tag:blogger.com,1999:blog-37148773.post2025355051812304420..comments2024-03-27T14:50:47.345-04:00Comments on <center>Sandwalk</center>: Creationists discover that human and chimp genomes are only about 70% similar!!!Larry Moranhttp://www.blogger.com/profile/05756598746605455848noreply@blogger.comBlogger193125tag:blogger.com,1999:blog-37148773.post-33164249018437869172015-06-25T17:30:15.918-04:002015-06-25T17:30:15.918-04:00The fusion apparently took place prior to the spli...The fusion apparently took place prior to the split of modern humans from Denisovans and Neanderthals. It is mentioned on pp. 64-65 of the supplementary information file for Prufer et al’s January 2014 paper in Nature on the Altai Neanderthal genome sequence. I believe it is still availbale here:<br />http://www.nature.com/nature/journal/v505/n7481/extref/nature12886-s1.pdf<br />Anonymoushttps://www.blogger.com/profile/05851334023571071184noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-25642337014136275622015-06-25T17:29:26.131-04:002015-06-25T17:29:26.131-04:00John, surely this would be misleading? Wouldn'...John, surely this would be misleading? Wouldn't many of these substitutions have happened as part of the same process that lead to the shortening of these telomeres in an individual prior to the fusion event?<br /><br />According to Carl Zimmer <a href="http://blogs.discovermagazine.com/loom/2012/07/23/and-finally-the-hounding-duck-can-rest/#.VYxx1vlVjLk" rel="nofollow">in this article</a>:<br /><br />> So the small quantity of telomere DNA does not, in fact, raise grievous doubts about the evolution of fused chromosomes. Nor does the fact that the repeating DNA in the fused chromsome has mutations in it. Telomere DNA is just prone to mutation. In fact, if you look at the telomere on a chromosome, you’ll typically find that the newest pieces of repeating DNA are correct, but the older segments further from the loop’s end are slightly garbled. These errors arise in your own body. If a chromosome’s telomeres are damaged, you might well expect the new ones to be gone, and the garbled ones remain.Aceofspadeshttps://www.blogger.com/profile/09534611408824723712noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-72621549541579434942015-06-25T13:31:46.967-04:002015-06-25T13:31:46.967-04:00Hi Tom - thanks!Hi Tom - thanks!AllanMillerhttps://www.blogger.com/profile/05955231828424156641noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-77364701368290215732015-06-25T12:09:33.411-04:002015-06-25T12:09:33.411-04:00If I remember correctly, the dating of the fusion ...If I remember correctly, the dating of the fusion comes from counting substitutions in the inactive former telomeric repeats.John Harshmanhttps://www.blogger.com/profile/06705501480675917237noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-18418401659578473822015-06-25T11:35:06.557-04:002015-06-25T11:35:06.557-04:00Glenn,
Can you explain the evidence that the fusi...Glenn,<br /><br /><i>Can you explain the evidence that the fusion occurred well after the chimpanzee split? I actually thought the fusion might have been one of the triggers for speciation </i><br /><br />I don't think there is a strong reason to associate such a translocation with speciation. True single biological species can be heterozygous for a fusion/break without any apparent phenotypic or meiotic fitness effect. eg http://www.nature.com/hdy/journal/v50/n3/abs/hdy198332a.html. <br /><br />More generally, karyotype evolution on a broader scale appears to follow a regular switch in the polarity of female meiosis - http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1461872/pdf/11729161.pdf . Although the authors' first sentence is "Speciation is often accompanied by changes in chromosomal number or form even though such changes significantly reduce the fertility of hybrid intermediates", the data they report actually argues against hybrid-unfitness speciation being the typical consequence of translocation.AllanMillerhttps://www.blogger.com/profile/05955231828424156641noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-66504619690155717872015-06-25T09:20:07.017-04:002015-06-25T09:20:07.017-04:00My understanding, though, is that the fusion could...My understanding, though, is that the fusion could have played a role in speciation, in that it promoted a relative reproductive isolation among those with the fusion, who would be more likely to successfully reproduce with each other than with those who did not have the fusion . Am I correct on that?Faizal Alihttps://www.blogger.com/profile/00937075798809265805noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-40562040758348679732015-06-25T07:06:39.868-04:002015-06-25T07:06:39.868-04:00Hi Allan
Your ears must have been ringing...
htt...Hi Allan<br /><br />Your ears must have been ringing...<br /><br />http://tinyurl.com/ofeyjd8<br /><br />best<br />Tom Muellerhttps://www.blogger.com/profile/09829281784362177069noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-29485682364936823502015-06-25T06:54:52.586-04:002015-06-25T06:54:52.586-04:00Interesting that the corrected alignment returns t...Interesting that the corrected alignment returns towards the values given by the now-superseded hybridisation method. The 'gapping' parameter is particularly relevant to this. Complementary pairing will rapidly realign either side of an indel in a physical system, affecting the 'melting' temperature, which an ungapped search would miss. AllanMillerhttps://www.blogger.com/profile/05955231828424156641noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-43253690818681213582015-06-25T02:32:09.502-04:002015-06-25T02:32:09.502-04:00If there was a fusion event 3 million years ago, t...If there was a fusion event 3 million years ago, that does not mean that the human-ancestor population at that time was as small as 2. It means that the ancestry for the fused region was a single chromosome. But because of recombination, all other regions of the genome were most likely descended from other individuals at that time.<br /><br />That is widely misunderstood for mitochondria and Y-chromosomes (the other chromosomes come from ancestors other than Mitochondrial Eve and Y-chomosome Adam, in fact each region of the genome comes from a different ancestor, down to chunks the size of a gene). It is also true for the fusion region versus nearby regions of chromosome 2. Joe Felsensteinhttps://www.blogger.com/profile/06359126552631140000noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-15103175506178044432015-06-23T23:01:07.035-04:002015-06-23T23:01:07.035-04:00Ken,
Thanks for joining the discussion. This threa...Ken,<br />Thanks for joining the discussion. This thread is like a Christmas where I got everything on my list.<br /><br />Did Tompkins really say DDX11L2 was "highly expressed"? Seems a bit brazen.<br /><br />I don't know how you keep your cool arguing with these people.Diogeneshttps://www.blogger.com/profile/15551943619872944637noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-88669536679316206342015-06-23T22:53:37.312-04:002015-06-23T22:53:37.312-04:003 million eh? The date works for me!
https://whye...3 million eh? The date works for me!<br /><br /><a href="https://whyevolutionistrue.wordpress.com/2011/09/18/how-big-was-the-human-population-bottleneck-not-anything-close-to-2/#comment-135151" rel="nofollow">https://whyevolutionistrue.wordpress.com/2011/09/18/how-big-was-the-human-population-bottleneck-not-anything-close-to-2/#comment-135151</a><br /><br />Thanks for the good news Ken.<br />Gary Gaulinhttps://www.blogger.com/profile/10925297296758439900noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-82791355886677927502015-06-23T22:28:27.612-04:002015-06-23T22:28:27.612-04:00Glenn - I'm pretty sure I've run across a ...Glenn - I'm pretty sure I've run across a study or two dating the fusion event to the last 2 or 3 million years. If I remember correctly, the fusion site is present in Neanderthal and Denisovan DNA. I can check this out if you like.Ken Millerhttps://www.blogger.com/profile/01385746839062291054noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-80091970722354024652015-06-23T19:49:53.178-04:002015-06-23T19:49:53.178-04:00Hi Ken, thanks for your comments!
I also want to ...Hi Ken, thanks for your comments!<br /><br />I also want to chime in on the "highly expressed" claim, which I can't help but think is a blatant lie. DDX11L2 is nowhere near as highly expressed as DDX11 itself, and secondly, the transcripts that cross the fusion site only make up about 20% of the DDX11L2 transcripts. It's demonstrably "lowly expressed" :D<br /><br />Can you explain the evidence that the fusion occurred well after the chimpanzee split? I actually thought the fusion might have been one of the triggers for speciation ..Glennhttps://www.blogger.com/profile/03419669114209732527noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-56066977612535834132015-06-23T19:23:41.233-04:002015-06-23T19:23:41.233-04:00I’m happy to be dragged into the discussion!
I ex...I’m happy to be dragged into the discussion!<br /><br />I exchanged a couple of emails with Tomkins last year, pointing out the errors in his papers (in creationist journals) on the Chromosome 2 fusion site. As you all know, he’s very excited that he’s found a “highly-expressed” gene that “spans” the fusion site. This means, he claims, that the fusion site couldn’t possibly be what it seems.<br /><br />He’s wrong, and many of the reasons why have already been pointed out in this discussion. First and foremost, the gene in question (actually a pseudogene with no known function) is a member of a transcript family known as DDX11L. Tomkins pointedly ignores the Costa (2009) paper, which identified 18 members of this gene family. Each of them is next to a sequence known as “WASH,” which is transcribed in the opposite direction of the DDX11L pseudogene. And, more to the point, each and every one of them is located right next to a telomere – except for one. That’s the DDX11L2 sequence, which is parked right next to the fusion site. That alone is very strong evidence that site is exactly what it seems to be – the remnant of a telomere-to-telomere fusion.<br /><br />Most of the genome databases show the DDX11L2 sequence as off to one side of the fusion site, so it really doesn’t span it. However, in some of the databases there are transcript variants that include the head-to-head telomere sequence motifs as one of the introns in the primary transcript. That is basis on which Tomkins claims that the gene spans the site. But the very same data are easily explained by variability in the termination of transcription so that occasionally a somewhat longer RNA is produced. This is exactly what I pointed out to Tomkins…. So that any claim that I “admitted” he was right about his interpretation is bogus.<br /><br />And, if Larry permits me to rant on a bit:<br /><br />• Tomkins said that “some” chromosome banding patterns were similar between humans and other great apes. Some? The matches were so extensive that Yunis & Prakash (1982) were able to align each and every chromosome from four different species!<br /><br />• He said there were too few telomere repeats in the fusion site. A “pristine” site would have 20,000 – 30,000 bases. But the fact is that “pristine” telomeres would prevent fusion, and treatments that dramatically shorten telomeres actually cause fusion, which is why there are so few repeats in chromosome 2. The small number of telomere repeats is exactly what should be expected at a fusion site.<br /><br />• Tomkins said that the DDX11L2 gene was unique to humans. Wrong. As Costa (2009) showed, there are members of this family in chimpanzees and gorillas. And, as you might expect, they are located right next to telomeres.<br /><br />• Finally, Tomkins lays great emphasis on the observation that transcription factor binding has been found throughout this region. But simple binding says nothing about the specificity of binding or its biological importance.<br /><br />• Tomkins has constructed a straw man in which an authentic fusion site would have to be an exact replica of the ends of two present day chimpanzee chromosomes to be valid. What he does not seem to realize is that the fusion occurred millions of years after our lineage separated from chimpanzees, and that both lines have continued to evolve along separate pathways. That accounts for the differences he regards as so significant.<br /><br />The evidence for a chromosomal fusion in the ancestry of our species is on very solid ground, and has been greatly strengthened by the very research he wishes to use against this idea.<br />Ken Millerhttps://www.blogger.com/profile/01385746839062291054noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-86632516965602773122015-06-23T01:26:46.300-04:002015-06-23T01:26:46.300-04:00Hello Photosynthesis
Notice that I did not insult...Hello Photosynthesis<br /><br /><i>Notice that I did not insult you (I hope I didn't). I just noticed that there were some problems with mixed understandings and misunderstandings, so I pointed them out. I often use my own concepts loosely.</i><br /><br />Not at all – I appreciate your patience and your indulgence for bringing me, an aging and non-current high school teacher, up to speed. Again, I thank you and John both for correcting any misconceptions on my part.<br /><br />I took up pencil and paper and was about to do some rough calculations to contradict the IDiot rendition I just cited above, when it suddenly occurred to me that recombination in diploids greatly complicates the story. I then did some google-whacking and was chagrined that my efforts had already been better tackled elsewhere:<br /><br />I direct your attention to Allan Miller’s insightful posts on<br /><br />http://sandwalk.blogspot.ca/2012/01/understanding-mutation-rates-and.html<br /><br />I am very grateful for this opportunity to refocus my thoughts and rewrite my exercises for the benefit of my students.<br /><br />Basically, I want to explain to my students that the point mutation rate is astonishingly high (~100 mutations per generation) and that in the ~600 000 generations since our human lineage diverged from chimpanzees, the number of “collective mutation hits” in a population averaging ~1 000 000 would exceed the size of our genome, ergo the importance of distinguishing mutation rate from fixation rate for a variety of complicated reasons including Muller’s ratchet.<br /><br />Going back to Muller’s ratchet, I reckon off hand that the number of mutation hits per human chromosome is roughly equal to the number of chiasmata per human chromosome. Is this just a coincidence or does this ratio hold across species and is less than coincidental from a Mullerian ratchet POV? It’s late at night and I am thinking out loud, I hope I am not embarrassing myself in public.<br /><br />Meanwhile, given an already astonishingly high mutation rate that may in fact be highly variable (Susan Rosenberg’s findings jump to mind) and that for every recombination event that diminishes “mutational load” half of the reciprocal products are in fact accumulating “mutational load”; IDiot contentions that Evolution could not produce those highly divergent HARs (as cited above) is not even wrong any more (to paraphrase Wolfgang Pauli)<br />Tom Muellerhttps://www.blogger.com/profile/09829281784362177069noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-77185594324449664262015-06-22T14:39:18.067-04:002015-06-22T14:39:18.067-04:00Hi Tom,
I understand. Notice that I did not insul...Hi Tom,<br /><br />I understand. Notice that I did not insult you (I hope I didn't). I just noticed that there were some problems with mixed understandings and misunderstandings, so I pointed them out. I often use my own concepts loosely. But when dealing with creationists we have to be careful and not let us go by mistaken notions, but rather try and understand what those notions are about. Concepts help understand, but they should not be mistaken with the things those concepts are trying to describe. With this distinction it becomes easier to explain when we misspeak and focus on the phenomena, better than playing word games. Remember that creationists are all about rhetoric, and a good deal of sophistry consists on using equivocations. Sometimes subtle ones, sometimes obvious ones.<br /><br />For some reason, equivocation fallacies seem hard for creationists to visualize and understand (or they're just dishonest and don't want to admit those equivocations).Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-37148773.post-1632637472731744832015-06-22T13:24:57.491-04:002015-06-22T13:24:57.491-04:00Hi John - Hi Photosynthesis
Re: the confusion bet...Hi John - Hi Photosynthesis<br /><br />Re: the confusion between mutation vs fixation rates.<br /><br />Please do not attack the messenger. I am merely reporting the sophistry of the IDiots. Frankly I reckon too much band width has been wasted on their sillier strawman arguments and not enough effort on some of their more subtle albeit still spurious suggestions.<br /><br />That said, I do welcome any efforts on your part to correct any lingering naïveté on my part. I thank you both.<br /><br />It could be argued that biased gene conversion increasing the GC content of the genome may be responsible for any HACSN1 –driven human chimp divergence.<br /><br />Check out this intriguing paper:<br /><br /><b>Hotspots of Biased Nucleotide Substitutions in Human Genes</b><br /><br />http://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.1000026<br /><br />I think IDiots miss the crucial point. <br /><br />I checked the original 81 nucleotide sequence of HACSN1; 12 of the 13 of the total base pair variations are AT-to-GC “biased” substitutions. But hey, that is still a cluster 4 X faster than would be anticipated by "neutral substitutions" as compared to the rest of the genome... bringing us back to your distinction between mutation vs. fixation rates.<br /><br />In other words- the IDiots have been summarily contradicted and further rebuttal on their part is futile.<br /><br /><i>These findings indicate that a recombination-associated process, such as biased gene conversion (BGC), is driving fixation of GC alleles in the human genome. This process can lead to accelerated evolution in coding sequences and excess amino acid replacement substitutions, thereby generating significant results for tests of positive selection.</i>Tom Muellerhttps://www.blogger.com/profile/09829281784362177069noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-51811092922910539792015-06-22T12:20:29.259-04:002015-06-22T12:20:29.259-04:00Tom,
Re:
So there was no such thing as a mutation...Tom,<br /><br /><i>Re:<br />So there was no such thing as a mutational hot-spot.<br /><br />To my understanding there in fact are mutational hotspots for two reasons:<br />1 - Highly unstable regions of the genome<br />2 - Genomic regions subject to intense positive selection</i><br /><br />I did not actually mean to say that mutations hot spots don't exist. I said that in that instance there was no such thing. I added that to find actual mutational hot-spots you have to do more than assume that concentrated mutations meant hot-spot.Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-37148773.post-33495759336325103652015-06-22T12:16:44.158-04:002015-06-22T12:16:44.158-04:00Strong positive selection doesn't increase the...<i>Strong positive selection doesn't increase the mutation rate; it increases the fixation rate.</i><br /><br />And so does population bottlenecks.<br /><br />Tom, you also seem to mistake "random genetic drift" with one of its potential consequences, namely the potential for a molecular clock.Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-37148773.post-25548145000098109482015-06-22T11:43:23.412-04:002015-06-22T11:43:23.412-04:00I think you are confusing mutation with fixation. ...I think you are confusing mutation with fixation. Nobody claims that HARs are mutational hotspots, as far as I know. Strong positive selection doesn't increase the mutation rate; it increases the fixation rate.John Harshmanhttps://www.blogger.com/profile/06705501480675917237noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-71163873922491598712015-06-22T10:18:58.831-04:002015-06-22T10:18:58.831-04:00Hi Photosynthesis
Re:
Regions of the human and ch...Hi Photosynthesis<br /><br />Re:<br /><i>Regions of the human and chimps genomes might differ by more than 30%. That doesn't mean that they are "crucial."</i><br /><br />Agreed – such regions do not <b>have to be</b> crucial; any such contention would admittedly be contingent and not necessary. <br /><br />That said, it appears that Human Accelerated Regions do indeed represent both mutational “hotspots” not due to regions of genomic instability but rather positive selection in functional regions of the genome. In fact, that is exactly how these regions were discovered (i.e hypermutability) <b>AND </b> it turns out these HARs are crucial in explaining human-chimp divergence.<br /><br />Re:<br /><i>So there was no such thing as a mutational hot-spot.</i><br /><br />To my understanding there in fact are mutational hotspots for two reasons:<br />1 - Highly unstable regions of the genome<br />2 - Genomic regions subject to intense positive selection<br /><br />For example, I direct your attention to <br /><br />http://www.sciencemag.org/content/314/5800/786.abstract<br /><br />Re:<br /><i>the molecular clock doesn't have to explain everything.</i><br /><br />Agreed! That was my whole point, the inexorable ticking of a molecular clock cannot explain HARs.<br /><br />Re:<br /><i>Concentrated mutations don't just open the door for an intelligent designer…Not knowing why there's a concentrated amount of mutations somewhere in the genome doesn't mean that some "intelligent designer" is the answer. It would just mean that we don't know how that happened.</i><br /><br />Hmmm – but I direct your attention to Larry’s challenge:<br /><br /><b> Laurence Moran:</b><i>”The onus is now on Intelligent Design Creationists to prove that the creation of an irreducibly complex system requires a step that cannot possibly be due to natural selection (or random genetic drift?)…<br /><br />I don't know of a single example of such an irreducibly complex system.</i><br /><br />And I counter that some of Dembski/Behe’s acolites are indeed citing HARs as proof positive that ID must be correct because of a false syllogism as outlined above. The major premise of Neutral Theory and the minor premise of HARs elicit the inevitable conclusion that Larry’s version of Evolution must be false. <br /><br /> Of course, the rebuttal is trivial: As Aceofspades explains, Neutral Theory does not deny any and all occurrences of intense positive selection; adaptation can be invoked to explain mutational hotspots such as HARs.<br /><br />The champions of ID counter that such mutational clusters would have required fixation within a generation for divergence to proceed thereby invalidating evolution even at the level of intense positive selection. Too much/too fast dontchya know.<br /><br />Here is a worksheet I provide my highschool students on the very subject:<br />http://www.indiana.edu/~ensiweb/lessons/Hum-Chimp%20DNA.pdf<br /><br />I built it before I became a regular at sandwalk. Rereading it permits me to recognize some errors of omission and commission that require “tweaking”. This activity's next incarnation will focus on this article instead:<br /><br />http://phenomena.nationalgeographic.com/2008/09/04/did-a-gene-enhancer-humanise-our-thumbs/<br />Tom Muellerhttps://www.blogger.com/profile/09829281784362177069noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-16783187017659044182015-06-22T09:08:29.892-04:002015-06-22T09:08:29.892-04:00The thing about HAR regions is that they are rare ...The thing about HAR regions is that they are rare and <a href="https://en.wikipedia.org/wiki/Human_accelerated_regions" rel="nofollow">incredibly small</a>. They have on the order of about 100 base pairs each.<br /><br />Even if these regions were under intense selective pressure, they represent such a tiny fraction of our genome that I don't see how they challenge neutral theory.Aceofspadeshttps://www.blogger.com/profile/09534611408824723712noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-78611168717973727472015-06-22T08:53:55.185-04:002015-06-22T08:53:55.185-04:00Tom,
1 crucial regions of genome between chimps a...Tom,<br /><br /><i>1 crucial regions of genome between chimps and humans differ by more than 30%</i><br /><br /><br />Regions of the human and chimps genomes might differ by more than 30%. That doesn't mean that they are "crucial."<br /><br /><i>2 and such differences cannot be explained by the inexhorable ticking of a molecular clock as suggested by Neutral Theory leaving open the door for ID</i><br /><br />Oh, but you're jumping here. Random mutation doesn't mean equidistant and homogeneous mutation. It just means random mutation. Some time ago, people thought they had found "mutational hot spots," and a scientist with a bit better understanding of what random means showed that these "hot spots" did not occur at a higher frequency than expected from a random distribution of mutations. So there was no such thing as a mutational hot-spot. There might be, but finding them is a tad more difficult that just pointing to a region that has more mutations that other regions, since the distribution of mutations should actually vary.<br /><br />Then, the molecular clock doesn't have to explain everything. When conceptualizing of the clock most scientists think of point mutations. Rearrangements, DNA insertions, retroviruses, etc, are not point mutations, yet they are just as natural. Etc. Etc.<br /><br />So, no. Concentrated mutations don't just open the door for an intelligent designer. Now, more deeply, if we knew nothing about what random actually means, about population bottlenecks, about insertion elements, about etc and etc, that would still not leave the door open for an intelligent designer because, well, intelligent designers have a track record for being imaginary answers to open questions. Like volcanoes and thunder. Not knowing why there's a concentrated amount of mutations somewhere in the genome doesn't mean that some "intelligent designer" is the answer. It would just mean that we don't know how that happened.<br /><br />Have a great week!Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-37148773.post-40466205178477295252015-06-22T08:25:47.483-04:002015-06-22T08:25:47.483-04:00I would love to - alas, I have been unable to find...I would love to - alas, I have been unable to find the graph they sent me, but I will keep looking!nmanninghttps://www.blogger.com/profile/14767343547942014627noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-262478297932928852015-06-22T08:23:11.882-04:002015-06-22T08:23:11.882-04:00It is so cute when creationist want to bring up Ha...It is so cute when creationist want to bring up Haldane's dilemma, as they so often do not have a clue as to what the 'dilemma' even was supposed to be - or the fact that it was not a universally accepted issue:<br /><br />"Perhaps the only disagreement I ever had with Crow concerned the substitutional load, because I never thought that the calculations concerning this load, which he and others carried out, were appropriate. From the very start, my own calculations suggested to me that Haldane’s arguments were misguided and indeed erroneous, and that there is no practical upper limit to the rate at which substitutions can occur under Darwinian natural selection."<br />- Warren Ewens<br /><br />nmanninghttps://www.blogger.com/profile/14767343547942014627noreply@blogger.com