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<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"
}
] |
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