <a href=\"https://i.stack.imgur.com/yZuoB.jpg\" rel=\"noreferrer\"><img src=\"https://i.stack.imgur.com/yZuoB.jpg\" alt=\"enter image description here\"></a></p>\n\n<p>which is a more sophisticated pumping vessel with two chambers.</p>\n\n<p>Amphibians evolved from fish, reptiles from amphibians, and mammals from reptiles. In this diagram, you will find that the heart becomes more sophisticated and efficient in each:\n<a href=\"https://i.stack.imgur.com/QU3mF.jpg\" rel=\"noreferrer\"><img src=\"https://i.stack.imgur.com/QU3mF.jpg\" alt=\"enter image description here\"></a></p>\n\n<p>So, this should give you a good idea of the evolution of the human heart from simpler, working system. I won't take the time to draw out the evolution of blood vessels or lungs; maybe someone else will, or you can google them yourself, the information is readily out there. But they all follow the same pattern: gradual, incremental improvements on working, simpler systems. </p>\n"
}
] |
[
{
"answer_id": 49211,
"pm_score": 3,
"text": "<p>This is a good question, but it has a vast scope, as you're talking about the progression of millions of different living animals over hundreds of millions of years, none of which are still alive, so we have to make inferences based on what we observe in their surviving offspring.</p>\n\n<p>That means if you want to learn how 'intermediate' (say, not-quite-lungs, not-quite-heart, not-quite-brain) body systems could function, you'd first need to learn about the biology of lots of other animals. Not all animals have lungs or hearts or nervous systems. Not all animals have blood.</p>\n\n<p>More to the point, though, the key factor is that several hundred million years is a <em>really, really, really</em> long time. It's such a long time that it's well outside any typical human scale of comprehension. Consider the entirety of your life experience thus far and everything you've seen change. In comparison to how long the evolutionary process has been operating, your life's span has been on the order of a millisecond out of a day.</p>\n"
},
{
"answer_id": 49215,
"pm_score": 4,
"text": "<p>This kind of question was raised in a book called \"Darwin's Black Box\" by Michael Behe, who is a biochemistry professor in the U.S. - he calls this '<a href=\"https://en.wikipedia.org/wiki/Irreducible_complexity\" rel=\"noreferrer\">irreducible complexity</a>' (IC). For example, the blood clotting cascade system where you have a large number of components that are all apparently essential for the process.</p>\n\n<p>Now I have to say I find the idea that this is a problem very unconvincing, to say the least. However, it's a reasonable question to ask; how does a system of interdependent elements evolve, if we assume that no part can change gradually without the whole system breaking?</p>\n\n<p>There are - at least - two major problems with this. Firstly, the assumption that you can't change any part of such a system has mostly turned out to be false. Secondly, systems would obviously evolve from other, simpler systems which are just as effective.</p>\n\n<p>Say I start out with three elements in my system (three proteins, for example). They are all <em>essential</em> as each requires the other to function properly. Now I introduce another protein to the system and make it dependent on only <em>one</em> of the existing proteins. Is this system IC? No, we can remove the new protein and the whole thing still works. Gradually, we make the other parts of the system dependent on the new protein and suddenly we have an 'IC' system.</p>\n\n<p>In other words, the 'problem' lies in imagining that you have to go from nothing to a complete working mousetrap. What seems more likely is that elements of a system are changed one by one, and that the system evolves through a series of states where you could point to some element and claim that it is essential.</p>\n\n<p>One final point to note is that no multicellular organism is born whole in one step. The processes that an embryo goes through are conceptually similar (though <a href=\"https://en.wikipedia.org/wiki/Recapitulation_theory\" rel=\"noreferrer\">not exactly</a> ) to evolution in that you can have different organs developing at different times, or simpler versions of them that can work together as a simpler system.</p>\n\n<hr>\n\n<p>To make this a little less abstract, consider the earthworm example given in the top answer. It has just a simple heart(s) and blood vessels - it doesn't seem that difficult, therefore to add in some lungs. Here's a trivial diagram:</p>\n\n<p><a href=\"https://i.stack.imgur.com/hL93C.png\" rel=\"noreferrer\"><img src=\"https://i.stack.imgur.com/hL93C.png\" alt=\"heart, blood, and lung interaction\"></a></p>\n\n<p>The lines here are interactions between the organs - the heart pumps blood through the vessels, and the lungs (if any) oxygenate the blood. We evolve from the simpler system (1) to the more complex system (2) just by adding another element.</p>\n\n<p>However, the difficulty with some systems is that the interactions between the parts are dependencies. A very simple example could be proteins that activate/deactivate other proteins (by phosphorylation, say). Then we could theoretically get a situation like this:</p>\n\n<p><a href=\"https://i.stack.imgur.com/nGmcP.png\" rel=\"noreferrer\"><img src=\"https://i.stack.imgur.com/nGmcP.png\" alt=\"protein activation systems\"></a> </p>\n\n<p>Here, the final system (4) looks like it is 'irreducibly' complex because you can't remove any of (A, B, C, D) without breaking the cycle. However, at each step, we only added or removed one dependency. This also shows the importance of redundancy in biological systems. If you knock out either C or D from system (3) then it still works.</p>\n"
},
{
"answer_id": 49216,
"pm_score": 0,
"text": "<p>A good question, indeed, and not easy to answer (or grasp). I'll give a very simplified answer. Bear in mind that the processess I'll describe are REALLY complex.</p>\n\n<p>You have to think way before blood, brains, etc. Billions of years ago, organic molecules were formed in the planet. These organic molecules started to \"\"\"join\"\"\". Millions of years latter, simple cells which didn't even have a nucleus were formed. Some millions of years latter, cells with nucleus started to form. Latter, these cells started to agreggate, turning into colonies of unicellular individuals. In time, these colonies turned into multicellular individuals, but with all cells being equal to one another. After that, cells in one organism started to differentiate into some functions (digestive and neural, for example). Slowly, more complex organisms were formed, as the cells which formed these organisms started to differentiate and form various kinds of tissues, which, through millions of years, developed into more and more complex organisms. Think of Cnidarians, for example. They are very \"simple\" (I use \"simple\" as a proxy for \"not complex\") beings. They have no circulatory system. A circulatory system developed in latter groups: the first, \"simple\" circulatory system appeared in Nematodeans (if I'm not mistaken). But it was really \"simple\". With time, other, more complex, circulatory systems started to originate due to various evolutionary pressures. The same applies to every type of cell, tissue or organ you can think about in any organism: <strong>complex organisms are the result of millions of years of simpler organisms which generated more complex organisms, by really little steps.</strong></p>\n\n<p>I hope you get the idea of what I'm trying to say. For really grasping all this, you have to study a lot of evolution, because it is a hard concept for us to deeply understand.</p>\n"
},
{
"answer_id": 49219,
"pm_score": 2,
"text": "<p>Simpler forms developed to handle simpler requirements. Take planarians, for instance, which are thin and small enough that they can receive their oxygen supply by diffusion straight through their surface. Now imagine a slightly bigger animal that needs a slightly more sophisticated system to oxygenate their internal regions well. A muscle with an aberrant, autonomous twitch would be enough to stir/circulate more oxygenated fluids through the body. Past that, any little accident that facilitates this (e.g. some cells bind to oxygen a little better, the muscle twitches a little stronger or more regularly, etc.) is another form closer to what we see today.</p>\n"
}
] |
49,214 |
<p>In the Krebs cycle, where do the hydrogens and electrons that NAD+ and FAD accept come from? It seems that citric acid only loses two hydrogens because it starts out with eight hydrogens and then becomes oxaloacetic acid, which has four hydrogens. </p>
|
[
{
"answer_id": 49218,
"pm_score": 6,
"text": "<p>While others have addressed the big picture aspects of your question, I think it would be useful to look at the specifics. </p>\n\n<p>Have a look at the heart (or more accurately, the <em>hearts</em>) of the earthworm: <a href=\"https://i.stack.imgur.com/VD1up.jpg\" rel=\"noreferrer\"><img src=\"https://i.stack.imgur.com/VD1up.jpg\" alt=\"enter image description here\"></a> </p>\n\n<p>They're nothing more than veins with some pumping muscles wrapped around them. It seems almost a stretch to call them hearts, they are shaped so different from what we think of as a heart proper.</p>\n\n<p>Also, note the earthworm's lungs, or rather, lack of them. It doesn't have any! Why not? It doesn't need them. It gets enough oxygen through its skin via osmosis. It's only larger organisms that need dedicated systems to concentrate oxygen from the surrounding environment.</p>\n\n<p>So, the worm has a simpler system (no chambered heart, no lungs) that works.</p>\n\n<p>All vertebrates descended from a common ancestor that was very similar to this earthworm. It had simple hearts, and no lungs. You can follow the evolution of the human heart through fish heart: <a href=\"https://i.stack.imgur.com/yZuoB.jpg\" rel=\"noreferrer\"><img src=\"https://i.stack.imgur.com/yZuoB.jpg\" alt=\"enter image description here\"></a></p>\n\n<p>which is a more sophisticated pumping vessel with two chambers.</p>\n\n<p>Amphibians evolved from fish, reptiles from amphibians, and mammals from reptiles. In this diagram, you will find that the heart becomes more sophisticated and efficient in each:\n<a href=\"https://i.stack.imgur.com/QU3mF.jpg\" rel=\"noreferrer\"><img src=\"https://i.stack.imgur.com/QU3mF.jpg\" alt=\"enter image description here\"></a></p>\n\n<p>So, this should give you a good idea of the evolution of the human heart from simpler, working system. I won't take the time to draw out the evolution of blood vessels or lungs; maybe someone else will, or you can google them yourself, the information is readily out there. But they all follow the same pattern: gradual, incremental improvements on working, simpler systems. </p>\n"
}
] |
[
{
"answer_id": 49211,
"pm_score": 3,
"text": "<p>This is a good question, but it has a vast scope, as you're talking about the progression of millions of different living animals over hundreds of millions of years, none of which are still alive, so we have to make inferences based on what we observe in their surviving offspring.</p>\n\n<p>That means if you want to learn how 'intermediate' (say, not-quite-lungs, not-quite-heart, not-quite-brain) body systems could function, you'd first need to learn about the biology of lots of other animals. Not all animals have lungs or hearts or nervous systems. Not all animals have blood.</p>\n\n<p>More to the point, though, the key factor is that several hundred million years is a <em>really, really, really</em> long time. It's such a long time that it's well outside any typical human scale of comprehension. Consider the entirety of your life experience thus far and everything you've seen change. In comparison to how long the evolutionary process has been operating, your life's span has been on the order of a millisecond out of a day.</p>\n"
},
{
"answer_id": 49215,
"pm_score": 4,
"text": "<p>This kind of question was raised in a book called \"Darwin's Black Box\" by Michael Behe, who is a biochemistry professor in the U.S. - he calls this '<a href=\"https://en.wikipedia.org/wiki/Irreducible_complexity\" rel=\"noreferrer\">irreducible complexity</a>' (IC). For example, the blood clotting cascade system where you have a large number of components that are all apparently essential for the process.</p>\n\n<p>Now I have to say I find the idea that this is a problem very unconvincing, to say the least. However, it's a reasonable question to ask; how does a system of interdependent elements evolve, if we assume that no part can change gradually without the whole system breaking?</p>\n\n<p>There are - at least - two major problems with this. Firstly, the assumption that you can't change any part of such a system has mostly turned out to be false. Secondly, systems would obviously evolve from other, simpler systems which are just as effective.</p>\n\n<p>Say I start out with three elements in my system (three proteins, for example). They are all <em>essential</em> as each requires the other to function properly. Now I introduce another protein to the system and make it dependent on only <em>one</em> of the existing proteins. Is this system IC? No, we can remove the new protein and the whole thing still works. Gradually, we make the other parts of the system dependent on the new protein and suddenly we have an 'IC' system.</p>\n\n<p>In other words, the 'problem' lies in imagining that you have to go from nothing to a complete working mousetrap. What seems more likely is that elements of a system are changed one by one, and that the system evolves through a series of states where you could point to some element and claim that it is essential.</p>\n\n<p>One final point to note is that no multicellular organism is born whole in one step. The processes that an embryo goes through are conceptually similar (though <a href=\"https://en.wikipedia.org/wiki/Recapitulation_theory\" rel=\"noreferrer\">not exactly</a> ) to evolution in that you can have different organs developing at different times, or simpler versions of them that can work together as a simpler system.</p>\n\n<hr>\n\n<p>To make this a little less abstract, consider the earthworm example given in the top answer. It has just a simple heart(s) and blood vessels - it doesn't seem that difficult, therefore to add in some lungs. Here's a trivial diagram:</p>\n\n<p><a href=\"https://i.stack.imgur.com/hL93C.png\" rel=\"noreferrer\"><img src=\"https://i.stack.imgur.com/hL93C.png\" alt=\"heart, blood, and lung interaction\"></a></p>\n\n<p>The lines here are interactions between the organs - the heart pumps blood through the vessels, and the lungs (if any) oxygenate the blood. We evolve from the simpler system (1) to the more complex system (2) just by adding another element.</p>\n\n<p>However, the difficulty with some systems is that the interactions between the parts are dependencies. A very simple example could be proteins that activate/deactivate other proteins (by phosphorylation, say). Then we could theoretically get a situation like this:</p>\n\n<p><a href=\"https://i.stack.imgur.com/nGmcP.png\" rel=\"noreferrer\"><img src=\"https://i.stack.imgur.com/nGmcP.png\" alt=\"protein activation systems\"></a> </p>\n\n<p>Here, the final system (4) looks like it is 'irreducibly' complex because you can't remove any of (A, B, C, D) without breaking the cycle. However, at each step, we only added or removed one dependency. This also shows the importance of redundancy in biological systems. If you knock out either C or D from system (3) then it still works.</p>\n"
},
{
"answer_id": 49216,
"pm_score": 0,
"text": "<p>A good question, indeed, and not easy to answer (or grasp). I'll give a very simplified answer. Bear in mind that the processess I'll describe are REALLY complex.</p>\n\n<p>You have to think way before blood, brains, etc. Billions of years ago, organic molecules were formed in the planet. These organic molecules started to \"\"\"join\"\"\". Millions of years latter, simple cells which didn't even have a nucleus were formed. Some millions of years latter, cells with nucleus started to form. Latter, these cells started to agreggate, turning into colonies of unicellular individuals. In time, these colonies turned into multicellular individuals, but with all cells being equal to one another. After that, cells in one organism started to differentiate into some functions (digestive and neural, for example). Slowly, more complex organisms were formed, as the cells which formed these organisms started to differentiate and form various kinds of tissues, which, through millions of years, developed into more and more complex organisms. Think of Cnidarians, for example. They are very \"simple\" (I use \"simple\" as a proxy for \"not complex\") beings. They have no circulatory system. A circulatory system developed in latter groups: the first, \"simple\" circulatory system appeared in Nematodeans (if I'm not mistaken). But it was really \"simple\". With time, other, more complex, circulatory systems started to originate due to various evolutionary pressures. The same applies to every type of cell, tissue or organ you can think about in any organism: <strong>complex organisms are the result of millions of years of simpler organisms which generated more complex organisms, by really little steps.</strong></p>\n\n<p>I hope you get the idea of what I'm trying to say. For really grasping all this, you have to study a lot of evolution, because it is a hard concept for us to deeply understand.</p>\n"
},
{
"answer_id": 49219,
"pm_score": 2,
"text": "<p>Simpler forms developed to handle simpler requirements. Take planarians, for instance, which are thin and small enough that they can receive their oxygen supply by diffusion straight through their surface. Now imagine a slightly bigger animal that needs a slightly more sophisticated system to oxygenate their internal regions well. A muscle with an aberrant, autonomous twitch would be enough to stir/circulate more oxygenated fluids through the body. Past that, any little accident that facilitates this (e.g. some cells bind to oxygen a little better, the muscle twitches a little stronger or more regularly, etc.) is another form closer to what we see today.</p>\n"
}
] |
50,420 |
<p>What was the first piece of work in computational biology? I'm ideally looking for a paper.</p>
<p>I am not interested in works that involve data management or data analysis but work that model biological processes through numerical simulations or numerical approximations of analytical results.</p>
|
[
{
"answer_id": 50445,
"pm_score": 4,
"text": "<p>Another nomination, if you include infectious disease epidemiology as part of biology and hence computational simulations of epidemics as part of computational biology:</p>\n\n<p><a href=\"http://www.jstor.org/stable/2342553\" rel=\"noreferrer\">Measles periodicity and Community Size</a>, M. S. Bartlett, <em>J. Roy. Stat Soc. A</em>, 120(1), 1957.</p>\n\n<p>The computations were run on the Manchester computer. Possibly the most entertaining part of the paper is the discussion afterwards from one of the computing assistants:</p>\n\n<blockquote>\n <p>Mr. J. C. GOWER: I should like to describe in a little more detail the programme for the Manchester computer which has produced the results that Professor Bartlett has been discussing ... Owing to the fact that the computer makes not infrequent mistakes and in view of the apparent impossibility of getting an overall check ... it is necessary to repeat the calculations ... The random numbers are produced in batches of 64. Each batch is tested for divergence from the expected number of unit digits. If the test fails a new batch is produced and tested. If three successive batches fail the machine stops and hoots continuously.</p>\n \n <p>Only once in the sixteen months during which the programme has been running have three successive batches failed ...</p>\n</blockquote>\n\n<p>But the winner (also in population biology) might be the one linked in the comments to a Biostars discussion, <a href=\"https://digital.library.adelaide.edu.au/dspace/bitstream/2440/15146/1/238.pdf\" rel=\"noreferrer\">Gene frequencies in a cline determined by selection and diffusion</a> R.A. Fisher <em>Biometrics</em> 1950. On p. 169 the author says</p>\n\n<blockquote>\n <p>I owe this tabulation to <a href=\"https://en.wikipedia.org/wiki/Maurice_Wilkes\" rel=\"noreferrer\">Dr. M. V. Wilkes</a> and <a href=\"https://en.wikipedia.org/wiki/David_Wheeler_(British_computer_scientist)\" rel=\"noreferrer\">Mr. D. J. Wheeler</a>, operating the <a href=\"https://en.wikipedia.org/wiki/Electronic_delay_storage_automatic_calculator\" rel=\"noreferrer\">EDSAC electronic computer</a></p>\n</blockquote>\n\n<p>(the tabulation is the solution of the differential equation $\\frac{d^2 q}{dx^2} = 4 x (1-q)q$ with boundary conditions $q=1/2$ at $x=0$ and $q=0$ as $x \\to \\infty$); the Wikipedia page about EDSAC (linked above) claims</p>\n\n<blockquote>\n <p>[Fisher's study] represents the first use of a computer for a problem in the field of biology</p>\n</blockquote>\n"
}
] |
[
{
"answer_id": 50423,
"pm_score": 3,
"text": "<p>I don't believe you'll ever find the <em>first</em> work in bioinformatics (or computational biology, as you put it), however the field really <strong>began</strong> in the times of accumulating data about protein biochemistry. Computational biologists (before they had access to the computer) would be writing and analyzing morphologies and types of proteins with pencil and paper. </p>\n\n<p>But you can go even further back than this. \"Alignment\" is another old technique used in bioinformatics. This is establishing the amount of similarity between two DNA sequences, or rather the degree of similarity between any two objects or data sets in computational biology.</p>\n\n<p>Your question, though, asks for a scientific paper (one of the oldest) on bioinformatics. This is arguably M. O. Dayhoff's paper: \"A Computer Program to Aid Primary Protein Structure Determination.\" (1962)</p>\n\n<p>This is the first formal paper that limits the scope of computational biology to the definition provided by this <a href=\"http://www.bioplanet.com/what-is-bioinformatics/\">BioPlanet article</a> and generally agreed by many:</p>\n\n<blockquote>\n <p>Bioinformatics is the application of computer technology to the management of biological information. </p>\n</blockquote>\n"
},
{
"answer_id": 50424,
"pm_score": 1,
"text": "<p>There is some ambiguity in words; however \"computational biology\" is often used to stress that work extends beyond sequence information (and sequence derived properties) and data management (which would rather be described by \"bioinformatics\").</p>\n\n<p>If the question is about the first work that used computer simulations, and algorithms to discover and mechanistically explain some complex biological problem, the work of Hans Meinhardt and colleagues comes very close to a first piece of computational biology.</p>\n\n<p>For instance they discovered how patterns could form; <a href=\"https://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=1&cad=rja&uact=8&ved=0ahUKEwjf-4b5iajOAhUk5IMKHTVnDeUQFggjMAA&url=http%3A%2F%2Fjxshix.people.wm.edu%2F2009-harbin-course%2Fclassic%2Fgierer-meinhardt-1972.pdf&usg=AFQjCNER-mV1Dq_VkvTsd_cL-B_PjluhDg&sig2=SEBMgZz6p5gqPx3VYIHCmQ\" rel=\"nofollow\">Gierer et Meinhadt 1972</a>, and other references contained in <a href=\"http://dev.biologists.org/content/develop/early/2016/03/22/dev.137414.full.pdf\" rel=\"nofollow\">his obituary</a></p>\n"
},
{
"answer_id": 50430,
"pm_score": 2,
"text": "<p>I don't have any idea about the <strong>first</strong> paper in computation biology (interpreted by me as papers that use computers and computer simulations to solve biological problems). However, some population ecologists were early in adopting computer simulations to solve population models. Your should look at <a href=\"https://en.wikipedia.org/wiki/Michael_Hassell\" rel=\"nofollow\">Micheal Hassell</a>, which I know was early in using computer simulations. One of his first papers is <a href=\"http://www.nature.com/nature/journal/v223/n5211/abs/2231133a0.html\" rel=\"nofollow\"><em>New inductive population model for insect parasites and its bearing on biological control.</em></a> from 1969 (<a href=\"http://www.nhm.ac.uk/resources/research-curation/projects/chalcidoids/pdf_Y/HasselVa969.pdf\" rel=\"nofollow\">pdf</a>), where models are simulated on the \"Oxford KDF9 computer\". His other papers and his collaborators could be a starting point.</p>\n"
},
{
"answer_id": 50459,
"pm_score": 2,
"text": "<p>Depending on your definition of computational biology (e.g. bioinformatics and mathematical modelling can be quite different), there is an oft-cited reference to Alan Turing's work after the second world war, modelling what he called \"morphogens\" in the emergence of mathematical patterns in nature. As I understand it he modelled diffusion of antagonistic and complementary hypothetical molecules in space and time. I'm fairly sure this is one of the first examples of using the very early computers, while they were still reminiscent of counting machines for biological problems.</p>\n\n<p>I don't have an exact reference for you right now, but some google-fu of \"Turing\" and \"morphogens\" will drag something up.</p>\n\n<p>EDIT: here's the paper, 1952 is the year to beat!:</p>\n\n<p><a href=\"http://www.dna.caltech.edu/courses/cs191/paperscs191/turing.pdf\" rel=\"nofollow\">http://www.dna.caltech.edu/courses/cs191/paperscs191/turing.pdf</a></p>\n"
}
] |
50,599 |
<p>I have a modest collection of insect specimens that I caught, prepared, mounted, and dried myself. I'm entirely an amateur collector, so my procedure may be causing me this trouble now, but here's how I preserved them.</p>
<ol>
<li>Killed in the freezer</li>
<li>Placed in a sealed container on a dry platform, with a 50% isopropyl alcohol solution under it. This lets the specimen thaw and remain moist, while the alcohol prevents rotting.</li>
<li>Kept in container for two to three days.</li>
<li>Stretched over foam and held in place with paper and pins.</li>
<li>Kept on stretching board for three weeks.</li>
<li>Placed in a consumer grade display box.</li>
<li>Stored in a dark, dry closet.</li>
</ol>
<p>It's been a while since I worked on this hobby, but I do like to pull the collection out from time to time and admire it. Today, I was surprised and disappointed to find that some of my best specimens have been turned to dust by a small caterpillar type bug. There are live bugs in my display case, eating my bugs!</p>
<p>I've had these for years without issue, and now I find this. What can I do about it? How can I keep this from happening again? Should my preservation procedure include some other step? How are they even surviving? There's no moisture in there at all!</p>
<p>I'd rather not put something toxic in my display case, as I like to take them out and examine them without the glass in the way. I don't want to be exposed to toxic things every time I look at them. I hope there's some effective, cheap, and safe thing I can do. I've become rather proud of my collection, but it's disheartening to have worms eating them before they've even eaten me.</p>
<p>Here's some pictures of the devastation:</p>
<p><a href="https://i.stack.imgur.com/pAAvf.jpg" rel="nofollow noreferrer"><img src="https://i.stack.imgur.com/pAAvf.jpg" alt="Bird's eye view."></a></p>
<p>That stain on the right used to be a specimen.</p>
<p><a href="https://i.stack.imgur.com/6f0N7.jpg" rel="nofollow noreferrer"><img src="https://i.stack.imgur.com/6f0N7.jpg" alt="Formerly a praying mantis."></a>
The big pile of dust there on the left used to be a praying mantis. I don't even know what the pile on the right use to be.</p>
<p><a href="https://i.stack.imgur.com/L0LUV.jpg" rel="nofollow noreferrer"><img src="https://i.stack.imgur.com/L0LUV.jpg" alt="Beetle missing insides"></a>
This beetle's entire insides have been eaten.</p>
<p><a href="https://i.stack.imgur.com/jkjDE.jpg" rel="nofollow noreferrer"><img src="https://i.stack.imgur.com/jkjDE.jpg" alt="Horsefly is now dust."></a>
This horsefly looks like it was mounted a hundred years ago.</p>
<p><a href="https://i.stack.imgur.com/eYvng.jpg" rel="nofollow noreferrer"><img src="https://i.stack.imgur.com/eYvng.jpg" alt="Butterflies and moths don't taste very good."></a>
Apparently moths and butterflies don't taste very good.</p>
<p><a href="https://i.stack.imgur.com/J2wJY.jpg" rel="nofollow noreferrer"><img src="https://i.stack.imgur.com/J2wJY.jpg" alt="The culprit!"></a>
The culprit! This little guy and his pals are responsible. You can see exoskeleton sheddings all throughout the other pictures.</p>
|
[
{
"answer_id": 50619,
"pm_score": 5,
"text": "<p>I ran into the same issue when collecting bees in a hot, humid environment. As <code>arboviral</code>stated, freezing is a great way to help with the infection but keep in mind:</p>\n\n<ul>\n<li>It may not kill all of your pests</li>\n<li>It will not keep your specimen from future pests</li>\n<li>It may damage your samples</li>\n</ul>\n\n<p>From the <a href=\"http://www.ars.usda.gov/News/docs.htm?docid=10141&page=11\">USDA website</a>, you could pretty cheaply use paradichlorobenzene or naphthalene:</p>\n\n<blockquote>\n <p>Two of the most widely used fumigants are paradichlorobenzene (PDB)\n and naphthalene, both of which are obtainable in balls or flakes.\n Never mix PDB with naphthalene as they react chemically and produce a\n liquid that may damage the collection. It should be noted, that most\n major collections are now moving away from the use of solid fumigants\n because of health concerns and in some jurisdictions, it is now\n against regulations to use some fumigants.</p>\n</blockquote>\n\n<p>That being said, I used a combination of freezing and then naphthalene (moth balls). It's cheap and anecdotally pretty effective for my purposes. I also didn't access my collection frequently once established, so the health concerns were less of a worry for me. </p>\n\n<p>Definitely worth mentioning that there has been talk that using naphthalene or PDB may damage DNA and hurt DNA extractions on down the road, but this is <a href=\"https://frontiersinzoology.biomedcentral.com/articles/10.1186/1742-9994-7-2\">demonstrably false</a>. That being said, keep in mind these chemicals still pose some heath effects - especially with prolonged or occupational exposure - such as <a href=\"https://medlineplus.gov/ency/article/002477.htm\">poisoning</a> and <a href=\"http://monographs.iarc.fr/ENG/Monographs/vol82/index.php\">carcinogenic risk</a>. </p>\n"
}
] |
[
{
"answer_id": 50613,
"pm_score": 3,
"text": "<p>As @picapica says, these look like beetles of the genus <em>Anthrena</em>: museum beetles, furniture carpet beetles or something similar. I'd lean towards furniture carpet beetle (<em>Anthrena flavipes</em>) myself, but this isn't a species ID question.</p>\n\n<p>Your best bet would be to use an insecticide. However, pages 18-19 of <a href=\"http://www.si.edu/mci/downloads/articles/AtPMiM1998-Update.pdf\" rel=\"noreferrer\">Story (1998) \"Approaches to pest management in museums\"</a> list 15 non-chemical ways to deal with these beetles. Based on this source, I suggest you:</p>\n\n<ol>\n<li><strong>physically remove as much of the infestation as you can</strong>, then</li>\n<li><strong>freeze the whole collection</strong> (again, as first suggested in the comment by @picapica).</li>\n</ol>\n\n<p>Dermestid beetles like <em>Anthrena</em> are relatively heat-tolerant and the other control methods are more based around reducing the chance of an infestation in the first place. <strong>To be effective, freezing may need to be as low as -30°C (generally domestic freezers will only maintain temperatures from −23 to −18°C) and sustained for up to three days.</strong></p>\n\n<p>Once you've got rid of this infestation, some of the other suggestions to avoid reinfestation may be useful, such as sealing or screening possible routes of entry in the cases to stop beetles getting back in.</p>\n\n<p>Nice collection, by the way!</p>\n"
},
{
"answer_id": 50656,
"pm_score": 2,
"text": "<p>Use borates, like for wood treatment. It's not a repellent like moth balls but it will kill them and not be smelly and it has low toxicity.</p>\n\n<p>Borates are also used in taxidermy, especially for controlling dermestid beetles, however salty crusts can develop so, you might have to play around with the concentration- so that you don't use too much.</p>\n\n<p>Also, peppermint and citronella are fine repellents. There are repellent satchets on the market, but you could probably save your money and just get a dram of peppermint oil or (pure) citronella oil (soak a piece of wood- like cedar).</p>\n\n<p>Also, DEET is good repellent. But these repellents won't last as long as moth balls.</p>\n"
},
{
"answer_id": 51123,
"pm_score": 2,
"text": "<p>Adding to the allready fine answers, I would suggest to use some <a href=\"https://en.wikipedia.org/wiki/Camphor\" rel=\"nofollow\">camphor</a>. Camphor is relatively inexpensive. I could buy it at the local pharmacy, but depending on your location, it might or might not be available there.</p>\n\n<p>I successfully used camphor to get rid of Dermestids. However, it is much more effective to <em>prevent</em> infestation than to get rid of one.</p>\n\n<p>However, if you use it, you might not want to store your collection in a part of a building where people spend prolonged times. Also, you definitely want to put your collection in a near-airtight container. Camphor evaporates quickly, and an airtight container is important to keep the atmosphere more or less saturated. Glass, of course, is best. Plastic might permeable, and even get brtittle, depending on the specific material. Sidenote: Professional and (very expensive cabinets) use hardwood boxes with a glass cover cemented in the lid, which have the additional advantage of making it difficult for dermestids to get in.</p>\n\n<p>You should apply it using a watch glass, and not let it come into direct contact with both your collections and the material the specimens are pinned on.</p>\n"
},
{
"answer_id": 63925,
"pm_score": 1,
"text": "<p>I like your collection! I am sorry about the beetle tragedy.<br>\nI recommend that in addition to killing the ones you have in the collection (freezing) that you put your collection in a <strong>beetle proof container</strong> to save what is left. That is not practical for a mounted water buffalo but I am sure you can find a Tupperware-type container that can house your collection and prevent beetle entry. </p>\n\n<p>Also: check the rest of that closet. Those beetles came from somewhere. Carpet beetles ate tracks in one of my nice coats a few years back. You might have a colony in the closet. Remove the stuff, shake it out and spray the floor with roach spray. </p>\n"
},
{
"answer_id": 65156,
"pm_score": 2,
"text": "<p>Another addition.\nIf you like to avoid chemicals, I recommend using vacuum bags that are meant to store clothes in, which you can easily buy. They are like big zipper bags that close airtight and keep away the pests. This is an alternative to very expensive airtight boxes.\nTo get rid of beetle larvae that are in your collection, you need to kill them. For me, it always sufficed to freeze at -18, but this might not always work. My home freezer is quite small, so I would re-pin the insects to a smaller box, clean up the 'main box' very thoroughly (also removing bottom plate!!!), and after 3 days of freezing put the insects back. Check your collection at least once a year. \nI have old museum boxes with lids that do not close so well anymore. Since I use vacuum bags I (5 years now) had no beetle infestation so far. </p>\n\n<p>\"Apparently moths and butterflies don't taste very good.\"\nWell, you were lucky. These beetles love moths and butterflies the most!</p>\n"
},
{
"answer_id": 76565,
"pm_score": 2,
"text": "<p>I preserve all my bugs in resin. It is an absolute ton of work, and not always guaranteed to turn out, but I have successfully done over 150 bugs. <img src=\"https://i.stack.imgur.com/MHMp9.jpg\" alt=\"enter image description here\"></p>\n"
}
] |
51,556 |
<p>We heard this animal outside in Western Washington (Port Townsend area) during the late evening. I think it is a bird, but it honestly sounds sort of like some creepy woman singing or something. The audio is linked below. The sound (in the audio) was repeated for a long time at random intervals averaging probably every ten seconds. </p>
<p><a href="https://clyp.it/tzybty1w" rel="nofollow">https://clyp.it/tzybty1w</a></p>
<p>Anyone know for certain?</p>
|
[
{
"answer_id": 51572,
"pm_score": 3,
"text": "<p>I asked the same question on another forum here: <a href=\"http://www.birdforum.net/showthread.php?p=3454684\" rel=\"nofollow\">http://www.birdforum.net/showthread.php?p=3454684</a>. </p>\n\n<p>It looks like another possibility is a <strong>barred owl</strong>. It also <a href=\"https://www.youtube.com/watch?v=NtRPYpklhiA\" rel=\"nofollow\">sounds somewhat similar</a>.</p>\n"
}
] |
[
{
"answer_id": 51563,
"pm_score": 2,
"text": "<p>My guess is an owl, possibly a great horned owl, which are found in the <a href=\"https://www.google.com.sg/search?q=owls+in+western+washington&gws_rd=cr&ei=IQnZV8GdMMLO0gT6gqCQAg\" rel=\"nofollow\">area</a> and can <a href=\"http://www.learner.org/jnorth/sounds/Owl_GreatHorned_Duet.mp3\" rel=\"nofollow\">sound similar</a>.</p>\n\n<p>Alternatively, it could be a mourning dove, which <a href=\"http://www.learner.org/jnorth/sounds/Dove_Mourning.mp3\" rel=\"nofollow\">sounds similar again</a>, and is <a href=\"http://www.birdweb.org/birdweb/bird/mourning_dove\" rel=\"nofollow\">common throughout the USA</a>.</p>\n"
},
{
"answer_id": 100525,
"pm_score": -1,
"text": "<p>It could be the Sri Lankan spot-bellied eagle-owl lost in America.</p>\n<p>Link = [https://www.google.com/search?q=spot-bellied+eagle-owl&oq=spot-bellied+eagle-owl&aqs=chrome..69i57j46j0i22i30l7.931j0j7&sourceid=chrome&ie=UTF-8][1]</p>\n"
},
{
"answer_id": 100531,
"pm_score": 1,
"text": "<p>This does sound like the characteristic "who cooks for you" call of a distant <a href=\"https://en.wikipedia.org/wiki/Barred_owl\" rel=\"nofollow noreferrer\"><strong>barred owl</strong> (<em>Strix varia</em>)</a>. You can hear this call at <a href=\"https://www.allaboutbirds.org/guide/Barred_Owl/sounds\" rel=\"nofollow noreferrer\">All About Birds</a> run by Cornell Ornithology Lab.</p>\n<ul>\n<li><p>The <a href=\"https://macaulaylibrary.org/asset/21681321\" rel=\"nofollow noreferrer\">recording by\nAndrew Spencer</a> is most similar to yours given the distance it was recorded (though, he suggests it's a subspecies out of range that was recorded).</p>\n</li>\n<li><p>You might also try <a href=\"https://www.audubon.org/field-guide/bird/barred-owl\" rel=\"nofollow noreferrer\">Audobon's</a> sound clips as they were recorded at farther distance than those at Cornell and so better represent what you're hearing.</p>\n</li>\n</ul>\n<p>You're in range of these owls in Port Townsend:</p>\n<p><a href=\"https://i.stack.imgur.com/aCK8zm.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/aCK8zm.jpg\" alt=\"enter image description here\" /></a></p>\n<p> Source: <a href=\"https://www.allaboutbirds.org/guide/Barred_Owl/maps-range\" rel=\"nofollow noreferrer\">All About Birds</a></p>\n"
},
{
"answer_id": 100532,
"pm_score": -1,
"text": "<p>No question ; barred owl. There are a few in the subdivision and presently I hear them fairly often. I think it may be fledging practicing the call. I am in E TX at the southern end of the range on the shown map.</p>\n"
}
] |
52,046 |
<p>I hope this is a good place to ask such question. I have to do some data analysis on RNA-seq data from human cells. I am currently searching for tools to help me with that. Specifically, I would need some tools to analyze the gene expression from the data. Something to help me plot the expression of selected genes in each fastq file and compare the differences in the expression with the possibility to export the results or some command line interface for scripting. Basically I need something where I can put a fastq file and perhaps also a human genome annotation file as input and get gene expression as output. I have looked at bioconductor and it's packages and on <a href="https://en.wikipedia.org/wiki/List_of_RNA-Seq_bioinformatics_tools">Wikipedia's List of RNA-Seq bioinformatics tools</a>. I suppose some of these tools have to be able to do what I need, but I have been unable to find out which one and how should they be used to achieve that. Could someone please give me some advice?</p>
|
[
{
"answer_id": 52112,
"pm_score": 4,
"text": "<p>You will likely need a tool to \"map\" the reads on the reference genome.\nYou may find such a reference genome, together with annotations, here:\n<a href=\"ftp://ussd-ftp.illumina.com/\" rel=\"nofollow noreferrer\">ftp://ussd-ftp.illumina.com/</a>.</p>\n\n<p>Mapping tools such as bowtie2 or bwa take fastq files and reference genomes and output mapping results in a format called <a href=\"https://samtools.github.io/hts-specs/SAMv1.pdf\" rel=\"nofollow noreferrer\">sam</a>.</p>\n\n<p>You then have a lot of options to estimate gene expression.</p>\n\n<ul>\n<li><p>You can write your own algorithm to parse sam format and estimate normalized read counts on each gene.</p></li>\n<li><p>You can combine more or less low-level tools such as samtools, pysam, htseq with some scripting to do this.</p></li>\n<li><p>You can use tools that do the counting (like bedtools ot htseq-count) and differential expression analysis (like deseq2).</p></li>\n</ul>\n\n<p>In the last case, I would advice to start from the documentation of the final tool to find out what are the tools you need to generate the output of the preceding step.</p>\n\n<p>It is very likely you will use some R or Python, or use the web platform <a href=\"https://galaxyproject.org/\" rel=\"nofollow noreferrer\">galaxy</a> for some of the steps.</p>\n\n<h3>Edits</h3>\n\n<p>As mentioned by @scribaniwannabe in <a href=\"https://biology.stackexchange.com/a/52327/1486\">this answer</a>, the paper about the <a href=\"http://dx.doi.org/10.1038/nprot.2016.095\" rel=\"nofollow noreferrer\">Tuxedo suite of tools</a> gives a good example of the steps to carry out an RNA-seq analysis using recent tools (as of October 2016).</p>\n\n<p>As @Student T reminds in <a href=\"https://biology.stackexchange.com/a/52261/1486\">this answer</a>, RNA-seq data contain reads that can come from exon-exon junctions, so the read mapper has to be set up in such a way as not to discard reads not mapping continuously on all their length on the genome. To my knowledge, <a href=\"https://ccb.jhu.edu/software/hisat2/index.shtml\" rel=\"nofollow noreferrer\">HISAT2</a> and <a href=\"http://crac.gforge.inria.fr/\" rel=\"nofollow noreferrer\">CRAC</a> do this by default. Bowtie2 needs special settings.</p>\n"
}
] |
[
{
"answer_id": 52261,
"pm_score": 2,
"text": "<p>While I also agree @bli that R and Python (in particular <code>Bioconductor</code>) have more than enough packages for you to compare gene expression. You <em>shouldn't</em> align your reads with bwa or bowtie because they don't take introns into consideration. You should use <code>TopHat</code> or <code>STAR</code>. </p>\n"
},
{
"answer_id": 52327,
"pm_score": 2,
"text": "<p>The answer @bli gave is great. I thought I would point out that Johns Hopkins also recently upgraded their <a href=\"http://www.nature.com/nprot/journal/v11/n9/full/nprot.2016.095.html\" rel=\"nofollow\" title=\"tuxedo suite\">tuxedo suite</a>. Looks promising and has great instructions for use.</p>\n\n<p>Also, I've begun to grow quite fond of the <a href=\"http://genetrail2.bioinf.uni-sb.de/\" rel=\"nofollow\">GeneTrail 2 tool</a> for my RNA-Seq secondary analysis. Gives great results for enrichment analyses.</p>\n\n<p>Hope this is helpful.</p>\n"
},
{
"answer_id": 52709,
"pm_score": 2,
"text": "<p>I think that STAR is the preferred splice-aware aligner nowadays. STAR can output counts by gene or by transcript. Assuming you have Illumina data, you can try using the tools on Illumina's BaseSpace. RNASeq might be one of the things that you can do for free there.</p>\n"
},
{
"answer_id": 100435,
"pm_score": 0,
"text": "<p>I think <a href=\"https://htseq.readthedocs.io/en/master/index.html\" rel=\"nofollow noreferrer\">HTSeq</a> does almost that. It outputs a matrix of read counts per gene given a fastq sample and annotation file</p>\n"
},
{
"answer_id": 104706,
"pm_score": 1,
"text": "<p><a href=\"https://github.com/urmi-21/pyrpipe\" rel=\"nofollow noreferrer\">pyrpipe</a> claims to be a one-stop python library for RNA-seq analysis. Here is an illustration from their <a href=\"https://academic.oup.com/nargab/article/3/2/lqab049/6290623\" rel=\"nofollow noreferrer\">paper</a>:</p>\n<p><a href=\"https://i.stack.imgur.com/TwNl6.png\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/TwNl6.png\" alt=\"enter image description here\" /></a></p>\n<p>Furthermore, I would like to draw attention to ENCODE's official RNA-seq pipeline, which is actively maintained on ENCODE-DCC's <a href=\"https://github.com/ENCODE-DCC/rna-seq-pipeline\" rel=\"nofollow noreferrer\">GitHub repository</a>.</p>\n"
}
] |
53,313 |
<p>Is there a lower limit to the difference in wavelength (colour) our eyes can detect? If so, is this consistent between individuals? Are there any other traits correlated with precise colour vision?</p>
|
[
{
"answer_id": 54449,
"pm_score": 3,
"text": "<p>The eye really on can sense 3 colors, or to be more precise it only has three types color sensitive each of which detects a large range of wavelengths with no way to distinguish between them within the same cone. We only determine color by the different levels of activation between the different cone cells. This means we need a lot of light to see color and our ability to detect differences in color really depend greatly on where on the visible spectrum that color falls. \n<a href=\"https://i.stack.imgur.com/PONuV.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/PONuV.jpg\" alt=\"enter image description here\"></a></p>\n\n<p>As for more precise color vision. The greater the number of types of cones cells the more color sensitive the eye ,birds and reptiles can see far more colors than use becasue they have 4 types of color sensitive cells as opposed to the human 3. More widely spaces base colors will give greater sensitivity. This is why even among trichromats human color vision is poor becasue two of our base colors are close together and overlap greatly. That is because humans (and primates) are secondarily trichromats, gaining a third base color from a recent mutation. <a href=\"https://en.wikipedia.org/wiki/Evolution_of_color_vision_in_primates\" rel=\"nofollow noreferrer\">wiki on the subject</a><br>\n<a href=\"https://i.stack.imgur.com/Pxl2h.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/Pxl2h.jpg\" alt=\"http://www.webexhibits.org/causesofcolor/images/content/Absorption_peaks.jpg\"></a></p>\n"
}
] |
[
{
"answer_id": 53472,
"pm_score": 0,
"text": "<p>First, it depends a lot of the brightness. And also, of the part of the spectrum: we have high accuracy between red-green (since 2 of the cone have close sensitiveness), and very few in deep red and violet (were mostly a single cone reacts).</p>\n\n<p>As always, you do have differences between individuals. Small ones, + big ones related to the variations in cone peak sensitiveness (or missing or extra cone).</p>\n\n<p>In addition, it seems that there is a cultural factor: some cultures are more trained to pay attention to differences within blues, or reds, or greys.</p>\n"
},
{
"answer_id": 54447,
"pm_score": 2,
"text": "<p>I am unable to answer the first question.</p>\n\n<p>But yes, there is an upper ad lower limit to what frequency of light the human eye can detect. This is why you cannot see microwaves, infra-red, ultraviolet or gamma rays. Given the light cones humans have, the limits is consistent within the species. However given that the exact number of each light cone (red, blue, green) varies between individuals, sensitivity to a particular colour will vary between individuals. So both of us can see blue. But my blue maybe bluer than yours.</p>\n\n<p>Should be noted that there are two variants of the green light cone in the human population. One has a sensitivity that is slighted to the red. And the gene for the green light cone is on the X chromosome. So about 2-3% of the women in the world have both variants and thus better colour discrimination. </p>\n\n<p><a href=\"https://en.wikipedia.org/wiki/Tetrachromacy\" rel=\"nofollow noreferrer\">https://en.wikipedia.org/wiki/Tetrachromacy</a></p>\n\n<p>PS: Yes.. there are colour blind people. And if you include colour blind people then there are some people who have a narrower range of colour perception than most of the human population.</p>\n"
},
{
"answer_id": 74594,
"pm_score": -1,
"text": "<p>About 2 nm wavelength difference. The human eye can detect about 150 different hues in a rainbow, which for us consists of a visible light 380-700nm. About 300nm/150hues = 2nm per smallest detectable difference between two hues. I guess that's the answer you were looking for?</p>\n"
},
{
"answer_id": 84450,
"pm_score": 2,
"text": "<blockquote>\n <p>Is there a lower limit to the difference in wavelength (colour) our eyes can detect?</p>\n</blockquote>\n\n<p>The average human can detect differences in color as low a 1 <a href=\"https://en.wikipedia.org/wiki/Nanometre\" rel=\"nofollow noreferrer\">nm</a> depending on color subject to:</p>\n\n<ul>\n<li><p>minimum spot size - \"<a href=\"http://www.jneurosci.org/content/34/16/5667\" rel=\"nofollow noreferrer\">Mapping the Perceptual Grain of the Human Retina</a>\", by Wolf M. Harmening, William S. Tuten, Austin Roorda and Lawrence C. Sincich in the Journal of Neuroscience 16 April 2014, 34 (16) 5667-5677; DOI: <a href=\"https://doi.org/10.1523/JNEUROSCI.5191-13.2014\" rel=\"nofollow noreferrer\">https://doi.org/10.1523/JNEUROSCI.5191-13.2014</a> </p></li>\n<li><p>background color - \"<a href=\"https://www.nature.com/articles/s41598-018-26754-1\" rel=\"nofollow noreferrer\">Sensations from a single M-cone depend on the activity of surrounding S-cones</a>\", by Brian P. Schmidt, Ramkumar Sabesan, William S. Tuten, Jay Neitz and Austin Roorda in Scientific Reports volume 8, Article number: 8561 (2018) DOI: <a href=\"https://dx.doi.org/10.1038%2Fs41598-018-26754-1\" rel=\"nofollow noreferrer\">https://dx.doi.org/10.1038%2Fs41598-018-26754-1</a></p></li>\n<li><p>location of cone, proximity to blood vessels - \"<a href=\"https://www.researchgate.net/publication/276170738_Selective_Stimulation_of_Penumbral_Cones_Reveals_Perception_in_the_Shadow_of_Retinal_Blood_Vessels\" rel=\"nofollow noreferrer\">Selective Stimulation of Penumbral Cones Reveals Perception in the Shadow of Retinal Blood Vessels</a>\", by Manuel Spitschan, Geoffrey K. Aguirre, and David H. Brainard, in PLoS ONE 10(4):e0124328 (April 2015) DOI: <a href=\"https://doi.org/10.1371/journal.pone.0124328\" rel=\"nofollow noreferrer\">https://doi.org/10.1371/journal.pone.0124328</a></p></li>\n</ul>\n\n<p>The following graph shows the minimum and maximum discrimination values at various frequencies:</p>\n\n<p><a href=\"https://i.stack.imgur.com/TmJuK.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/TmJuK.jpg\" alt=\"Mean Wavelength Discrimination Curve\"></a></p>\n\n<p>Figure 13. Mean wavelength discrimination curve. (From Davson, H., The Eye, vol 2. London, Academic Press, 1962)</p>\n\n<p>Source: <a href=\"https://webvision.med.utah.edu/book/part-viii-psychophysics-of-vision/color-perception/\" rel=\"nofollow noreferrer\">Color Perception</a> by Michael Kalloniatis and Charles Luu</p>\n\n<p><a href=\"https://i.stack.imgur.com/sYzqf.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/sYzqf.jpg\" alt=\"Computation of Cone Fundamentals\"></a></p>\n\n<p>Source: Computation of Cone Fundamentals (Color Matching Functions) in Terms of Energy for Various Field Sizes and Ages Based on CIE 170-1, Spreadsheet Prepared By Mark Fairchild (mdf@cis.rit.edu), RIT Munsell Color Science Laboratory (mcsl.rit.edu), from Rochester Institute of Technology, Program of Color Science: <a href=\"https://www.rit.edu/science/pocs/useful-data\" rel=\"nofollow noreferrer\">Useful Color Data</a>.</p>\n\n<blockquote>\n <p>If so, is this consistent between individuals? </p>\n</blockquote>\n\n<p>No.</p>\n\n<p><a href=\"https://i.stack.imgur.com/CYDSB.gif\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/CYDSB.gif\" alt=\"xxxxxxxxxx\"></a></p>\n\n<p><a href=\"https://www.handprint.com/HP/WCL/color2.html#individualdiffs\" rel=\"nofollow noreferrer\">Individual variations in photopic sensitivity</a></p>\n\n<p>Results for 52 individuals, based on heterochromatic step by step brightness matching; \"The visibility of radiant energy\" Gibson, Tyndall and Kasson (1923)</p>\n\n<p>A newer study, \"<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4757445/\" rel=\"nofollow noreferrer\">Individual Differences in Scotopic Visual Acuity and Contrast Sensitivity: Genetic and Non-Genetic Influences</a>\" (Feb 17 2016), by Alex J. Bartholomew, Eleonora M. Lad, et al., PLoS One. 2016; 11(2): e0148192. DOI: 10.1371/journal.pone.0148192\nPMCID: PMC4757445, offers a different variance plot (without nm):</p>\n\n<p><a href=\"https://i.stack.imgur.com/bXtnX.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/bXtnX.jpg\" alt=\"Individual Differences in Scotopic Visual Acuity and Contrast Sensitivity\"></a></p>\n\n<p>Fig 1. Test-retest assessment. Four data sets are depicted: Visual acuity (left panel) and contrast sensitivity (right panel) at photopic luminance (green triangles, near top left and at scotopic luminance (blue discs, near bottom left). Result of the first test on the abscissa, second test on the ordinate. Grey 45°- line is the identity line, next to it the ± limits of agreement (photopic, dashed; scotopic, dotted). Visual acuity in logMAR units have an inverted scale, and contrast sensitivity is in logCSWeber units, meaning that better performance corresponds to the top right for both graphs. As expected, photopic measures of VA or CS are markedly better than scotopic ones. The 95% limits of agreement are remarkably similar. All in all, there is no marked deviation from a normal\ndistribution, and the reliability is good for the range measured.</p>\n\n<blockquote>\n <p>Are there any other traits correlated with precise colour vision?</p>\n</blockquote>\n\n<p>For your third question, above the one question per post limit, I'll offer these links (I may come back to this as time permits):</p>\n\n<p>The website Handprint has these webpages:</p>\n\n<ul>\n<li><p><a href=\"https://www.handprint.com/HP/WCL/color2.html#discrimination\" rel=\"nofollow noreferrer\">Measuring Perceptual Discrimination</a></p></li>\n<li><p><a href=\"https://www.handprint.com/HP/WCL/color2.html#individualdiffs\" rel=\"nofollow noreferrer\">Individual Differences in Color Experience</a></p></li>\n<li><p><a href=\"https://www.handprint.com/HP/WCL/color2.html#language\" rel=\"nofollow noreferrer\">Color and Language</a></p></li>\n</ul>\n\n<p>See also: </p>\n\n<ul>\n<li><p>\"<a href=\"https://www.pnas.org/content/114/40/10785\" rel=\"nofollow noreferrer\">Color naming across languages reflects color use</a>\", by Edward Gibson, Richard Futrell, Julian Jara-Ettinger, Kyle Mahowald, Leon Bergen, Sivalogeswaran Ratnasingam, Mitchell Gibson, Steven T. Piantadosi, and Bevil R. Conway in PNAS October 3, 2017 114 (40) 10785-10790; first published September 18, 2017 <a href=\"https://doi.org/10.1073/pnas.1619666114\" rel=\"nofollow noreferrer\">https://doi.org/10.1073/pnas.1619666114</a></p></li>\n<li><p><a href=\"https://midimagic.sgc-hosting.com/huvision.htm\" rel=\"nofollow noreferrer\">Human Color Vision</a></p></li>\n<li><p><a href=\"https://midimagic.sgc-hosting.com/pricol.htm\" rel=\"nofollow noreferrer\">Teach the Correct Color Theory in School</a></p></li>\n</ul>\n\n<p>Briefly: Precise color perception is not only the capability of the eye but the training of the brain (seeing different similar colors and having a need to differentiate between them) and the teaching of the vocabulary, the learning of the differences, and learned application of this in practice. </p>\n"
}
] |
53,328 |
<p>Imagine you hit your foot at a table leg and it hurts a while or you got a tiny graze. Those injuries aren't an infection but could these things still be called an inflammation?</p>
<p>Is it necessary that in both cases cells are damaged to induce a cascade of hormones? Or with other words, is there always an inflammation when cells are damaged or is needed more?</p>
|
[
{
"answer_id": 54449,
"pm_score": 3,
"text": "<p>The eye really on can sense 3 colors, or to be more precise it only has three types color sensitive each of which detects a large range of wavelengths with no way to distinguish between them within the same cone. We only determine color by the different levels of activation between the different cone cells. This means we need a lot of light to see color and our ability to detect differences in color really depend greatly on where on the visible spectrum that color falls. \n<a href=\"https://i.stack.imgur.com/PONuV.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/PONuV.jpg\" alt=\"enter image description here\"></a></p>\n\n<p>As for more precise color vision. The greater the number of types of cones cells the more color sensitive the eye ,birds and reptiles can see far more colors than use becasue they have 4 types of color sensitive cells as opposed to the human 3. More widely spaces base colors will give greater sensitivity. This is why even among trichromats human color vision is poor becasue two of our base colors are close together and overlap greatly. That is because humans (and primates) are secondarily trichromats, gaining a third base color from a recent mutation. <a href=\"https://en.wikipedia.org/wiki/Evolution_of_color_vision_in_primates\" rel=\"nofollow noreferrer\">wiki on the subject</a><br>\n<a href=\"https://i.stack.imgur.com/Pxl2h.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/Pxl2h.jpg\" alt=\"http://www.webexhibits.org/causesofcolor/images/content/Absorption_peaks.jpg\"></a></p>\n"
}
] |
[
{
"answer_id": 53472,
"pm_score": 0,
"text": "<p>First, it depends a lot of the brightness. And also, of the part of the spectrum: we have high accuracy between red-green (since 2 of the cone have close sensitiveness), and very few in deep red and violet (were mostly a single cone reacts).</p>\n\n<p>As always, you do have differences between individuals. Small ones, + big ones related to the variations in cone peak sensitiveness (or missing or extra cone).</p>\n\n<p>In addition, it seems that there is a cultural factor: some cultures are more trained to pay attention to differences within blues, or reds, or greys.</p>\n"
},
{
"answer_id": 54447,
"pm_score": 2,
"text": "<p>I am unable to answer the first question.</p>\n\n<p>But yes, there is an upper ad lower limit to what frequency of light the human eye can detect. This is why you cannot see microwaves, infra-red, ultraviolet or gamma rays. Given the light cones humans have, the limits is consistent within the species. However given that the exact number of each light cone (red, blue, green) varies between individuals, sensitivity to a particular colour will vary between individuals. So both of us can see blue. But my blue maybe bluer than yours.</p>\n\n<p>Should be noted that there are two variants of the green light cone in the human population. One has a sensitivity that is slighted to the red. And the gene for the green light cone is on the X chromosome. So about 2-3% of the women in the world have both variants and thus better colour discrimination. </p>\n\n<p><a href=\"https://en.wikipedia.org/wiki/Tetrachromacy\" rel=\"nofollow noreferrer\">https://en.wikipedia.org/wiki/Tetrachromacy</a></p>\n\n<p>PS: Yes.. there are colour blind people. And if you include colour blind people then there are some people who have a narrower range of colour perception than most of the human population.</p>\n"
},
{
"answer_id": 74594,
"pm_score": -1,
"text": "<p>About 2 nm wavelength difference. The human eye can detect about 150 different hues in a rainbow, which for us consists of a visible light 380-700nm. About 300nm/150hues = 2nm per smallest detectable difference between two hues. I guess that's the answer you were looking for?</p>\n"
},
{
"answer_id": 84450,
"pm_score": 2,
"text": "<blockquote>\n <p>Is there a lower limit to the difference in wavelength (colour) our eyes can detect?</p>\n</blockquote>\n\n<p>The average human can detect differences in color as low a 1 <a href=\"https://en.wikipedia.org/wiki/Nanometre\" rel=\"nofollow noreferrer\">nm</a> depending on color subject to:</p>\n\n<ul>\n<li><p>minimum spot size - \"<a href=\"http://www.jneurosci.org/content/34/16/5667\" rel=\"nofollow noreferrer\">Mapping the Perceptual Grain of the Human Retina</a>\", by Wolf M. Harmening, William S. Tuten, Austin Roorda and Lawrence C. Sincich in the Journal of Neuroscience 16 April 2014, 34 (16) 5667-5677; DOI: <a href=\"https://doi.org/10.1523/JNEUROSCI.5191-13.2014\" rel=\"nofollow noreferrer\">https://doi.org/10.1523/JNEUROSCI.5191-13.2014</a> </p></li>\n<li><p>background color - \"<a href=\"https://www.nature.com/articles/s41598-018-26754-1\" rel=\"nofollow noreferrer\">Sensations from a single M-cone depend on the activity of surrounding S-cones</a>\", by Brian P. Schmidt, Ramkumar Sabesan, William S. Tuten, Jay Neitz and Austin Roorda in Scientific Reports volume 8, Article number: 8561 (2018) DOI: <a href=\"https://dx.doi.org/10.1038%2Fs41598-018-26754-1\" rel=\"nofollow noreferrer\">https://dx.doi.org/10.1038%2Fs41598-018-26754-1</a></p></li>\n<li><p>location of cone, proximity to blood vessels - \"<a href=\"https://www.researchgate.net/publication/276170738_Selective_Stimulation_of_Penumbral_Cones_Reveals_Perception_in_the_Shadow_of_Retinal_Blood_Vessels\" rel=\"nofollow noreferrer\">Selective Stimulation of Penumbral Cones Reveals Perception in the Shadow of Retinal Blood Vessels</a>\", by Manuel Spitschan, Geoffrey K. Aguirre, and David H. Brainard, in PLoS ONE 10(4):e0124328 (April 2015) DOI: <a href=\"https://doi.org/10.1371/journal.pone.0124328\" rel=\"nofollow noreferrer\">https://doi.org/10.1371/journal.pone.0124328</a></p></li>\n</ul>\n\n<p>The following graph shows the minimum and maximum discrimination values at various frequencies:</p>\n\n<p><a href=\"https://i.stack.imgur.com/TmJuK.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/TmJuK.jpg\" alt=\"Mean Wavelength Discrimination Curve\"></a></p>\n\n<p>Figure 13. Mean wavelength discrimination curve. (From Davson, H., The Eye, vol 2. London, Academic Press, 1962)</p>\n\n<p>Source: <a href=\"https://webvision.med.utah.edu/book/part-viii-psychophysics-of-vision/color-perception/\" rel=\"nofollow noreferrer\">Color Perception</a> by Michael Kalloniatis and Charles Luu</p>\n\n<p><a href=\"https://i.stack.imgur.com/sYzqf.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/sYzqf.jpg\" alt=\"Computation of Cone Fundamentals\"></a></p>\n\n<p>Source: Computation of Cone Fundamentals (Color Matching Functions) in Terms of Energy for Various Field Sizes and Ages Based on CIE 170-1, Spreadsheet Prepared By Mark Fairchild (mdf@cis.rit.edu), RIT Munsell Color Science Laboratory (mcsl.rit.edu), from Rochester Institute of Technology, Program of Color Science: <a href=\"https://www.rit.edu/science/pocs/useful-data\" rel=\"nofollow noreferrer\">Useful Color Data</a>.</p>\n\n<blockquote>\n <p>If so, is this consistent between individuals? </p>\n</blockquote>\n\n<p>No.</p>\n\n<p><a href=\"https://i.stack.imgur.com/CYDSB.gif\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/CYDSB.gif\" alt=\"xxxxxxxxxx\"></a></p>\n\n<p><a href=\"https://www.handprint.com/HP/WCL/color2.html#individualdiffs\" rel=\"nofollow noreferrer\">Individual variations in photopic sensitivity</a></p>\n\n<p>Results for 52 individuals, based on heterochromatic step by step brightness matching; \"The visibility of radiant energy\" Gibson, Tyndall and Kasson (1923)</p>\n\n<p>A newer study, \"<a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4757445/\" rel=\"nofollow noreferrer\">Individual Differences in Scotopic Visual Acuity and Contrast Sensitivity: Genetic and Non-Genetic Influences</a>\" (Feb 17 2016), by Alex J. Bartholomew, Eleonora M. Lad, et al., PLoS One. 2016; 11(2): e0148192. DOI: 10.1371/journal.pone.0148192\nPMCID: PMC4757445, offers a different variance plot (without nm):</p>\n\n<p><a href=\"https://i.stack.imgur.com/bXtnX.jpg\" rel=\"nofollow noreferrer\"><img src=\"https://i.stack.imgur.com/bXtnX.jpg\" alt=\"Individual Differences in Scotopic Visual Acuity and Contrast Sensitivity\"></a></p>\n\n<p>Fig 1. Test-retest assessment. Four data sets are depicted: Visual acuity (left panel) and contrast sensitivity (right panel) at photopic luminance (green triangles, near top left and at scotopic luminance (blue discs, near bottom left). Result of the first test on the abscissa, second test on the ordinate. Grey 45°- line is the identity line, next to it the ± limits of agreement (photopic, dashed; scotopic, dotted). Visual acuity in logMAR units have an inverted scale, and contrast sensitivity is in logCSWeber units, meaning that better performance corresponds to the top right for both graphs. As expected, photopic measures of VA or CS are markedly better than scotopic ones. The 95% limits of agreement are remarkably similar. All in all, there is no marked deviation from a normal\ndistribution, and the reliability is good for the range measured.</p>\n\n<blockquote>\n <p>Are there any other traits correlated with precise colour vision?</p>\n</blockquote>\n\n<p>For your third question, above the one question per post limit, I'll offer these links (I may come back to this as time permits):</p>\n\n<p>The website Handprint has these webpages:</p>\n\n<ul>\n<li><p><a href=\"https://www.handprint.com/HP/WCL/color2.html#discrimination\" rel=\"nofollow noreferrer\">Measuring Perceptual Discrimination</a></p></li>\n<li><p><a href=\"https://www.handprint.com/HP/WCL/color2.html#individualdiffs\" rel=\"nofollow noreferrer\">Individual Differences in Color Experience</a></p></li>\n<li><p><a href=\"https://www.handprint.com/HP/WCL/color2.html#language\" rel=\"nofollow noreferrer\">Color and Language</a></p></li>\n</ul>\n\n<p>See also: </p>\n\n<ul>\n<li><p>\"<a href=\"https://www.pnas.org/content/114/40/10785\" rel=\"nofollow noreferrer\">Color naming across languages reflects color use</a>\", by Edward Gibson, Richard Futrell, Julian Jara-Ettinger, Kyle Mahowald, Leon Bergen, Sivalogeswaran Ratnasingam, Mitchell Gibson, Steven T. Piantadosi, and Bevil R. Conway in PNAS October 3, 2017 114 (40) 10785-10790; first published September 18, 2017 <a href=\"https://doi.org/10.1073/pnas.1619666114\" rel=\"nofollow noreferrer\">https://doi.org/10.1073/pnas.1619666114</a></p></li>\n<li><p><a href=\"https://midimagic.sgc-hosting.com/huvision.htm\" rel=\"nofollow noreferrer\">Human Color Vision</a></p></li>\n<li><p><a href=\"https://midimagic.sgc-hosting.com/pricol.htm\" rel=\"nofollow noreferrer\">Teach the Correct Color Theory in School</a></p></li>\n</ul>\n\n<p>Briefly: Precise color perception is not only the capability of the eye but the training of the brain (seeing different similar colors and having a need to differentiate between them) and the teaching of the vocabulary, the learning of the differences, and learned application of this in practice. </p>\n"
}
] |
57,128 |
<p>How forgetting things is helpful for the brain or the human body biologically? This <a href="https://www.google.co.in/url?sa=t&source=web&rct=j&url=https://www.psychologytoday.com/blog/mind-blender/201403/why-forgetting-the-past-can-be-good-thing&ved=0ahUKEwj41aGi1MjSAhWMtY8KHaoJBbwQFghaMAg&usg=AFQjCNFFycom7b3voykO4S9tVv62-a9kDQ" rel="noreferrer">web page</a></p>
<blockquote>
<p>After some moment of being rude, selfish, or weak, either we are able to put it behind us, or the person who suffered at the result of our imperfection moves on. The reason for this is our ability to forget about it. We forget not because we have an imperfect hippocampus (our brain’s memory organ); it's actually an evolved solution. The ability to lose information allows new information to come in that is more relevant, more pertinent to an ongoing reality. Forgetting allows us to update.</p>
</blockquote>
<p>and this Huffington post <a href="http://www.huffingtonpost.com/hale-dwoskin/the-benefits-of-forgettin_b_6117964.html" rel="noreferrer">article</a></p>
<blockquote>
<p>According to a study in Nature, our awareness is limited to only three or four objects at any given time. To be able to think at your highest level, you therefore must be very efficient at filtering out all of the background noise: Your racing thoughts, the ringing phone, your neighbor’s barking dog, and the list goes on.</p>
<p>The Nature study found that when participants were asked to “hold in mind” certain objects while ignoring others, there are significant variations in how well each of us can keep irrelevant objects out of our awareness.</p>
<p>The researchers concluded that our memory capacity is therefore not simply about storage space, but rather “how efficiently irrelevant information is excluded from using up vital storage capacity.”</p>
</blockquote>
<p>provide some backgrounds.</p>
|
[
{
"answer_id": 57136,
"pm_score": 6,
"text": "<p><strong>Short answer</strong><br>\nIt has been shown that loss of long-term memories may enhance the retrieval of others. Short-term working memory is explicitly designed to be volatile and non-lasting. However, there are many other types of memories where memory loss may not be explicitly beneficial, or even outright debilitating such as in the case of Alzheimer's or stroke.</p>\n\n<p><strong>Background</strong><br>\nFirst off all, there are many types of <a href=\"http://www.human-memory.net/types.html\" rel=\"noreferrer\">memories</a>, including sensory memory, motor memory, short-term (working) memory, long-term memory, explicit & implicit memory, declarative & procedural memory and so on. Hence, because the question is quite broad, I will focus on long-term memory, short term-memory and sensory memory to discuss that memory loss can be beneficial, neutral, or detrimental. </p>\n\n<ul>\n<li><strong>Beneficial effects of loosing memories</strong><br>\n<a href=\"http://www.human-memory.net/types.html\" rel=\"noreferrer\"><strong>Long-term memory</strong></a> is probably what you are after and there are studies in that field that have linked the loss of memories to enhanced processing of other memories. More specifically, there are adaptive benefits of forgetting, namely a reduced demand on cognitive controls during future acts of remembering of other stored information. Even more specific: retrieval of memories after forgetting others are thought to reduce the necessary engagement of functionally coupled cognitive control mechanisms that <strong>detect</strong> (<em>anterior cingulate</em> cortex) and <strong>resolve</strong> (<em>dorsolateral</em> and <em>ventrolateral prefrontal cortex</em>) mnemonic competition <a href=\"http://www.nature.com/neuro/journal/v10/n7/abs/nn1918.html\" rel=\"noreferrer\">(Kuhl <em>et al</em>., 2007)</a>. The improvement of particular memory processes by forgetting others may be linked to them being closely related. Indeed, motor tasks more remote do not benefit much from forgetting unrelated ones <a href=\"http://shapeamerica.tandfonline.com/doi/abs/10.1080/02701367.1991.10608726\" rel=\"noreferrer\">(Shea & Right, 1991)</a>. </li>\n<li><strong>Inherently volatile memory</strong><br>\n<strong><a href=\"http://www.human-memory.net/types_short.html\" rel=\"noreferrer\">Short-term working memory</a></strong> is explicitly designed to aid in on-demand task performance. Short term memory is for example used to remember a set of components (e.g., colors) and use that information to deal with a certain task at hand (<em>which objects depicted here match the colors you just saw?</em>). If all these memories would be retained, <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3721021/\" rel=\"noreferrer\">tasks dependent on working memory</a> would not be possible. <a href=\"http://www.human-memory.net/types_sensory.html\" rel=\"noreferrer\">Sensory memory</a> an ultra-short term memory that is kept only for very short amounts of time, allowing people to, <em>e.g.</em>, track a light and make a symbol or letter out of it before the information is funneled to the short term-memory. </li>\n<li><strong>Neutral effects of loss of neural function: a side track off memory lane</strong><br>\nHowever, forgetting may be simply another example of the <strong><em><a href=\"http://hearinghealthfoundation.org/blog?blogid=119\" rel=\"noreferrer\">use it or lose it</a></em></strong> principle that applies to pretty much everything in the human body; when you don't walk, the bones in the legs will weaken along with the musculature used for locomotion. Similarly, when the inner ear or the retina becomes dysfunctional and degenerate, the deafferented auditory nerve and optic nerve start to degenerate, respectively. The associated deafferented sensory cortices will slowly be taken over by other adjacent cortical areas due to the <strong>plasticity of the cortex</strong>. In blind folks, for example, the tactile and auditory cortices have been shown to take over the primary visual cortex. Given that the visual cortex is huge compared to the tactile and auditory cortex, one would expect substantial increase in performance on tactile and acoustic tasks in blind folks. Yet, this is debated <a href=\"http://www.sciencedirect.com/science/article/pii/S0006899315005156\" rel=\"noreferrer\">(Stronks et al, 2015)</a>. In fact, normally sighted folks can learn braille as well as their blind peers, suffice they get an equal amount of practice. In other words, practice is the key, not enhanced areas of cortex being available <em>per se</em>. Hence, <strong>'forgetting' to see or 'forgetting' to hear is, as far as my knowledge goes, not associated with any benefits whatsoever</strong>, barred a minority of studies that showed a slight benefit of being blind in auditory tasks <a href=\"http://www.sciencedirect.com/science/article/pii/S0006899315005156\" rel=\"noreferrer\">(Stronks et al., 2015)</a>.</li>\n<li><strong>Pathological memory loss - not so good</strong>:<br>\nHowever, forgetting of memories may also be pathological; think of the impaired short-term memory of <a href=\"http://www.alz.org/alzheimers_disease_what_is_alzheimers.asp\" rel=\"noreferrer\">Alzheimer's</a> patients, or <a href=\"http://www.disabilitysecrets.com/resources/social-security-disability-benefits-and-memory-loss.htm\" rel=\"noreferrer\">amnesia due to stroke</a>. Forgetting is not always beneficial.</li>\n</ul>\n\n<p><sub><strong>References</strong><br>\n<strong>-</strong> <a href=\"http://www.nature.com/neuro/journal/v10/n7/abs/nn1918.html\" rel=\"noreferrer\">Kuhl <em>et al</em>., <em>Nature Neurosci</em> (2007); <strong>10</strong>: 908-14</a><br>\n<strong>-</strong> <a href=\"http://shapeamerica.tandfonline.com/doi/abs/10.1080/02701367.1991.10608726\" rel=\"noreferrer\">Shea & Right, <em>Res Quarterly Exercise Sport</em> (1991); <strong>62</strong>(3)</a><br>\n<strong>-</strong> <a href=\"http://www.sciencedirect.com/science/article/pii/S0006899315005156\" rel=\"noreferrer\">Stronks <em>et al</em>., <em>Brain Res</em> (2015); <strong>1624</strong>: 140–52</a></sub></p>\n"
}
] |
[
{
"answer_id": 57133,
"pm_score": 3,
"text": "<p>Memory is formed by building connections between nerve cells (i.e. neurons). These connections are called synapses. The synapses form a network between several (or tens or hundreds) of neurons, therefore giving us the ability to retrieve something we had memorized before. </p>\n\n<p>Learning something new requires building new connections, but the older connections might interfere with the new ones and thereby interrupt our memory or what we have learnt. So sometimes older connections must be broken in favor to new connections and new abilities. For instance, you might remember crawling on both hands and knees as a child, but slowly you practiced walking and at one point you stood up and never crawled again. Children crawl like it's no big deal, but grown-ups have to think and struggle and in the end it's not gonna be very good. That's because older connections regarding crawling have been broken in favor to new connections for walking.</p>\n\n<p>Check out: <a href=\"https://dx.doi.org/10.1007/978-3-319-06716-2\" rel=\"nofollow noreferrer\">Izquierdo, Ivan. \"The art of forgetting.\" Springer International Publishing, 2015.</a></p>\n"
},
{
"answer_id": 57148,
"pm_score": 3,
"text": "<p><strong>Who says it has to be good?</strong>\nWe cannot assume that every trait that evolves is beneficial to the species. A lot of people assume that the species of an ecosystem will evolve optimally; that is, they assume each species evolves to have the best possible genes for its environment. My understanding is this is not the case. Species have to adapt or face extinction, but they only have to adapt to be good enough. Perhaps it's not that forgetting is good, but rather it just doesn't impede survival or reproduction. (Well, except when you forget your spouse's anniversary!) Which leads us to the next point...</p>\n\n<p><strong>It's a side effect of how human memory works.</strong>\nFirst off, storing a memory in the brain is not like running a tape recorder or camera. The brain actually stores very little of the information coming into it, just enough so that it can later fill in the blanks and make a decent reproduction. In computer terms, the data is filtered through a very lossy compression algorithm before being stored. It's just good enough that we usually don't notice, but sometimes things go wrong and we get phenomena like <a href=\"https://en.wikipedia.org/wiki/Confabulation\" rel=\"nofollow noreferrer\">confabulation</a>.</p>\n\n<p>Now about how that data is stored. As you know, the data is stored by the synapses in the neurons. But here's the thing: <strong>those synapses aren't dedicated to that specific memory!</strong> Storing a new memory affects synapses that are part of other memories. One synapse might be storing a piece of information for any number of memories, because those memories all have some tiny thing in common. I wish I could explain this better and in more detail, but this became pretty obvious to me when I read up on artificial neural networks, which are crude models of brains.</p>\n\n<p><strong>Sometimes, neurons just die.</strong> Obviously this is going to affect the brain's ability to recall the information the dead synapses contained. There's enough redundancy built into the brain that this is rarely a problem, except in cases like Alzheimer's, where the brain just suffers too much damage.</p>\n\n<p>To me, the question isn't why we forget. The question is how we can remember stuff at all!</p>\n"
},
{
"answer_id": 57149,
"pm_score": 3,
"text": "<p>One famous person, <a href=\"https://edubloxtutor.com/solomon-shereshevsky/\" rel=\"noreferrer\">Solomon Shereshevsky</a>, had an unusual ability to remember everything he encountered: sights, numbers, words in foreign languages, events from infancy, and more.</p>\n\n<blockquote>\n <p>Unfortunately, S’s gift was a serious handicap. He was unable to block unwanted memories. Also, he had a terrible memory for faces because he memorized them so exactly. People’s faces change with time, lighting, mood, and expression. S had difficulty recognizing faces because they looked so different to him from the ones he had completely memorized in the past.</p>\n</blockquote>\n\n<p>Extrapolating from that, one could conclude that the inability to block unwanted memories could easily lead to the development of PTSD — especially if, as in Shereshevsky's case, the total recall is combined with synaesthesia.</p>\n"
},
{
"answer_id": 57300,
"pm_score": 2,
"text": "<blockquote>\n <p>What are the advantages of forgetting?</p>\n</blockquote>\n\n<p>Perhaps the question asked should be what is the disadvantage of remembering every little detail?</p>\n\n<p>The answer is cost. It cost energy/neuron to remember everything. Neural tissue are expensive to maintain and feed. At rest, the human brain consume 20% of all calories. And that is alot of energy when the human brain is only 1% of all tissue in the body.(<a href=\"http://www.nature.com/neuro/journal/v1/n1/full/nn0598_36.html\" rel=\"nofollow noreferrer\">http://www.nature.com/neuro/journal/v1/n1/full/nn0598_36.html</a>)</p>\n\n<p>It is also inefficient. If you remember everything, it will take time to reach the appropriate memory. When time is life, it is inefficient to have a large store of unimportant memories to search through for the one important memory.</p>\n\n<p>Also, this being biology... is there a selective drive for perfect memory? Without a section pressure for perfect memory, it won't evolve. Memory that is good enough to survive is what we will get. We do not get cheetahs which are as fast as biologically possible. We get the cheetah that can catch the slowest gazelle. </p>\n"
}
] |
57,145 |
<blockquote>
<p>A recent study has provided evidence that two types of equine (horse) herpes viruses have an unusually broad host range. This fact supports which of the following statements?</p>
<p>a. The lytic cylce occurs in horses while the lysogenic cycle occurs only in other species.</p>
<p>b. The virus is transmitted from one host to another by mosquitoes.</p>
<p>c. In a population of horses, many of the individuals will become infected</p>
<p>d. Horses, rhinoceroses, and polar bear can become infected</p>
<p>e. In an individual horse, many different type of cells will be infected</p>
</blockquote>
<p>According to the answer key, the answer is D. My question is why isn't E also a correct answer? I thought host range means "the range of cells that can act as a host to a virus".</p>
|
[
{
"answer_id": 57136,
"pm_score": 6,
"text": "<p><strong>Short answer</strong><br>\nIt has been shown that loss of long-term memories may enhance the retrieval of others. Short-term working memory is explicitly designed to be volatile and non-lasting. However, there are many other types of memories where memory loss may not be explicitly beneficial, or even outright debilitating such as in the case of Alzheimer's or stroke.</p>\n\n<p><strong>Background</strong><br>\nFirst off all, there are many types of <a href=\"http://www.human-memory.net/types.html\" rel=\"noreferrer\">memories</a>, including sensory memory, motor memory, short-term (working) memory, long-term memory, explicit & implicit memory, declarative & procedural memory and so on. Hence, because the question is quite broad, I will focus on long-term memory, short term-memory and sensory memory to discuss that memory loss can be beneficial, neutral, or detrimental. </p>\n\n<ul>\n<li><strong>Beneficial effects of loosing memories</strong><br>\n<a href=\"http://www.human-memory.net/types.html\" rel=\"noreferrer\"><strong>Long-term memory</strong></a> is probably what you are after and there are studies in that field that have linked the loss of memories to enhanced processing of other memories. More specifically, there are adaptive benefits of forgetting, namely a reduced demand on cognitive controls during future acts of remembering of other stored information. Even more specific: retrieval of memories after forgetting others are thought to reduce the necessary engagement of functionally coupled cognitive control mechanisms that <strong>detect</strong> (<em>anterior cingulate</em> cortex) and <strong>resolve</strong> (<em>dorsolateral</em> and <em>ventrolateral prefrontal cortex</em>) mnemonic competition <a href=\"http://www.nature.com/neuro/journal/v10/n7/abs/nn1918.html\" rel=\"noreferrer\">(Kuhl <em>et al</em>., 2007)</a>. The improvement of particular memory processes by forgetting others may be linked to them being closely related. Indeed, motor tasks more remote do not benefit much from forgetting unrelated ones <a href=\"http://shapeamerica.tandfonline.com/doi/abs/10.1080/02701367.1991.10608726\" rel=\"noreferrer\">(Shea & Right, 1991)</a>. </li>\n<li><strong>Inherently volatile memory</strong><br>\n<strong><a href=\"http://www.human-memory.net/types_short.html\" rel=\"noreferrer\">Short-term working memory</a></strong> is explicitly designed to aid in on-demand task performance. Short term memory is for example used to remember a set of components (e.g., colors) and use that information to deal with a certain task at hand (<em>which objects depicted here match the colors you just saw?</em>). If all these memories would be retained, <a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3721021/\" rel=\"noreferrer\">tasks dependent on working memory</a> would not be possible. <a href=\"http://www.human-memory.net/types_sensory.html\" rel=\"noreferrer\">Sensory memory</a> an ultra-short term memory that is kept only for very short amounts of time, allowing people to, <em>e.g.</em>, track a light and make a symbol or letter out of it before the information is funneled to the short term-memory. </li>\n<li><strong>Neutral effects of loss of neural function: a side track off memory lane</strong><br>\nHowever, forgetting may be simply another example of the <strong><em><a href=\"http://hearinghealthfoundation.org/blog?blogid=119\" rel=\"noreferrer\">use it or lose it</a></em></strong> principle that applies to pretty much everything in the human body; when you don't walk, the bones in the legs will weaken along with the musculature used for locomotion. Similarly, when the inner ear or the retina becomes dysfunctional and degenerate, the deafferented auditory nerve and optic nerve start to degenerate, respectively. The associated deafferented sensory cortices will slowly be taken over by other adjacent cortical areas due to the <strong>plasticity of the cortex</strong>. In blind folks, for example, the tactile and auditory cortices have been shown to take over the primary visual cortex. Given that the visual cortex is huge compared to the tactile and auditory cortex, one would expect substantial increase in performance on tactile and acoustic tasks in blind folks. Yet, this is debated <a href=\"http://www.sciencedirect.com/science/article/pii/S0006899315005156\" rel=\"noreferrer\">(Stronks et al, 2015)</a>. In fact, normally sighted folks can learn braille as well as their blind peers, suffice they get an equal amount of practice. In other words, practice is the key, not enhanced areas of cortex being available <em>per se</em>. Hence, <strong>'forgetting' to see or 'forgetting' to hear is, as far as my knowledge goes, not associated with any benefits whatsoever</strong>, barred a minority of studies that showed a slight benefit of being blind in auditory tasks <a href=\"http://www.sciencedirect.com/science/article/pii/S0006899315005156\" rel=\"noreferrer\">(Stronks et al., 2015)</a>.</li>\n<li><strong>Pathological memory loss - not so good</strong>:<br>\nHowever, forgetting of memories may also be pathological; think of the impaired short-term memory of <a href=\"http://www.alz.org/alzheimers_disease_what_is_alzheimers.asp\" rel=\"noreferrer\">Alzheimer's</a> patients, or <a href=\"http://www.disabilitysecrets.com/resources/social-security-disability-benefits-and-memory-loss.htm\" rel=\"noreferrer\">amnesia due to stroke</a>. Forgetting is not always beneficial.</li>\n</ul>\n\n<p><sub><strong>References</strong><br>\n<strong>-</strong> <a href=\"http://www.nature.com/neuro/journal/v10/n7/abs/nn1918.html\" rel=\"noreferrer\">Kuhl <em>et al</em>., <em>Nature Neurosci</em> (2007); <strong>10</strong>: 908-14</a><br>\n<strong>-</strong> <a href=\"http://shapeamerica.tandfonline.com/doi/abs/10.1080/02701367.1991.10608726\" rel=\"noreferrer\">Shea & Right, <em>Res Quarterly Exercise Sport</em> (1991); <strong>62</strong>(3)</a><br>\n<strong>-</strong> <a href=\"http://www.sciencedirect.com/science/article/pii/S0006899315005156\" rel=\"noreferrer\">Stronks <em>et al</em>., <em>Brain Res</em> (2015); <strong>1624</strong>: 140–52</a></sub></p>\n"
}
] |
[
{
"answer_id": 57133,
"pm_score": 3,
"text": "<p>Memory is formed by building connections between nerve cells (i.e. neurons). These connections are called synapses. The synapses form a network between several (or tens or hundreds) of neurons, therefore giving us the ability to retrieve something we had memorized before. </p>\n\n<p>Learning something new requires building new connections, but the older connections might interfere with the new ones and thereby interrupt our memory or what we have learnt. So sometimes older connections must be broken in favor to new connections and new abilities. For instance, you might remember crawling on both hands and knees as a child, but slowly you practiced walking and at one point you stood up and never crawled again. Children crawl like it's no big deal, but grown-ups have to think and struggle and in the end it's not gonna be very good. That's because older connections regarding crawling have been broken in favor to new connections for walking.</p>\n\n<p>Check out: <a href=\"https://dx.doi.org/10.1007/978-3-319-06716-2\" rel=\"nofollow noreferrer\">Izquierdo, Ivan. \"The art of forgetting.\" Springer International Publishing, 2015.</a></p>\n"
},
{
"answer_id": 57148,
"pm_score": 3,
"text": "<p><strong>Who says it has to be good?</strong>\nWe cannot assume that every trait that evolves is beneficial to the species. A lot of people assume that the species of an ecosystem will evolve optimally; that is, they assume each species evolves to have the best possible genes for its environment. My understanding is this is not the case. Species have to adapt or face extinction, but they only have to adapt to be good enough. Perhaps it's not that forgetting is good, but rather it just doesn't impede survival or reproduction. (Well, except when you forget your spouse's anniversary!) Which leads us to the next point...</p>\n\n<p><strong>It's a side effect of how human memory works.</strong>\nFirst off, storing a memory in the brain is not like running a tape recorder or camera. The brain actually stores very little of the information coming into it, just enough so that it can later fill in the blanks and make a decent reproduction. In computer terms, the data is filtered through a very lossy compression algorithm before being stored. It's just good enough that we usually don't notice, but sometimes things go wrong and we get phenomena like <a href=\"https://en.wikipedia.org/wiki/Confabulation\" rel=\"nofollow noreferrer\">confabulation</a>.</p>\n\n<p>Now about how that data is stored. As you know, the data is stored by the synapses in the neurons. But here's the thing: <strong>those synapses aren't dedicated to that specific memory!</strong> Storing a new memory affects synapses that are part of other memories. One synapse might be storing a piece of information for any number of memories, because those memories all have some tiny thing in common. I wish I could explain this better and in more detail, but this became pretty obvious to me when I read up on artificial neural networks, which are crude models of brains.</p>\n\n<p><strong>Sometimes, neurons just die.</strong> Obviously this is going to affect the brain's ability to recall the information the dead synapses contained. There's enough redundancy built into the brain that this is rarely a problem, except in cases like Alzheimer's, where the brain just suffers too much damage.</p>\n\n<p>To me, the question isn't why we forget. The question is how we can remember stuff at all!</p>\n"
},
{
"answer_id": 57149,
"pm_score": 3,
"text": "<p>One famous person, <a href=\"https://edubloxtutor.com/solomon-shereshevsky/\" rel=\"noreferrer\">Solomon Shereshevsky</a>, had an unusual ability to remember everything he encountered: sights, numbers, words in foreign languages, events from infancy, and more.</p>\n\n<blockquote>\n <p>Unfortunately, S’s gift was a serious handicap. He was unable to block unwanted memories. Also, he had a terrible memory for faces because he memorized them so exactly. People’s faces change with time, lighting, mood, and expression. S had difficulty recognizing faces because they looked so different to him from the ones he had completely memorized in the past.</p>\n</blockquote>\n\n<p>Extrapolating from that, one could conclude that the inability to block unwanted memories could easily lead to the development of PTSD — especially if, as in Shereshevsky's case, the total recall is combined with synaesthesia.</p>\n"
},
{
"answer_id": 57300,
"pm_score": 2,
"text": "<blockquote>\n <p>What are the advantages of forgetting?</p>\n</blockquote>\n\n<p>Perhaps the question asked should be what is the disadvantage of remembering every little detail?</p>\n\n<p>The answer is cost. It cost energy/neuron to remember everything. Neural tissue are expensive to maintain and feed. At rest, the human brain consume 20% of all calories. And that is alot of energy when the human brain is only 1% of all tissue in the body.(<a href=\"http://www.nature.com/neuro/journal/v1/n1/full/nn0598_36.html\" rel=\"nofollow noreferrer\">http://www.nature.com/neuro/journal/v1/n1/full/nn0598_36.html</a>)</p>\n\n<p>It is also inefficient. If you remember everything, it will take time to reach the appropriate memory. When time is life, it is inefficient to have a large store of unimportant memories to search through for the one important memory.</p>\n\n<p>Also, this being biology... is there a selective drive for perfect memory? Without a section pressure for perfect memory, it won't evolve. Memory that is good enough to survive is what we will get. We do not get cheetahs which are as fast as biologically possible. We get the cheetah that can catch the slowest gazelle. </p>\n"
}
] |
57,356 |
<p>My science textbook says this:</p>
<blockquote>
<p>Evolution should not be equated with progress. In fact, there is no real 'progress' in the idea of evolution. Evolution is simply the generation of diversity and the shaping of the diversity by environmental factors. The only progressive trend in evolution seems to be that more and more complex body designs have emerged over time. However, again it is not as if older designs are inefficient! So many of the older and simpler designs still survive [..] In other words, human beings are not the pinnacle of evolution, but simply yet another species in the teeming spectrum of life.</p>
</blockquote>
<p>I am not sure if I agree with this; after all, humans do seem to be more <strong>advanced</strong> than dogs. Many people have asked me why I thought this was true, so here is my answer: <em>Today, humans could wipe out dogs from Earth if they wanted, but you can hardly imagine a scenario in which dogs would do the same to humans.</em></p>
<p><em><strong>What am I missing here?</strong></em></p>
|
[
{
"answer_id": 57454,
"pm_score": 5,
"text": "<p>I'm glad you've asked the question as it is a common layman misunderstanding.</p>\n\n<h1>Dog vs Human</h1>\n\n<p>Your example comparing humans and dogs is actually very central to the logical flaw that yields many to equate evolution with progress.</p>\n\n<p>There are several issues when you say</p>\n\n<blockquote>\n <p>humans do seem to be more advanced than dogs</p>\n</blockquote>\n\n<ol>\n<li><p><strong>Humans are not more evolved than dogs</strong></p>\n\n<ul>\n<li>Humans, dogs, jellyfish, oak tree, fungi, bacteria, .... we have all evolved during about 3.5 billion years. None of the extant lineages is more evolved than any other at least in terms of the number of years of evolution. Note, however, that what matters most when considering evolutionary time is the number of generations. Humans having a rather long generation time, it tends to make fewer generations. In this regard, one could expect a dog to have been through more generations than humans and could eventually be called more evolved but even there it is not that easy. See also <a href=\"https://biology.stackexchange.com/questions/71229/are-we-more-evolved-than-present-day-bacteria\">Are we “more evolved” than present-day bacteria?</a></li>\n</ul></li>\n<li><p><strong>You are a human, be aware of your biases</strong></p>\n\n<ul>\n<li>As @Jamesqf rightly said in the comments, you did not feel like considering the dog's extraordinary sense of smell, better hearing, higher jumps, stronger jaws or protective fur. Not to mention, dogs can typically raise way more offsprings than humans can. Not to become personal but my 8 months old, 9 kg Cocker Spaniel runs 300 meters at the same time Usain Bolt runs 200 meters! You seem to have only considered things that make you human such as opposable thumbs and high cognitive abilities. Coming to cognitive abilities you will note that a puppy learns by association faster than a baby human. Dogs just plateau much quicker than humans.</li>\n<li>Make sure that you understand that high cognitive abilities are not a goal or a direction of evolution. While it is hard to measure the evolution of intelligence for both a question of definition and question of measurement tools, it is very very likely that many lineages (incl. eventually the <em>Homo</em> lineage) have evolved toward reducing intelligence at some point (see <a href=\"https://biology.stackexchange.com/questions/52478/have-creatures-ever-evolved-to-become-less-intelligent\">this post</a>).</li>\n<li>You say <code>humans could wipe out dogs from Earth</code> however again it feels very human (and awkwardly combative and hostile) to consider the ability to kill as a measure of progress.</li>\n</ul></li>\n<li><p><strong>The illusion of considering two variables</strong></p>\n\n<ul>\n<li>You consider a correlation between two variables 1) how evolved a lineage is and 2) how advanced a lineage is. (As discussed in the first point, there is actually no variance in how evolved lineages are if we consider evolutionary time). You are determining those that are more evolved by how \"advanced\" you visualize the lineage. Your explanatory and response variables are therefore the same and you do not explain anything by saying 'humans are both more advanced and more evolved than dogs so evolution should equate progress'</li>\n</ul></li>\n</ol>\n\n<h1>Definition of progress</h1>\n\n<p>A big issue in your question is the definition of progress. For example, if you define progress as an increase of mean fitness (the concept of fitness in biology has nothing to do with bodybuilding, see <a href=\"https://en.wikipedia.org/wiki/Fitness_(biology)\" rel=\"noreferrer\">here</a>) over time, then yes evolution is in part to be equated with progress as increase in mean fitness over time is exactly what natural selection is doing (see the so-called <a href=\"https://en.wikipedia.org/wiki/Fisher's_fundamental_theorem_of_natural_selection\" rel=\"noreferrer\">Fundamental Theorem of Natural Selection</a>).</p>\n\n<h1>Evolution ≠ Natural Selection</h1>\n\n<p>So, let's assume we define progress as an increase in mean <a href=\"https://en.wikipedia.org/wiki/Fitness_(biology)\" rel=\"noreferrer\">fitness</a> over time. As stated in the previous section, this is exactly what natural selection is doing. So, instead of saying <code>Evolution should not be equated with progress</code>, one could say <code>Natural selection is to be equated with progress</code> (as a reminder this assumes a very specific definition of progress)</p>\n\n<p>You will note that I replace the term <code>evolution</code> with <code>natural selection</code>. It is often unclear to laymen but these two terms, while related, are different. </p>\n\n<p>Evolution is a change of <a href=\"https://en.wikipedia.org/wiki/Allele\" rel=\"noreferrer\">allele</a> (loosely speaking, an allele is a variant of a gene) frequency over time. There are a number of mechanisms that can cause evolution, one of which is natural selection (which itself is caused by a fitness differential associated with genetic variance). But there is way more to evolution than just natural selection. Genetic drift, mutations, migration and other demographic elements are all important factors causing the evolution of populations.</p>\n\n<p>You should have a look at <a href=\"http://evolution.berkeley.edu/evolibrary/article/evo_01\" rel=\"noreferrer\">Understanding Evolution by UC Berkeley</a>. It is a very introductory online course on evolutionary biology that will teach you about the basic forces that cause evolution.</p>\n"
}
] |
[
{
"answer_id": 57360,
"pm_score": 2,
"text": "<p>When you say, humans are more advanced than dogs, from what perspective are you saying that from? Is it in the capacity to use intelligence, to build and create, to do the math, to climb trees? If it is any of these, you are right: humans are better at using intelligence to build and create, at doing the math and at climbing trees than dogs do. However, from the perspective of, say, hunting down a rabbit or detecting by smell some chemical component at very low concentrations in a suitcase, dogs are indubitably better.</p>\n\n<p>So which is actually more advanced? The answer is none, they are just differently <strong>adapted</strong> to be better at some things - the things they needed to be better at to survive, and which evolution created and preserved. So <strong>evolution</strong> here simply means the constant modification of living organisms and the perseverance of those who become better adapted to the conditions they live in - this means that a bacteria today is as evolved as a human being, his dog or the tree that dog is peeing on. Now when we talk about <strong>progress</strong>, we're talking about something which function or capacity improves over a continuum. Evolution does make progress sometimes, such as the progression from initial photoreceptors to the organs of vision we have today (called eyes), and the increasing capacity of some bacteria strains to resist antibiotics - both are signs of progress, and both are made possible through the process of evolution.</p>\n\n<p>At a larger level, we see that life, though <strong>evolution</strong>, has been <strong>progressively</strong> more able to create more and more complex organisms (complexity here meaning the amount of information necessary to describe the organism), through the principle of \"<em>complexity allows for the creation of more complexity</em>\". Today, there are indubitably more complex organisms that there was in the beginnings of life, and yes, we can say humans are one of the most (if not the most, because of brain complexity) complex beings alive, and also complex <em>things</em> in the universe. So we can say that <strong>evolution</strong> is a <strong>process</strong> which made possible the <strong>progress</strong> towards more and more complex things.</p>\n\n<p>What I hope to have helped understand is that evolution and progress are correlated and interdependent, but not the same thing. Evolution is a process which allows for progress, but not always and not necessarily.</p>\n\n<p>I am not including any sources or background because this question relates more to etymology and meaning than scientific research.</p>\n\n<p>EDIT: interesting things you may like to watch about the progress and evolution of complexity:</p>\n\n<p><a href=\"https://www.youtube.com/watch?v=MTFY0H4EZx4\" rel=\"nofollow noreferrer\">https://www.youtube.com/watch?v=MTFY0H4EZx4</a></p>\n\n<p><a href=\"https://school.bighistoryproject.com/bhplive\" rel=\"nofollow noreferrer\">https://school.bighistoryproject.com/bhplive</a></p>\n\n<p><a href=\"https://www.ted.com/talks/david_christian_big_history\" rel=\"nofollow noreferrer\">https://www.ted.com/talks/david_christian_big_history</a></p>\n"
},
{
"answer_id": 57362,
"pm_score": 2,
"text": "<p>There are two issues here; defining \"progress\" and equating evolution with it. I'll take the second one first.</p>\n\n<p>When we \"equate evolution with progress\" we are typically making specific claims (sometimes without thinking about it). We mean that progress is an important priority of evolution or even its goal. We mean that evolution always leads to progress. And when we say \"don't equate evolution with progress\" we're saying that neither of those things is implied in the Theory of Evolution, and in fact, there isn't much evidence for either.</p>\n\n<p>Humans are more advanced than dogs (again, skipping the question of defining \"progress\" for now), but humans and dogs aren't the only organisms around. E.coli is as much the outcome of 4 billion years of evolution as we are, yet we didn't \"progress\" in the same way at all.</p>\n\n<p>One way of looking at it is thinking of diffusion. When I release a dot of dye into the water, it expands outward. Is there a specific force pushing it outward? Are any of the molecules <em>trying</em> to go outward? No, and no; all the molecules are moving randomly, and it is statistics that make it so their overall movement is outward; there simply is more space to move outside of the dot than inside.</p>\n\n<p>And if I put that dye on the right edge of a water container, it would expand leftward. Again, is there a leftward force? Do all the molecules want to go left? No, and no: all the molecules are moving randomly, they just can't go further right than they already are, so for a molecule by the edge any random movement right keeps them where they are and any random movement left takes them left. And the overall average of the molecule's positions will move leftward, even though no specific molecule has a leftward bent (if they did we might expect molecules to disappear from the right edge, and in a diffusion situation they don't). Moreover, if we took the leftmost molecule at a certain point and looked at its trajectory over time, it would sure <em>look</em> like it's deliberately moving leftward... But that deliberateness would be an illusion; out of trillions of molecules moving randomly the odds are good that one of them would have made only or mostly leftward movements, and obviously that's the kind of molecule that would end up being leftmost in the first place. That doesn't mean it is being pushed left, or that its <em>next</em> movement will be leftward.</p>\n\n<p>So applied to evolution, for almost all measures of \"progress\" we can come up with - size, intelligence, behavioral complexity, structural complexity, whatever - if evolution was pushing any lineage randomly along those variables we would still expect the maximum and even average size/intelligence/complexity to increase over time, because it would be very hard for life to become smaller, dumber or simpler than E.coli (harder but not impossible ! And we see examples of such trajectories, in parasites especially).</p>\n\n<p>Now, you will tell me, evolution isn't random! Through natural selection, it leads to adaptation. True; it leads to adaptation <em>to the environment</em>. Change the environment, you change the direction that evolution will \"push\" a given lineage. And in the case of things like complexity or intelligence (the usual markers for \"progress\" in evolution), those traits can be adaptive or not depending on the environment; complexity allows more variety in responding to the environment, intelligence allows more productive interactions with said environment, but both have a cost, in risks of errors, in energy consumption, and so on. And so while you might say <em>this lineage</em> over <em>this time period</em> (in <em>this environment</em>) shows a definite trend towards complexity or intelligence (or gaining flight, or losing sight...), it is impossible to say the same of <strong>Evolution as a whole</strong>.</p>\n\n<p>One point of evidence that the increase in maximum \"progress level\" is the result of diffusion and not a specific progress-ward force, is that as the right side of the container that still contained dye, the biosphere still contains tons of (a majority of in fact!) \"un-progressed\" organisms. This would not be true if Evolution as a whole were pushing toward progress. (in fact, you might note that I am not quite correct here! In a naturalistic view of abiogenesis, living things (or not-technically-living ancestors to living things) must have existed that were themselves outcomes of evolution but were incredibly simple compared to today's amazing bacteria, and <em>those</em> could be thought to be the lower bound in complexity, and Evolution <em>did</em> move life as a whole away from it! So we could argue that Evolution does move towards a minimal level of \"progress\" (the amount sufficient to compete against a bacterium). It's just that we reached that level over 3 billion years ago).</p>\n\n<p>And to get back to the first point about defining \"progress\", once you dig down into what that means it can become all the clearer that evolution doesn't push one way or another. Bacteria have more metabolic diversity than Eukaryotes could hope for. Humans are more intelligent than dogs but worse at smelling. It can be argued that from a <a href=\"https://en.wikipedia.org/wiki/Muller%27s_ratchet\" rel=\"nofollow noreferrer\">Müller's Ratchet</a> perspective, \"complexity\" in Eukaryotes is pretty much constant, and any progress in one domain is the result of tradeoffs in another domain. This doesn't mean humans aren't more \"advanced\" than dogs, but it does demonstrate you need to be more specific about what \"advanced\" means for that to be true.</p>\n"
},
{
"answer_id": 81881,
"pm_score": -1,
"text": "<ol>\n<li><p>There is no real progress behind the idea of evolution.</p></li>\n<li><p>Evolution is simply the generation of diversity and shaping of diversity by environmental selection.</p></li>\n<li><p>The only progressive trend in evolution seems to be that more and more complex body designs has emerged over time. It doesn't means that the older designs are inefficient.</p></li>\n<li><p>However, one of the simplest form of life (Bacteria) can even survive in harsh conditions such as hot springs or ice of Antarctica.</p></li>\n<li><p>Therefore, Human beings aren't the pinnacle of evolution, but simply yet another species in teeming spectrum of evolving life.</p></li>\n</ol>\n\n<p>SOURCE: NCERT Class 10 science textbook</p>\n"
},
{
"answer_id": 93549,
"pm_score": 1,
"text": "<p>Indeed evolution cannot be equated with progress, but that book's reasoning is misstated.</p>\n\n<p>The reason it cannot be equated is because of many distinctions between these 2 concepts, regardless of the fact that in many cases evolution is a vehicle or mechanism by which progress happens, by popular definitions of what we call progress at a given time. If survival and adaptation of a species in question, is what we would consider progress in whatever context, then evolution fuels that progress, and can reasonably be said to itself be progress in that context.</p>\n\n<p>Now let's say that you consider a finely balanced Ecosystem, and some species quickly evolves to better hunt another species, then from a short term perspective of the subject species, evolution is progress, but knowing that this will cause a population explosion and shortly after, mass starvation, it is clear that this was not progress, even for the hunter species -- however, it still cannot be said that evolution did not occur, so clearly evolution does not equate with progress on sematic or functional levels (the latter simply because there can be shown many situations where that is clearly not the case).</p>\n\n<p>Fun aside: Also consider that evolution cannot go backwards to pick another foregone path. But in some cases that would be required for progress being considered, like the perfection of human eyeballs, which are greatly evolved, but would/could have been much better if we didn't come from the water </p>\n"
},
{
"answer_id": 94717,
"pm_score": -1,
"text": "<p>Evolutionary biology cannot answer a question about "<em>progress</em>". Opinions are strong. For a good discussion see <a href=\"https://academic.oup.com/bioscience/article/50/5/451/264248\" rel=\"nofollow noreferrer\">https://academic.oup.com/bioscience/article/50/5/451/264248</a> and note comment by Stephen Jay Gould, “Progress is a noxious, culturally embedded, untestable, nonoperational, intractable idea that must be replaced if we wish to understand the patterns of history” (Gould 1988, p. 319) and William Provine “the problem is that there is no ultimate basis in the evolutionary process from which to judge true progress” (Provine 1988, p. 63).</p>\n<p>I believe this is because its mathematical formulation only looks backward. It presumes a parameter "fitness" which has a value in a particular environment, especially in what that environment WAS not what it IS or WILL BE. (For a clear treatment, not the usual overbearing textbook, see Gillespie, <em>Population Genetics - A Concise Guide</em>, 1998 <a href=\"https://public.wsu.edu/%7Egomulki/mathgen/materials/gillespie_book.pdf\" rel=\"nofollow noreferrer\">https://public.wsu.edu/~gomulki/mathgen/materials/gillespie_book.pdf</a> )</p>\n<p>That does not mean the question cannot be answered. But it requires a convincing definition of progress. There already is one in common use among futurists. And it leads to a convincing answer. However, there is disagreement as to whether humans are on the path to an answer.</p>\n<p>To obtain a definition of progress, only note which forms are most likely to remain viable in future environments.</p>\n<p>This requires forecasting of future environments, a difficulty I will pass over. While non-trivial, it is an entirely separate question.</p>\n<p>Looking far enough into the future, it is extremely easy to forecast that Earth (and the sun and moon and rest of it) will eventually meet some end and not even be available as an environment. It could be as simple as a focused gamma ray burst <a href=\"https://jatan.space/timeline-for-life-until-the-end-of-the-universe/\" rel=\"nofollow noreferrer\">https://jatan.space/timeline-for-life-until-the-end-of-the-universe/</a> . The only viable forms will be those which have left.</p>\n<p>There is a famous puzzle, named after Enrico Fermi though he didn't formulate the puzzle exactly. He just asked, "Where are all the Aliens?"</p>\n<p>Putting aside those who claim they are among us and we don't know it, and looking only at physical evidence, while some might keep themselves secret we can't think of a reason why they all would. We appear to be alone in the universe. There appear to be some barriers that prevent life from leaving its home planet. And I'm not talking about the long time travels required, etc. Those are not actually insurmountable. I worked for NASA for 45 years and studied this question often. Difficult is not insurmountable. Pass over that argument, it is a sidetrack.</p>\n<p>None of the solutions to the so-called Fermi Paradox are the least bit impressive. Not only to me, I never met anyone who was really impressed with any of them. They pick favorites, but everyone is puzzled. <em>It is not obvious humans are capable of solving this problem</em>. For the most concise (not too long, but still comprehensive, and very colorful) see the animated video short <a href=\"https://www.youtube.com/watch?v=sNhhvQGsMEc&t=6s\" rel=\"nofollow noreferrer\">https://www.youtube.com/watch?v=sNhhvQGsMEc&t=6s</a> , or look up the original paper by Michael Hart, 1975, "Explanation for the Absence of Extraterrestrials on Earth."</p>\n<p>If in the future humans become "advanced" enough to understand the problem and work out what its realistic features are, then we might be able to say if humans can solve it, or if dogs can solve it. So there is potential to define objective progress in evolution.</p>\n<p>It might require the evolution of life around red dwarfs to solve the problem. Such life might have a concept of much longer time intervals, for example, or be much more cooperative. We just don't know how such imponderable variables would affect evolution. The issues with life around Red Dwarfs is discussed here <a href=\"https://www.space.com/14659-red-dwarf-stars-planets-habitable-zones.html\" rel=\"nofollow noreferrer\">https://www.space.com/14659-red-dwarf-stars-planets-habitable-zones.html</a> and note that the timeline given earlier <a href=\"https://jatan.space/timeline-for-life-until-the-end-of-the-universe/\" rel=\"nofollow noreferrer\">https://jatan.space/timeline-for-life-until-the-end-of-the-universe/</a> suggests that in 1 trillion years Red Dwarfs will be all that is left. <em>Thus the future environment has already been predicted with high confidence.</em></p>\n<p>The ancestors of dogs evolved in surprising ways, achieving brains that rival our own. I'm thinking of the whales and dolphins, that presumably evolved from some predator hunting in shallow lagoons and gradually returning to the sea. <a href=\"https://evolution.berkeley.edu/evolibrary/article/evograms_03\" rel=\"nofollow noreferrer\">https://evolution.berkeley.edu/evolibrary/article/evograms_03</a></p>\n<p>In their present form they are unsuitable for spaceships. Suppose over a billion years the sea dried up, and they gradually adapted, developed an urgent need to free themselves from dependence on one single planet that could be so rude as to lose its oceans, and developed an instinctive collective urge to find other planets, instilling cooperation far beyond the human level. Then dogs might win.</p>\n<p>I personally believe the Achilles heel of the Fermi dilemma is cooperation. Much touted human cooperation is not what it appears. More intelligent people cooperate less. If you explain game theory to people they cooperate less (Nash Equilibrium and all that). A global society might not be a highly cooperative one. Interstellar travel might require global cooperation. Forcing everyone to take just one approach to any given problem might be the ruin of any civilization. It is certainly not the way of evolution.</p>\n<p>But not knowing who is going to solve the Fermi Paradox, if any species ever, does not detract from its value in defining progress in an extremely objective manner.</p>\n<p>And if you get past that, there is the end of what we call the universe. Cosmologists, at least some of them, now think it is not really the end. See Dyson et. al. Disturbing Implications of a Cosmological Constant <a href=\"https://arxiv.org/abs/hep-th/0208013\" rel=\"nofollow noreferrer\">https://arxiv.org/abs/hep-th/0208013</a> .</p>\n<p>But there might be ten to the 100th years of not very interesting non-entropic processes until there is a repeat, or approximate repeat, of the initial conditions, a Poincare Recurrence as Poincare proved a theorem that this would eventually happen over a hundred years ago. Who will survive that? We can't say it's impossible. We know next to nothing about non-entropic processes. But it is possible to define progress even then.</p>\n"
}
] |
57,479 |
<p>As far as I know, humans have 23 pairs of chromosomes, each one which contains a particular amount of genes. But in the "last" pair, men have a XY pair chromosome, and women have a XX pair chromosome. Does the missing "leg" of the XY pair make men to have fewer genes than women, and if so, how many genes do each sex have?</p>
|
[
{
"answer_id": 57480,
"pm_score": 6,
"text": "<p>It is true that the Y chromosome is shorter than the X chromosome and that there are more genes on the X chromosome.</p>\n\n<blockquote>\n <p>Do men have fewer genes?</p>\n</blockquote>\n\n<p>One could (mis)understand three things in the expression \"number of genes\". </p>\n\n<ol>\n<li>Number of gene copies (see <a href=\"https://en.wikipedia.org/wiki/Copy-number_variation\" rel=\"noreferrer\">Copy Number Variation</a>)</li>\n<li>Number of <a href=\"https://en.wikipedia.org/wiki/Gene\" rel=\"noreferrer\">genes</a></li>\n<li>Number of <a href=\"https://en.wikipedia.org/wiki/Allele\" rel=\"noreferrer\">alleles</a></li>\n</ol>\n\n<p>Thanks to @GerardoFurtado for correcting my semantic in the comments.</p>\n\n<p><strong>1. Number of gene copies</strong></p>\n\n<p>From the statement that there are fewer genes on the Y chromosome, one can conclude that men have fewer genes copies than woman.</p>\n\n<p>This is the intuition the OP seemed to have.</p>\n\n<p><strong>2. Number of genes</strong></p>\n\n<p>Men also have an X chromosome. So men have the standard genes present on the X chromosome (but they only have a single copy of it while women have two copies; btw you might be interested in <a href=\"https://en.wikipedia.org/wiki/Dosage_compensation\" rel=\"noreferrer\">dosage compensation</a>).</p>\n\n<p>Because women do not have a Y chromosome and because there are a number of genes on the Y chromosome that are not present on the X chromosome, men have genes that female don't have at all. Therefore women have fewer genes than men.</p>\n\n<p><strong>3. Number of alleles</strong></p>\n\n<p>There is not much reason to expect that one gender would be more heterozygote than the other at autosomes (=non sexual chromosomes). Some may hypothesize that women may have more heterozygosity than men if there is stronger selection among sperm than among ovules or things like that but let's not get down this complicated path.</p>\n\n<p>One one hand women have more gene copies and therefore might experience more heterozygosity, one the other hand, men have more genes and would therefore eventually carry more alleles. I don't know which side wins!</p>\n\n<p><strong>Did you mean number of genes per cell or per individual?</strong></p>\n\n<p>So far I assumed you were interested about the number of genes (or gene copies) per cells but if you want to compare whole individuals than it is a different story!</p>\n\n<p>Men are on average taller and therefore have more cells. Therefore if you compare the body-wide number of gene copies, women will have fewer gene copy on average (Thanks to @JM97 comment).</p>\n"
}
] |
[
{
"answer_id": 57501,
"pm_score": 0,
"text": "<p>Note - this is a very simple way to present things, and don't have the ambition to be a biology thesis. </p>\n\n<p>Men do not have fewer genes than women, but fewer allels (variations of a gene); the allels on the x-y chromosome pair are not necessarily the same on the x and on the y (for men) or second x (for women), but they are for a part of same kind - same gene. It's like if, for a part, the y chromosome was broken, missing a bar to be an x. </p>\n\n<p>One example of this is daltonism, linked to the xy chromosome pair.<br>\nLet's say that the daltonism allel is a corrupted existing allel (a variation of a gene).<br>\nTo be a daltonist, a woman must have the daltonism allel on both of his x chromosomes - the daltonism allel is not a dominant allel, and if there is one corrupted allel on one x chromosome, but a normal one on the other x, the woman won't be a daltonist. </p>\n\n<p>But a man is a daltonist only if his X chromosome do have the \"corrupted\" allel, because of the missing part of the y chromosome (compared to an x one).</p>\n\n<p>If a woman has both allels, one \"good\" and one \"corrupted\", she will transmit it or not to his child, depending on which X chromosome she will give to this child.</p>\n\n<p>If the father is a daltonist, he won't transmit it to his child if this child is a boy (he gives him his y chromosome genes and allels, not the x ones, and the boy takes an x from the mother, so he is xy).<br>\nBut if his child is a girl, the father will transmit it to her (the girl take an x from the two of his mother and the only x from the father, so she is xx)</p>\n\n<p>So, a child, to be a daltonist, must have at least a daltonist allel from his mother, no matter if the woman was daltonist or not (one x allel only corrupted or both).<br>\nThen, if this child is a girl, and is daltonist, it implies his father was daltonist too.<br>\nIf it's a boy, no matter if the father is daltonist or not, he will be a daltonist as soon as his mother transmitted him a corrupted allel.</p>\n\n<p>If the father is a daltonist, and if the mother has no daltonism allel at all, he will although transmit the allel to his daughters, who, while not being daltonists, will be able to transmit it to their own child.<br>\n In the same case (father daltonist, mother with no daltonism allel at all), if the child is a boy, he won't be a daltonist and won't be able to transmit it to his own child, etc, etc.</p>\n\n<p>Remember, this is a simple way to present things, and do not pretend to be at the top of today's science vision, and even more not the truth - above the fact I'm not a biology specialist, every scientific that deserves this name won't ever be claimed to say the truth, something reserved for religions - and that's why science and knowledge, in general as well as for each people in the same spirit state, progresses ...</p>\n\n<p>Last word, concerning the numbers of genes, according to Wikipedia - but you know that Wikipedia is not always the best source ;) - a human male has an estimated amount of 21 000 genes, and a woman, something between 0 and 50 fewer genes (800 genes on the x chromosome, 50 on the y one, but some of these are commons to both. How many, I don't know ...).<br>\nSorry for the multiple edits, I try to give my 2 cents on this question after 2 days and a night without sleeping</p>\n"
},
{
"answer_id": 57506,
"pm_score": 2,
"text": "<p>As @GerardoFurtado noted in his comment, males have more genes since there are genes unique to the Y chromosome, like <a href=\"https://en.wikipedia.org/wiki/SRY\" rel=\"nofollow noreferrer\">SRY</a>. Of course, the fact that males only have a single X chromosome means that males will only have a single <a href=\"https://en.wikipedia.org/wiki/Allele\" rel=\"nofollow noreferrer\">allele</a> of each gene encoded by the X chromosome, while females have two alleles for each gene they have.</p>\n"
},
{
"answer_id": 57551,
"pm_score": 0,
"text": "<p>As Remi.b said, there are different definitions of what a gene is. I found some more sources, if I understand correctly, according to the table in this wikipedia article with Data source of Ensembl genome browser release 87 <a href=\"https://en.wikipedia.org/wiki/Human_genome\" rel=\"nofollow noreferrer\">https://en.wikipedia.org/wiki/Human_genome</a>, a male human would have 14600 \"pseudogenes\" and a female human would have 14800 \"pseudogenes\" in each cell, and according this another table <a href=\"https://en.wikipedia.org/wiki/Chromosome#cite_note-26\" rel=\"nofollow noreferrer\">https://en.wikipedia.org/wiki/Chromosome#cite_note-26</a> , a male human would have 21000 genes and a female woman would have 21750 genes in each cell</p>\n"
},
{
"answer_id": 59654,
"pm_score": 2,
"text": "<p>Note : the number of genes evolves.\nFor who is interested and can understand french, heres a link speaking, in a short way, about that, and about the eventual disappearence of the y chromosom in human genom:<br>\n<a href=\"http://planet-vie.ens.fr/content/chromosome-y-humain\" rel=\"nofollow noreferrer\">http://planet-vie.ens.fr/content/chromosome-y-humain</a><br>\nAnd a link about the inactivation of one of the X chromosom in women genom (corpuscle of Barr) : <a href=\"http://www.snv.jussieu.fr/vie/dossiers/kx/kx.htm\" rel=\"nofollow noreferrer\">http://www.snv.jussieu.fr/vie/dossiers/kx/kx.htm</a></p>\n"
}
] |
58,769 |
<p>Inbreeding increases the risk of getting two identical recessive genes, alleles, that cause a disease which wouldn't have been activated with mixed genes. That's how I understand it anyway. But I sometimes read and hear that inbreeding among humans also causes decreased intelligence, especially emotional and social intelligence. Is there any support for such claims, and if so how does that work?</p>
|
[
{
"answer_id": 59018,
"pm_score": 4,
"text": "<p>There is indeed evidence that inbreeding in humans lowers intelligence of offspring. </p>\n\n<blockquote>\n <p>In summary, our comprehensive assessment revealed that parental consanguinity and degree of inbreeding was significantly associated with depression in intellectual behaviors among children. Factors other than inbreeding showed little influence, suggesting that genetic component (i.e., inbreeding) was more influential over these parameters under study. Moreover, the depression in cognitive abilities seems to be more prominent due to increase in the degree of inbreeding (F). </p>\n</blockquote>\n\n<p><a href=\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4196914/\" rel=\"nofollow noreferrer\">Estimating the Inbreeding Depression on Cognitive Behavior: A Population Based Study of Child Cohort</a></p>\n\n<blockquote>\n <p>A thorough literature search resulted in 95 studies. There were 15 studies that provided sufficient data for a meta-analysis. The studies were divided into four categories of inbreeding, showing values of an inbreeding coefficient (f) of .046, .063 (first cousin marriage), .125 (double first cousin marriage), and .25 (incest). The study’s hypothesis of a linear relationship was strongly confirmed. Over four categories, degree of inbreeding correlated highly with average IQ depression, r = .91. The current meta-analysis shows that the most common type of consanguinity, first cousin marriage (f = .063), may lead to a depression of about six IQ points, whereas incest (f = .25), the most severe type of consanguinity may cause a depression of about 28 IQ points. </p>\n</blockquote>\n\n<p><a href=\"http://scriptiesonline.uba.uva.nl/document/152307\" rel=\"nofollow noreferrer\">Is there a linear relationship between inbreeding and mental ability?: A meta-analysis </a></p>\n\n<p>Another study reaches a similar conclusion:</p>\n\n<blockquote>\n <p>This result is interpreted in light of cultural feedback theory, whereby it is suggested that consanguinity could subtly influence IQ at larger scales as a result of small IQ handicaps bought about through inbreeding being amplified into much larger differences through their effect on factors that maximize IQ such as access to education and adequate nutrition. </p>\n</blockquote>\n\n<p>About the mechanism behind the IQ decline caused by inbreeding:</p>\n\n<blockquote>\n <p>The study of Morton (1978) study revealed that the offspring of\n first-cousins had over a five times higher risk of mental retardation when compared to controls. The study concluded that declines in IQ and the increase of mental retardation are consistent with rare recessive alleles associated\n with around 325 loci, whose likelihood of being transmitted into offspring increases with the relatedness of the parents.</p>\n</blockquote>\n\n<p><a href=\"http://www.sciencedirect.com/science/article/pii/S0160289608001608\" rel=\"nofollow noreferrer\">Inbreeding depression and IQ in a study of 72 countries</a></p>\n"
}
] |
[
{
"answer_id": 59022,
"pm_score": 2,
"text": "<p>Inbreeding, in nature at large, has one primary effect, as you said. It increases the chances of two copies of harmful, recessive alleles. Consequently, offspring are much more likely to suffer from genetic and/or degenerative diseases.</p>\n\n<p>As for intelligence, some studies have indeed concluded that inbreeding can lead to a lower IQ (see <a href=\"https://biology.stackexchange.com/a/59018/31608\">this answer</a> for the exact quotations), it is possible that there are other factors at play. For instance, those from a lower socio-economic background tend to be of lower intelligence, although as with everything there are exceptions. Whilst I have struggled to find a source for this, it is statistically more likely that those of a lower socio-economic background will exhibit poor mental health and/or partake in the act of inbreeding.</p>\n\n<p>Consequently, due to the fact that intelligence is largely heriditary, the offspring of inbreeding will tend to be less intelligent. As a result, it is difficult to determine that there is a causal relationship between these correlating factors.</p>\n"
},
{
"answer_id": 59029,
"pm_score": 3,
"text": "<p>You are right. <strong>Inbreeding strongly increases overall homozygosity</strong> which subjects inbred individuals to diseases caused by rare recessive alleles. In non-inbred individuals the chance is quite low to receive those <a href=\"https://biology.stackexchange.com/questions/55676/why-are-most-mutations-recessive/55680#55680\">because many deleterious variants (and in fact, most segregating alleles we can observe) are recessive</a>. Most often, but depending on the dominance coefficient, these 'hide' in healthy heterozygous carriers and when <strong>very closely related individuals breed</strong> (with a lot of variants that are <a href=\"https://en.wikipedia.org/wiki/Identity_by_descent\" rel=\"nofollow noreferrer\">identical by descent</a>) there is a <strong>high chance that some of the 'hidden' deleterious variants are passed to the offspring</strong>.</p>\n\n<p>You have to be aware that there are in fact two conceptually different processes that can be both be referred to as inbreeding but are also somewhat continuously linked (see below): </p>\n\n<ol>\n<li><p>Mating systems that allow <strong>offspring between actually related individuals</strong> (measured by the <a href=\"https://en.wikipedia.org/wiki/Coefficient_of_relationship\" rel=\"nofollow noreferrer\">degree of relatedness</a>), what in humans often is referred to as incest or consanguinity.</p></li>\n<li><p>Populations with very low <a href=\"https://en.wikipedia.org/wiki/Effective_population_size\" rel=\"nofollow noreferrer\">effective population size</a> $N_e$ generally exhibit higher relatedness due to lack of genetic diversity (excess of homozygous sites). Therefore, <strong>populations with low $N_e$ are referred to as inbred even if no actually related individuals are mating.</strong> </p></li>\n</ol>\n\n<p>There is some evidence that <strong>inbreeding in the first sense is linked to cognitive abilities in humans</strong>:</p>\n\n<ul>\n<li><p><a href=\"https://www.nature.com/nature/journal/v266/n5601/abs/266440a0.html\" rel=\"nofollow noreferrer\">Bashi (1977)</a> investigated the effect of offspring having first-cousin (i.e. between children of siblings) and double first-cousin (i.e. between children of siblings and unrelated siblings, sharing as much variants as half-siblings but with more recombination events) parents while (at least somewhat) correcting for socioeconomic effects. He found an <strong>inbreeding depression with respect to cognition</strong> that could </p>\n\n<blockquote>\n <p>result either from the general increase in homozygosity [...] or from <strong>decrease in performance resulting from homozygosity for specific recessive alleles</strong> (highlighted by me). The higher variance of the double cousin group in some of the tests favours the second interpretation.</p>\n</blockquote></li>\n<li><p><a href=\"http://www.sciencedirect.com/science/article/pii/S0160289608001608\" rel=\"nofollow noreferrer\">Woodley (2012)</a> presents evidence for <strong>slightly lower IQs caused by inbreeding</strong>, however, he also mentions that the effect is way smaller than socioeconomic effects: </p>\n\n<blockquote>\n <p>Consanguinity could subtly influence IQ at larger scales as a result of small IQ handicaps bought about through inbreeding being amplified into much larger differences through their effect on factors that maximize IQ such as access to education and adequate nutrition.</p>\n</blockquote></li>\n<li><p><a href=\"http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0109585\" rel=\"nofollow noreferrer\">Fareed and Afzal (2014)</a> investigated verbal IQ, performance IQ, and full-scale IQ and found that all of these <strong>IQ parameters are significantly lower in inbred children compared to non-inbred children</strong> - actually the difference increases significantly with the degree of relatedness. They conclude that there is </p>\n\n<blockquote>\n <p>evidence for inbreeding depression on cognitive abilities among children.</p>\n</blockquote></li>\n</ul>\n\n<p>Please keep in mind that, for for sociological/ethical reasons, this is highly controversial, especially when the two concepts above are intermixed - human populations underwent differential and variably strong periods of low $N_e$, i.e. were subject to stronger or weaker inbreeding in the second sense. When reading the citation of Bashi (1977) above carefully, you will notice that he takes good care not to intermix those. <strong>Inbreeding in the first sense leaves large runs of homozygosity</strong> (ROH, blocks without heterozygous sites, i.e. a clustered and local lack of variation) whereas inbreeding in the second sense increases homozygosity in the genome less selectively. Therefore, the <strong>distribution of homozygous sites can be used to infer whether inbreeding is recent (first sense) or old (second sense)</strong> (see for example <a href=\"http://www.sciencedirect.com/science/article/pii/S000292970800445X\" rel=\"nofollow noreferrer\">McQuillan et al. (2008)</a> - here you see that both concepts form a continuum: where do you set the cutoff between recent and old? what is an appropriate threshold size for ROH? ...). Regardless, Bashi's findings indicate that <strong>effects of inbreeding are caused by recent inbreeding</strong> as he presents evidence that his results are rather driven by specific deleterious recessive variants than overall excess homozygosity. Finally, even though the study by Fareed and Afzal (2014) shows rather large effects of recent inbreeding in IQ measures, the results from Woodley (2012) show that one needs to be <strong>really careful to separate genetic from environmental components</strong> as his study suggests that the latter contribute more to the observed decrease in IQ.</p>\n"
},
{
"answer_id": 79228,
"pm_score": -1,
"text": "<p>My understanding, NOT based on any study, it purifies the gene 'pool' since mutation derived alleles variation will be lost thru' generations just like we don't have much of our grand grand's 'unique' allele.</p>\n\n<p>This is bad as it happens in farms, when an decease that infects one, could eliminates all the populations, to be exact, barring a few left.</p>\n\n<p>In the ever changing environment as in evolutions, singular gene pool will be hit with extinction even thought it might prosper if and only if the same good old 'environment' persists. Environment here includes everything in the ecosystems.</p>\n"
},
{
"answer_id": 107372,
"pm_score": 1,
"text": "<p>In addition to everything mentioned above, it should be noted that inbreeding leads to an increased chance at <a href=\"https://www.ingentaconnect.com/content/wk/mxe/2016/00000005/00000001/art00005\" rel=\"nofollow noreferrer\">schizophrenia</a> and <a href=\"https://europepmc.org/article/med/32627161\" rel=\"nofollow noreferrer\">bipolar</a> disorder. According to one of the studies called <strong>Inbreeding and serious mental illness in the first Spanish Bourbons</strong> states that inbreeding leads to a point where a person "accumulates pathogenic alleles", which is what leads to an increase risk of suffering from these particular mental disorders.</p>\n"
}
] |
59,062 |
<p>Some sources say that gametes are haploid, some say that they are diploid.</p>
<p>I'm confused.</p>
|
[
{
"answer_id": 59111,
"pm_score": 3,
"text": "<p>Actually there is some confusion here, and that's quite excusable, because it's extremely common reading that <strong>monoploid</strong> and <strong>haploid</strong> are synonyms and have the same meaning. However, they are different terms. According to Hartl and Ruvolo (2012):</p>\n\n<blockquote>\n <p>The potential confusion arises because of diploid organisms, in which the monoploid chromosome set and the haploid chromosome set are the same.</p>\n</blockquote>\n\n<p>As we, human beings, are diploid organisms, it's easy to see why haploid and monoploid ended up being considered as synonyms. </p>\n\n<p>However, a more precise terminology would be:</p>\n\n<ul>\n<li><strong>Monoploid</strong>: the total number of chromosomes in a single complete set of chromosomes (this does not change whether we are talking about a somatic cell or a gamete).</li>\n<li><strong>Haploid</strong>: half of the total number of chromosomes in a somatic cell. The haploid chromosome set is the set of chromosomes present in a gamete, irrespective of the chromosome number of the species.</li>\n</ul>\n\n<p>That being said, <em>diploid</em> and <em>haploid</em> are not antonyms nor mutually exclusive terms. A cell can be diploid <em>and</em> haploid at the same time. Let's exemplify this with organisms that perform gametic meiosis:</p>\n\n<p>Human beings have diploid somatic cells, with 46 chromosomes. When a somatic human cell perform meiosis, it produces <em>haploid</em> cells which are <em>monoploid</em>. Human gametes are haploid and monoploid.</p>\n\n<p>In wheat (<em>Triticum aestivum</em>), somatic cells are hexaploid, having 42 chromosomes (that is, 6 full sets of 7 chromosomes). When a wheat cell perform meiosis (producing micro and mega spores, and later on gametes), it produces <em>haploid</em> cells which are <em>triploid</em>. Wheat gametes are haploid and triploid.</p>\n\n<p>The same whay, a tetraploid organism would produce, by meiosis, a cell which is haploid <em>and</em> diploid. Thus, depending on the number of chromosome sets in the somatic cell of a given species, you can say that a gamete is diploid (as stated in this <a href=\"https://biology.stackexchange.com/a/59067/24284\">other answer</a>).</p>\n\n<p>In a nutshell, a gamete that was produced by meiosis (there are life cycles where the gamete is not produced meiotically) is <strong>always</strong> haploid, regardless the number of chromosome sets it has (which will determine if it is monoploid, diploid, triploid, hexaploid etc...). </p>\n\n<p>Sources:</p>\n\n<ul>\n<li><p><a href=\"https://books.google.com.au/books?id=cfvILxY9tCIC&pg=PA285&dq=haploid%20monoploid&hl=en&sa=X&redir_esc=y#v=onepage&q=haploid%20monoploid&f=false\" rel=\"nofollow noreferrer\">Hartl, D. and Ruvolo, M. (2012). Genetics. 1st ed. Burlingham, Mass.: Jones and Bartlett Learning.</a></p></li>\n<li><p><a href=\"https://genetics-notes.wikispaces.com/Ploidy\" rel=\"nofollow noreferrer\">Genetics-notes.wikispaces.com. (2017). genetics-notes - Ploidy. [online] Available at: https://genetics-notes.wikispaces.com/Ploidy [Accessed 1 May 2017].</a></p></li>\n</ul>\n"
}
] |
[
{
"answer_id": 59063,
"pm_score": 1,
"text": "<p>Don't get confused by the number of chromosomes. Haploid refers to 1 set of chromosome, diploid refers to 2 set of chromosomes, triploid means 3 set of chromosomes. They don't represent the numbers of chromosome present on a set. </p>\n\n<p>We human beings have 23 chromosomes on a single set. We are diploid organisms and thus all the cells of our body carries two set of chromosomes (thus 23*2=46). Our germ cells however are formed through meiosis cell division and thus they are haploid (23 chromosomes).</p>\n\n<p>So, sperm cell carries 23 chromosome and egg carries 23 chromosome each. When they fuse, zygote is formed and as you can see, zygote carries 23+23=46 chromosomes. Zygote undergoes mitotic cell division and a complete human is formed. So, human zygote definitely is diploid.</p>\n"
},
{
"answer_id": 59067,
"pm_score": 2,
"text": "<p>It depends on the organism in question. (<a href=\"https://en.wikipedia.org/wiki/Polyploid#Examples\" rel=\"nofollow noreferrer\">https://en.wikipedia.org/wiki/Polyploid#Examples</a>)</p>\n\n<p>Notice that the gametes carry half number of copies of the normal cells. As such a tetraploid organism will have diploid gametes. </p>\n"
},
{
"answer_id": 84680,
"pm_score": 0,
"text": "<p>Gametes must be haploid because they will be combining with another gamete. Sexual reproduction works to increase genetic diversity by having two haploid gametes combine to form a new organism that has a different combination of genes than either of its parents. The new organism has half the chromosomes from its mother and half from its father.</p>\n\n<p>Source from <a href=\"http://docsbay.net/chromosomes-and-meiosis\" rel=\"nofollow noreferrer\">Chromosomes and Meiosis Interactive</a> </p>\n\n<p>For example, in order for humans to reproduce, a sperm cell must fuse with an egg cell, producing a zygote that has a unique set of genetic information. If the gametes were diploid instead of haploid, the resulting organism would have too many chromosomes. By having two haploid gametes fuse together, it is ensured that the new organism will be genetically distinct and still have the correct number of chromosomes that it needs.</p>\n"
},
{
"answer_id": 106951,
"pm_score": 2,
"text": "<p>This is a confusing topic when it comes to polyploids. I don't believe the definition for haploid provided in the accepted answer is correct for all species.</p>\n<p><a href=\"https://www.genome.gov/genetics-glossary/haploid\" rel=\"nofollow noreferrer\">Haploid</a> refers to a cell or an organism that has only a single set of chromosomes - my interpretation is that it is only in a diploid organism such as a human that haploid means "half of the total number of chromosomes in a somatic cell", because diploid organisms produce haploid gametes.</p>\n<p>A diploid human produces haploid gametes.\nA hexaploid produces triploid gametes.</p>\n<p>I think the confusion in the accepted answer is that gamete means the same as haploid (which of course is true only for diploids, such as humans). The triploid gametes are not haploid. The definition in my answer supports that, and indeed if you search, other definitions state this also e.g. <a href=\"https://www.nature.com/scitable/definition/haploid-309/\" rel=\"nofollow noreferrer\">"Haploid describes a cell that contains a single set of chromosomes"</a>.</p>\n<p>I should add, to answer the question, that the gametes are diploid for a 4n tetraploid organism - when the gamete is produced 2 of these go to one gamete, and 2 to other (diploid). It may be that the source you read was referring to a tetraploid organism.</p>\n"
}
] |
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