Human and chimp DNA: They really are about 98% similar

_{vjtorley
October 22, 2015

Intelligent Design

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A few days ago, scientist and young-earth creationist Dr. Jay Wile wrote a post on his Proslogion blog, in which he reported that Dr. Jeff Tomkins had abandoned his claim that human and chimpanzee DNA are only about 70% similar, in favor of a revised figure of 88%. But even that figure is too low, according to the man who spotted the original flaw in Dr. Tomkins’s work.

Dr. Wile reports:

More than two years ago, Dr. Jeffrey P. Tomkins, a former director of the Clemson University Genomics Institute, performed a detailed, chromosome-by-chromosome comparison of human and chimpanzee DNA using a widely-recognized computer program known as BLAST. His analysis indicated that, on average, human and chimpanzee DNA are only about 70% similar. This is far, far, below the 95-99% numbers that are commonly cited by evolutionists, so once I read the study, I wrote a summary of it. Well, Dr. Tomkins has done a new study, and it invalidates the one he did two years ago.

The new study was done because last year, a computer programmer of financial trading algorithms (Glenn Williamson) discovered a bug in the BLAST algorithm that Tomkins used. This bug caused the program to ignore certain matches that should have been identified, which led to an artificially low similarity between the two genomes.

Here is what Glenn Williamson has to say about himself:

Yeah – 36 year old, stay-at-home father of four – including triplets, ha! 🙂

I don’t have any formal qualifications in genetics, or anything biological for that matter. I have a bachelors degree in computing science (i.e. programming) from the University of Technology in Sydney. Started my career as a programmer, but transitioned into derivatives trading, which is a lot more fun…

And for what it’s worth, I believe that my paper is more of a computing science paper than a genetics paper. It’s more my area of expertise than Jeff Tomkins’ area.

Glenn Williamson’s detailed takedown of Dr. Tomkins’s 70% similarity figure can be accessed here. Dr. Tomkins claims he submitted his paper to the creationist publication, Answers Research Journal, but it was never published. Here’s an excerpt from the paper (emphasis mine – VJT):

In this paper I carefully reproduce a subset of Dr Tomkins’ results, and show clearly and unambiguously that Dr Tomkins has fallen victim to a serious bug in the software used to obtain his results. It is this bug that causes Dr Tomkins to report the erroneous figure of 70% similarity. After correcting for both the effects of this bug and some non-trivial errors in Dr Tomkins’ methodology, I report an overall similarity of 96.90% with a standard error of ±0.21%. This figure includes indels, and the result is largely in line with the secular scientific consensus.

What happened next? Dr. Wile takes up the story:

As a result, Dr. Tomkins redid his study, using the one version of BLAST that did not contain the bug. His results are shown above… The overall similarity between the human and chimpanzee genomes was 88%.

In an update at the top of his post, Dr. Wile now admits to having cold feet, even about the revised 88% figure:

Based on comments below by Glenn (who is mentioned in the article) and Aceofspades25, there are questions regarding the analysis used in Dr. Tomkins’s study, upon which this article is based. Until Dr. Tomkins addresses these questions, it is best to be skeptical of his 88% similarity figure.

So what was wrong with Dr. Tomkins’s new study? I’ll let Glenn Williamson explain (emphasis mine – VJT):

October 16, 2015 4:22 pm

As I’ve said many times, if there is a single base pair indel in the middle of a 300bp sequence, Tomkins will say this is a 50% match.

Tomkins is most certainly aware of this, yet he chose to publish it. I think that says pretty much everything.

Another commenter named Aceofspades25 has this to add (emphases mine – VJT):

October 16, 2015 2:13 pm

The other obvious thing that Thompkins hasn’t dealt with in his BLASTN analysis, I talk about here.

There are a few cases where no match will be found because this entire sequence appears de-novo in Chimpanzees as the result of a single mutation (e.g. a novel transposable element – see here) or because humans have had a large deletion which other primates don’t. Deletions like this also likely occurred in a single mutation – see here

Thompkins (sic) would count both of these as being a 0% match (or 600 effective mutations if the sequences he was searching for were 300bp each). In reality, these probably represent just 2 mutations.

I’ll let Glenn Williamson have the final word (emphases mine – VJT):

Thanks Ace, for letting me know about this post. I reiterate here a few things about my (unpublished!) paper, and about Tomkins’ new paper.

The first thing is that he uses the “ungapped” parameter in his BLAST comparisons. As I’ve written in a few other places now, using this parameter, and calculating results in the way that Tomkins does is entirely disingenuous. If you are comparing two 300bp sequences, and one of those sequences has a single indel smack bang in the middle, Tomkins counts this as the sequences being only 50% identical.

I’ve told him at least twice that he cannot use ungapped and then calculate the result in this way. He can do one of two things:

1. Use ungapped, which ignores indels and therefore he can only report the substitution rate. (emphasis mine – VJT)If he did this, he would get a result of around 98.8%.

2. Allow gaps, and – this is what he fails to mention in his paper – get a result of around 96.9%. And this is using a very conservative method of calculation as well, since it counts a 50bp indel as having the same weight as 50 individual mutations. If you counted a 50bp indel as a single event (which it probably was), then the overall result would be pushed up towards 98%, which is the figure usually thrown around anyway.

In a comment dated 14 August 2015 (at 03:44) on an article titled, Chimp and Human DNA vs “Sophisticated Nonsense”! on a blog called Marmotism, Glenn Williamson adds:

I’ve actually written a paper on Tomkins’ 70% result, and have _ATTEMPTED_ to get it published in Answers Research Journal. Obviously they are not having a bar of it – Tomkins is the sole peer-reviewer, and he is currently refusing to provide any critique of my work – he has been silent for 8 months, while the ball is in his court ..

See the paper here:

https://www.dropbox.com/sh/dm2lgg0l93sjayv/AAATnWSJdER53EYEYZvcgiwma?dl=0

It’s the two PDFs ..

Dr. Tomkins’s latest article in Answers Research Journal (October 7, 2015) acknowledges Williamson’s work in a single sentence:

As of 2013, the issue of overall genome similarity between chimpanzee and humans seemed to be about 70% based on five different reports, three of which were based on actual data analyses. However, in 2014 , a computer programmer of financial trading algorithms discovered an apparent bug in the BLASTN algorithm and notified this author of the situation (Glenn Williamson, Tibra Capital, personal communication).

So, a submitted article only counts as a “personal communication”? Perhaps Dr. Tomkins needs to be a little more up-front about giving credit where credit is due, and acknowledging his mistakes. At any rate, the ball is definitely in his court, and his latest 88% similarity figure warrants skepticism. I have to say that Dr. Tomkins’s methodology sounds rather suspicious to me.

What do readers think?

Comments

This is the statement to which we objected. E. Coli didn’t choose. Rather, the results support random mutation.
LoL! It took the only gene the organism had to transport citrate and put it under the control of a promoter that allowed the gene to be expressed in the presence of O2. Why did it take so long? It wasn't a required change for survival and it isn't the only solution to the survival question.Virgil Cain_{October 23, 2015
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Vy: Except of course you want to lie and claim the e. coli didn’t already have the ability to use citrate under anaerobic conditions prior to forcing it use it under aerobic conditions which would be totally understandable BTW, it’s not like you guys are known for your honesty. As we never made that claim, or implied that claim, or held that view, your statement is false. Vy: * the organism controls the DNA not vice versa, so under the “eat_citrate_or_starve_to_death” lab conditions, the E. Coli chose to eat by tweaking already existing information to work under the lab environments. This is the statement to which we objected. E. Coli didn't choose. Rather, the results support random mutation. Zachriel: All evolution is a tweaked version of something that already existed. Vy: Finally, the honesty. With that, I say adaptation, not evolution. Evolution by natural selection is adaptation through modification of existing forms. See Darwin, Origin of Species, 1859. Vy: eat citrate aerobically or die. That's not the case. Citrate utilization evolved in the same medium that had been used for 30 thousand generations. Genomic studies show that the trait evolved through potentiating mutations in a single lineage, then a tandem duplication, followed by optimizing mutations. Most lineages never developed the trait, and the number of generations is consistent with random mutation. Vy: As for “random” mutations, that’s not an exact representation of reality. Mutations are not purely random. They have a number of causes and biases. However, they are random (uncorrelated) with respect to fitness. That's why Cit+ took so long for the potentiating mutations to occur.Zachriel_{October 23, 2015
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"This is false. We have never claimed that E. coli didn’t have the ability to utilize citrate under anaerobic conditions." Don't quote me out of context. Read it:
Except of course you want to lie and claim the e. coli didn’t already ...
"This is the statement we objected to, and the one that is unsupported." Actually, you quoted a large text with two "claims" and objected to it so there is no "this is the one". "Because if its a choice, all the bacteria would choose to have more resources. Again, because of? Why bother with something you might never encounter? "All evolution is a tweaked version of something that already existed. Finally, the honesty. With that, I say adaptation, not evolution. Please don't give me that story about adaptation being a mechanism of evolution or whatnot. "In this case, it requires potentiating mutations, a tandem duplication, then additional optimizing mutations." First, it required a reason, eat citrate aerobically or die. Everything else that happened was because of that. "The time it took to evolve is consistent with random mutation." There you go again with the equivocation. Sheesh! As for "random" mutations, that's not an exact representation of reality.Vy_{October 23, 2015
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Vy: you want to lie and claim the e. coli didn’t already have the ability to use citrate under anaerobic conditions prior to forcing it use it under aerobic conditions which would be totally understandable This is false. We have never claimed that E. coli didn't have the ability to utilize citrate under anaerobic conditions. Vy: the E. Coli chose to eat by tweaking already existing information to work under the lab environments. This is the statement we objected to, and the one that is unsupported. Vy: All because of? Because if its a choice, all the bacteria would choose to have more resources. Vy: So did Cit+ pop out of nowhere or is it a tweaked version of something that already existed? All evolution is a tweaked version of something that already existed. In this case, it requires potentiating mutations, a tandem duplication, then additional optimizing mutations. The time it took to evolve is consistent with random mutation.Zachriel_{October 23, 2015
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"But that’s not the claim you made" Sure? Here it is, again:
* the organism controls the DNA not vice versa, so under the "eat_citrate_or_starve_to_death” lab conditions, the E. Coli chose to eat by tweaking already existing information to work under the lab environments.
Wanna try again? "It’s clear the bacteria didn’t choose, or all the bacteria would have chosen to eat citrate in the aerobic conditions they found themselves in." Say what? All because of? "Instead, only after having tried billions of mutations was the pathway to Cit+ found, and only in a sub-population. So did Cit+ pop out of nowhere or is it a tweaked version of something that already existed? Was there or was there no reason for the e. coli to tweak this already existing functionality?Vy_{October 23, 2015
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It took 30 thousand generations for Cit+ to evolve, and then, only in some lineages.
That's because it wasn't a required change- it wasn't required for survival. How many generations did it take before humans discovered alternating current?Virgil Cain_{October 23, 2015
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Vy: Actually, it is. Except of course you want to lie and claim the e. coli didn’t already have the ability to use citrate under anaerobic conditions prior to forcing it use it under aerobic conditions which would be totally understandable BTW, it’s not like you guys are known for your honesty. But that's not the claim you made, which was that the bacteria "chose to eat by tweaking already existing information to work under the lab environments." It's clear the bacteria didn't choose, or all the bacteria would have chosen to eat citrate in the aerobic conditions they found themselves in. Instead, only after having tried billions of mutations was the pathway to Cit+ found, and only in a sub-population. bFast: BECAUSE EVERY SINGLE POINT MUTATION IS DELETERIOUS! Zachriel: Can you support this statement? bFast: No, I can’t. There are you are then. bFast: That said, simple logic, the 3d shape of the thing, strongly supports the “deleterious” hypothesis. Do you have support for that claim? bFast: So there are two options: 1 – All point mutation within the 180 are deleterious or 2 – There is something other than natural selection and known repair mechanisms conserving it. Or there were potentiating changes leading to accelerated evolution of the region.Zachriel_{October 23, 2015
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Zachriel (71) No, I can't. The reason I can't is that there seems to be DNA that is highly conserved even when it has no apparent purpose. As such, there is clearly some other preservative for DNA beside Natural Selection (and those pesky DNA repair systems ostensibly developed via RM+NS.) However, if we assume that natural selection (and its progeny which are presumably leaky) is the only preservative, then the fact that this 180 some odd nucleotide sequence is conserved through so many different species should be proof enough. So there are two options: 1 - All point mutation within the 180 are deleterious or 2 - There is something other than natural selection and known repair mechanisms conserving it. That said, simple logic, the 3d shape of the thing, strongly supports the "deleterious" hypothesis. Your theory still is best supported by the anathema principle.bFast_{October 23, 2015
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"That’s clearly not supported by the evidence." Actually, it is. Except of course you want to lie and claim the e. coli didn't already have the ability to use citrate under anaerobic conditions prior to forcing it use it under aerobic conditions which would be totally understandable BTW, it's not like you guys are known for your honesty. "It took 30 thousand generations for Cit+ to evolve, and then, only in some lineages." It took 30 thousand generations for e. coli to tweak it's DNA well enough to use citrate under aerobic conditions. "The results are consistent with random mutation." Right, they just randomly got stuck in a citrate-high petri dish, randomly already knew how to use citrate under anaerobic conditions, and many other "randoms". "The burst of evolution occurred after Cit+ evolved, as a mutator strain arose leading to rapid optimization of the trait." And here we go again.Vy_{October 23, 2015
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This is your claim. bFast: BECAUSE EVERY SINGLE POINT MUTATION IS DELETERIOUS! Can you support this statement?Zachriel_{October 23, 2015
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Zachriel, "What might be deleterious in one context might not be deleterious in another." Let me see, you are trying to tell me that in all of the contexts that all of the mammals and all of the birds experience the chimp way is the best, come human, poof now having mutations that destroy the 3d shape of this thing cease to be important. Why don't you get honest and say that you haven't a clue how the HAR1F pulled off this change -- but you are certain that it was naturalistic because the other option is anathema.bFast_{October 23, 2015
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bFast: Second — there is huge variability within mammals and birds. As is clear from the context, we were referring to humans. You ignored the point. You are claiming that the mutations must have been deleterious. What might be deleterious in one context might not be deleterious in another. Other changes in the human genome may have resulted in potentiating changes. Vy: * the organism controls the DNA not vice versa, so under the “eat_citrate_or_starve_to_death” lab conditions, the E. Coli chose to eat by tweaking already existing information to work under the lab environments. That's clearly not supported by the evidence. It took 30 thousand generations for Cit+ to evolve, and then, only in some lineages. The results are consistent with random mutation. Vy: * no new information was dropped from space, ergo, no evolution, whether burst, process or change. The burst of evolution occurred after Cit+ evolved, as a mutator strain arose leading to rapid optimization of the trait.Zachriel_{October 23, 2015
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"In this case, we have potentiating mutations AND gene-duplication with sequence divergence AND the gain of a new regulatory relationship AND a burst of optimizing mutations." * the E. Coli already had the ability to comfortably use citrate albeit under anaerobic conditions. * the organism controls the DNA not vice versa, so under the "eat_citrate_or_starve_to_death" lab conditions, the E. Coli chose to eat by tweaking already existing information to work under the lab environments. * no new information was dropped from space, ergo, no evolution, whether burst, process or change. Simply adaptation due to tweaking of already existing functionality to work under new conditions which conversely lead to a loss of function:
Each of these mutant strains has an antagonistic pleiotropy characteristic. An existing system is traded for an altered phenotype that is better suited to survive the specific stressful environment. Regulation is reduced to enable overexpression. DNA repair and DNA polymerase fidelity are reduced to enable increased mutation rates (increasing the probability of a “beneficial” mutation). A gene is inactivated by a process that concurrently activates a silent gene.Such trade-offs provide a temporary benefit to the bacterium, increasing its chances of surviving specific starvation conditions. However, these mutations do not account for the origin of the silenced genes, as their prior existence is essential for the mutation to be beneficial. (Anderson and Purdom)
We have adaptation and loss of function, clear enough?Vy_{October 23, 2015
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Zachriel (53): "There are actually 18 substitutions since the posited common ancestors with chimpanzees." That is correct. However, there is a change in the loop structure of one of the nodes. To invoke this loop structure change takes 6 mutations. (I give nature the HUGE benefit of the doubt that when the loop structure changed, the result was somehow at least as good as the non-human HAR1F.) Every possible single point mutation within this loop has been tried a gazillion times, and been removed a gazillion (minus 1) by natural selection. Why? BECAUSE EVERY SINGLE POINT MUTATION IS DELETERIOUS! That's what the theory says -- honest. If each individual mutation that forms the loop is deleterious, and if it takes 6 to re-form the loop, then a minimum of 5 deleterious mutations must have combined together waiting for lucky #6 to produce the loop transformation. "HAR1 is conserved, with only two point mutations since the common ancestor of chickens and non-human primates." Actually, on the tail of this 118 nucleotide RNA gene there are three points that wander like the wind. (One just happens to be the same with chickens and humans, but with other animals there is a third wanderer.) Except for these three wanderers, this thing is rock stable for all mammals and birds (but it doesn't exist at all in reptiles, go figure.) "A simple example would be a bigger skull being deleterious" That's a stupid statement Zachriel. First, still takes at least 6 approximately simultaneous mutations. Second -- there is huge variability within mammals and birds. Bet bones that whales have bigger skulls than humans. "A similar burst of evolution is seen in Lenski’s E. coli Long-term Evolution Experiment." Let me see, before there was a gene duplication (which was not deleterious) a point mutation wouldn't work. Once the duplication was there, the point mutation became effective. This is well inside the "edge of evolution". This is hardly a parallel to the HAR1F.bFast_{October 23, 2015
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A burst of evolution is expected if organisms are designed to evolve. The equivocation comes from using all examples of evolution as support for blind watchmaker evolution.Virgil Cain_{October 23, 2015
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Vy: So bacteria adapting to use citrate for carbon growth which it could already metabolize and transport is somehow a “burst of optimizing evolution”? Did you bother to read the paper? http://www.nature.com/nature/journal/v489/n7417/images_article/nature11514-f1.2.jpg Vy: Blount et al. have now reported that Behe was largely right. The key innovation was a shift in regulation of the citrate operon, caused by a rearrangement that brought it close to a new promoter. What Behe actually wrote was "If the phenotype is due to one or more mutations that result in, for example, the addition of a novel genetic regulatory element, gene-duplication with sequence divergence, or the gain of a new binding site, then it will be a noteworthy gain-of-FCT mutation." In this case, we have potentiating mutations AND gene-duplication with sequence divergence AND the gain of a new regulatory relationship AND a burst of optimizing mutations.Zachriel_{October 23, 2015
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If you guys want to explain what on earth you are going on about let me know. Like, what is contradictory about those terms Vy? A burst of evolution is obviously an evolutionary process and includes the accumulation of evolutionary changes? What's the bait? What's the switch?wd400_{October 23, 2015
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"No. It’s really really not at all like that. What are you going on about?" Could ask you the same. We've gone from "burst of evolution" to adaptation due to "evolutionary processes" to accumulation of "evolutionary changes". Pretty interesting use of terms. When someone gets around to ending the bait-and-switch, do inform me.Vy_{October 23, 2015
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wd400:
The “optimizing evolution” Zachriel is talking about is the pretty rapid accumulation of evolutionary changes that followed the establishment of the cit+ phenotype. In other words, there is a fairly long waiting time for the combination of mutations that create the new phenotype, but once that phenotype is established substitutions which increase its effectiveness are fixed rapidly.
And the equivocation continues. It is very telling that all our opponents can do is equivocate, erect strawman after strawman and misrepresent. Pathetic, actuallyVirgil Cain_{October 23, 2015
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"Accumulate rapidly" And that surely explains the differences between the chimp and the human?EugeneS_{October 23, 2015
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The mechanism of adaptation in Lenski’s Experiment was clearly due to evolutionary processes;
Zachriel's continued equivocation is duly noted.Virgil Cain_{October 23, 2015
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Vy,
That’s like saying the fact that a child born on Antarctica could survive a day in the Sahara desert is a “burst of optimizing evolution”.
No. It's really really not at all like that. What are you going on about? The "optimizing evolution" Zachriel is talking about is the pretty rapid accumulation of evolutionary changes that followed the establishment of the cit+ phenotype. In other words, there is a fairly long waiting time for the combination of mutations that create the new phenotype, but once that phenotype is established substitutions which increase its effectiveness are fixed rapidly.wd400_{October 23, 2015
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@VJTorley:
They really are about 98% similar
That number doesn't include sequences that are in one species but not the other. Is this comment 100% similar to your original post above because I quote you? I think it's more meaningful to cite numbers like these:
their genomes are not 98% or 99% identical ... One consequence of the numerous duplications, insertions, and deletions, is that the total DNA sequence similarity between humans and chimpanzees is not 98% to 99%, but instead closer to 95% to 96%, although the rearrangements are so extensive as to render one-dimensional comparisons overly simplistic -- Todd Preuss, PNAS, 2012
one finds that the human and chimpanzee genomes are indeed about 95% identical, genome wide -- Dennis Venema, of BioLogos
JoeCoder_{October 23, 2015
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"The mechanism of adaptation in Lenski’s Experiment was clearly due to evolutionary processes; in particular, the burst of optimizing evolution." Burst of optimizing evolution eh? So bacteria adapting to use citrate for carbon growth which it could already metabolize and transport is somehow a "burst of optimizing evolution"? That's like saying the fact that a child born on Antarctica could survive a day in the Sahara desert is a "burst of optimizing evolution". Total and utter crap! What I do see clearly is that you've answered my question, you do enjoy the mental gymnastics, that's why this ...
After an enormous amount of work, having sequenced the genomes of many clones along the lineages that led to the ability to use citrate, as well as lineages that never did, and testing the phenotypes of identified mutations, Blount et al. have now reported that Behe was largely right. The key innovation was a shift in regulation of the citrate operon, caused by a rearrangement that brought it close to a new promoter. ... It certainly is an example of reusing existing information in a new context, thus producing a new niche for E coli in lab cultures. But if the definition of innovation is something genuinely new, such as a new transport molecule or a new enzyme, then no, this adaptation falls short as an innovation. And no one should be surprised.
... translates to "clearly a burst of optimizing evolution" in your mind (or brain, considering that generally doesn't exist for you guys). And seriously, "optimizing" evolution??? Blindly "optimized" randomness???Vy_{October 23, 2015
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Vy: The only evolution that occurred in Lenski’s experiment is the one that exists only, and only, in the minds of Darwinists (theistic or otherwise) where adaptation (a fully valid pre-Darwinian mechanism) = evolution (an invalid representation of reality that elevates probablymaybecouldness, time, the laws of nature to “god”level). The mechanism of adaptation in Lenski's Experiment was clearly due to evolutionary processes; in particular, the burst of optimizing evolution. Many of the details of that historical transition are now known. See Blount, Genomic analysis of a key innovation in an experimental Escherichia coli population, Nature 2012.Zachriel_{October 23, 2015
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"A similar burst of evolution is seen in Lenski’s E. coli Long-term Evolution Experiment. There were potentiating mutations, then a tandem repeat, in a sub-population of bacteria under study. Once this occurred, it was followed by a burst of evolution, as multiple optimizing mutations became fixed in the citrate strain." The way you evos equivocate adaptation and evolution is truly amazing. Do you guys listen to yourselves or do you enjoy the mental gymnastics it takes to accomplish it? The only evolution that occurred in Lenski's experiment is the one that exists only, and only, in the minds of Darwinists (theistic or otherwise) where adaptation (a fully valid pre-Darwinian mechanism) = evolution (an invalid representation of reality that elevates probablymaybecouldness, time, the laws of nature etc. to "god"level).Vy_{October 23, 2015
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It is very telling that all our opponents can do is equivocate, erect strawman after strawman and misrepresent.Virgil Cain_{October 23, 2015
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bFast: Lets start with a serious look at the challenge of the HAR1F. I contend that a minimum of 6 mutations were required to cause the gene to choose the human looping pattern. There are actually 18 substitutions since the posited common ancestors with chimpanzees. bFast: We know from the fact that it is ultra-conserved between mice and chickens that every single point mutation is deleterious. HAR1 is conserved, with only two point mutations since the common ancestor of chickens and non-human primates. That doesn't mean every substitution will be deleterious if other aspects of the human lineage have changed. A simple example would be a bigger skull being deleterious, unless accompanied by wider hips for childbearing in the female (which is actually still deleterious in humans, leading to a higher risk for the mother and baby, but compensated for by the advantage of a larger brain). A similar burst of evolution is seen in Lenski's E. coli Long-term Evolution Experiment. There were potentiating mutations, then a tandem repeat, in a sub-population of bacteria under study. Once this occurred, it was followed by a burst of evolution, as multiple optimizing mutations became fixed in the citrate strain.Zachriel_{October 23, 2015
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"And, of course, the 98% similarity refers to 2% of the genomes in question." Right. So in essence, it's basically 1.6% - 1.8% of the entire genome, evodelusionary distinction between DNA and the mythical "junk" DNA notwithstanding.Vy_{October 23, 2015
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Further to Virgil Cain (46), "Then tell us how to test the claim that drift and natural selection didit." Lets start with a serious look at the challenge of the HAR1F. I contend that a minimum of 6 mutations were required to cause the gene to choose the human looping pattern. We know from the fact that it is ultra-conserved between mice and chickens that every single point mutation is deleterious. Any analysis of the 3d configuration of the gene would cause us to conclude that mutation 2, 3, 4 and 5 are deleterious also. This transformation is far above the edge of evolution.bFast_{October 23, 2015
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23
2015
07:25 AM
7
07
25
AM
PDT}

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