Sunday, April 06, 2014

Vincent Torley tries to understand fixation

I'm having an interesting discussion with some creationists. They claimed that the differences between the sequences of the human and chimpanzee genomes could not be explained by evolution. Therefore, it had to be due to design.

I wrote up a little post showing that there were about 44 million differences and that they could be accounted for by our understanding of population genetics and Neutral Theory. What his means is that the creationist explanation has to account for the fact that the vast majority of differences look like what we would expect if most of them were neutral and population genetics is correct. It's not good enough to simply invoke design and magic to explain the differences, you have to account for all the data.

Vincent Torley attempted to understand modern evolution theory. Some of these concepts were quite new to him because he doesn't have much of a biology background. We've had an exchange of posts were he expressed his astonishment and I try to explain evolution. You can find the links at: Vincent Torley apologizes and claims that he is not a liar.

I was thinking that this exchange would wind down but I was wrong. Vincent Torley is having second thoughts about accepting my explanation of Neutral Theory, population genetics, and mutation rates. He posted those second thoughts yesterday at: A Short Post on Fixation. My apologies if this is getting boring for Sandwalk readers but I feel an obligation to try and teach creationists about evolution, if for no other reason than being able to say that I tried.

Torley starts with ....
In a previous post, I asked for some experimental evidence to back up Professor Moran’s claim that 22.4 million nearly neutral alleles could have become fixed in the human genome during the last five million years. Were there any other organisms – bacteria, for instance – exhibiting the fixation rate predicted by evolutionary theory for neutral alleles?

Professor Moran kindly provided an example ...
The example I gave was from Richard Lenski's long-term evolution experiment where his group showed the the rate of fixation of neutral alleles corresponded to their mutation rate as predicted.
Initially, I was very impressed with Lenski’s paper, and I was inclined to think that Professor Moran had proved his point. Scientia locuta est, causa finita est. Or so I thought.

A skeptical biochemist

It was then that I was contacted by a scientist who wrote to me, arguing that the fixation of 22.4 million mutations in the human lineage during the last five million years by a combination of selection and genetic drift was impossible and nonsensical for any population of organisms, especially when we consider the pattern of fixation. Strong words! Who was this mysterious scientist? Readers might be surprised to learn that he’s a biochemist with a very impressive track record named Branko Kozulic, whom I introduced to readers in a previous post, titled, The Edge of Evolution? A short summary of his career achievements is available here. Dr. Kozulic also serves on the editorial board of the Intelligent Design journal Bio-Complexity.

By now I was intrigued. Here was a prominent biochemist disagreeing with the arguments of another prominent biochemist! (Larry Moran is a Professor of Biochemistry at the University of Toronto.) Who was right? I decided to investigate the matter further.
Fair enough. Let's see what Branko Kozulic has to say.

Torley begins by pointing out that there is some confusion about the term "mutation rate" and he's right. Sometimes it refers to the number of mutations per round of replication per nucleotide (or base pair). This value is roughly constant and equals about one mutation every 10 billion base pairs (10-10). Sometimes if refers to the number of mutations per generation or the number of new mutations in every new individual. That value depends on the size of the genome and the number of cell divisions per generation. For humans it's roughly 100 mutations per generation. This can also be expressed as the the number of mutations per base pair per generation. This is called μ (mu) in population genetics.

Theme

Mutation
In addition, you sometimes want to talk about the total number of mutations in a population per generation. That value is the mutation rate times the population size. (It's actually the "effective" population size and it only applies, strictly speaking, to populations that aren't growing or shrinking.)

In the experiment I mentioned (Wielgoss et al., 2011), the authors were testing their results against the predictions of population genetics. The prediction is that the rate of substitution of neutral alleles would be equal to the mutation rate of neutral alleles. They determined that there were 941,000 sites in the E. coli genome where a mutation would be neutral. If the mutation rate per replication per base pair was 10-10 then there would only be 0.0000941 mutations per individual per generation. They sequenced bacteria from the end results of 300,000 generations (multiple cultures at multiple time points). Remember that population genetics predicts that the overall rate of fixation will be equal to the mutation rate per individual per generation (μ).

You would predict 300,000 × 0.0000941 = 28 mutations and the authors found 25 mutations fixed in the population. They conclude that the mutations rate per nucleotide is a bit less than 10-10. (The paper is a bit confusing on this point since they actually found 35 neutral mutations but some were rejected.)

Thus, they have pretty much confirmed that the rate of fixation of neutral alleles in an evolving population corresponds to the mutation rate of neutral alleles per generation.

Vince Torley and his creationist biochemist aren't convinced. Torley says,
In the passage cited above, Professor Moran referred to Lenski’s long term evolution experiment:
If the fixation rate of neutral alleles was equal to the mutation rate then (as predicted by population genetics) then this should be observable in the experiment run by Lenski (now 60,000 generations).
Did you notice the reference to “the mutation rate”? As we saw above, there are three mutation rates. In chapter two of his book, Population Genetics: A Concise Guide (Johns Hopkins University Press, Baltimore, second edition, 2004), which I’ve been recently perusing, evolutionary biologist John Gillespie repeatedly refers to the mutation rate for a given locus. And in population genetics, altering the numerical relationship between the mutation rate and the (effective) population size can lead to dramatically different results. For example Gillespie, in the textbook referred to above, writes:
If 1/u << N, the time scale of mutation is much less than drift, leading to a population with many unique alleles. If N << 1/u, the time scale of drift is shorter, leading to a population devoid of variation. (2004, p. 31)


Professor Moran is kindly requested to state whether he agrees with this statement, and if not, to provide some references to support his views.
I admit that I should have specifically said "the mutation rate per generation at neutral sites." If that's the important criticism, then I concede that I could have been more clear about what the results were showing.

As for the question, I can't really answer it because I don't know what John Gillespie means by the mutation rate (μ). If it's 10-10 per bp per generation then 1/μ equals 1010, or 10 billion. There are very few population sizes that are larger than 10 billion. If Gillespie means something like 10-4 mutations per generation (E. coli) or 100 mutations per generation (Homo sapiens) then I agree with him, although it seems a bit silly to be talking about a population size of 1/100 (1/μ) in the case of humans.
In the passage cited above, Professor Moran referred to Lenski’s results with E. coli bacteria: a mere 35 fixations after 60,000 generations. That’s about 0.0006 fixation events per generation, for the population as a whole.

By contrast, the fixation rate which Professor Moran claims for human beings (130 per generation) was 200,000 times faster than the rate which Lenski observed for his bacteria. That’s a difference of over five orders of magnitude! This difference in fixation rates requires an explanation. Do we agree on this point, Professor Moran?
I suppose I should have realized that Vincent Torley would not read and/or understand the paper I cited. Maybe I should have explained the result more thoroughly if I want creationists to understand modern evolutionary theory. I hope my explanation in this post helps.

That explains why Vincent Torley had trouble understanding the result. It doesn't explain why "prominent biochemist," Branko Kozulic, who serves on the editorial board of the Intelligent Design journal Bio-Complexity, doesn't understand the scientific literature and evolutionary theory.
Finding the cause that explains the pattern

Now, clearly something was responsible for producing the 22.4 million neutral alleles that distinguish the human lineage from that of chimpanzees. Nobody disputes that. What Dr. Kozulic rejects is the idea that all these mutations could have been fixed by any undirected process (e.g. random mutations plus natural selection, or plus genetic drift), within the time available, especially when we consider the pattern of fixed mutations.
I guess Dr. Kozulic will have to contact me directly and let me know which part of evolutionary theory he doesn't get and which data he rejects.

Isn't it surprising that so many creationists don't understand evolution?


Wielgoss, S., Barrick, J. E., Tenaillon, O., Cruveiller, S., Chane-Woon-Ming, B., Médigue, C., Lenski, R. E. and D. Schneider (2011) Mutation rate inferred from synonymous substitutions in a long-term evolution experiment with Escherichia coli. G3: Genes, Genomes, Genetics 1, 183-186. [doi: 10.1534/g3.111.000406]

47 comments :

  1. I think John Gillespie was using mutation rates per locus (so multiples of the per-base rate). His 1/μ is the reciprocal of that number, not the reciprocal of the total number of mutations per generation in the a genome.

    Reading the comments after Torley's new post is appalling. Virtually all of the commenters get things badly wrong. Many assume that the point under discussion is how one accounts for adaptive changes. They do not get it that the 44 million changes are all the changes, adaptive, deletrious, and neutral, and that most of those are neutral. Torley somehow thinks that it is hard to explain how there could be that many neutral substitutions in the time allowed. One poster who has been opposed to creationist arguments (wd400) gets it right, and does a calculation much like Larry's, getting a very similar answer.

    Bornagain77 posts masses of stuff irrelevant to the question at hand, as is ba77's wont.

    One poster asks about polymerase errors. Polymerase errors may be relevant if we are detecting mutations -- they can give the false appearance of a change. But when a putative mutant is found, the experiment detecting it can easily be rechecked, so that there is no real need to worry about rates of polymerase errors. The actual mutations may or may not have been caused by the inaccuracy of a polymerase, but that is irrelevant, as the empirical rates of mutation are being measured.

    Finally commenter Charles tries to check the units in the wd400/Moran calculation and gets it wrong. Charles says:

    So I understand how you get “30″. But I don’t see how you get “mutations”:

    basepairs/generation * mutations/basepair/generation * generations

    which resolves to:

    basepairs/generation * mutations-generation/basepair * generations

    basepairs/generation cancels -generations/basepair leaving “mutation-generations”, not simply “mutations”

    This matters because if the units are incorrect, then the calculation is incorrect, or incorrectly explained or stated.


    Sorry, Charley. I get that

    basepairs/generation * mutations/basepair/generation * generations

    resolving to

    mutations / generation.

    How did Charley get anything else?

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    1. Actually, to answer my own question, what Charley might have done is mistakenly assume that mutations/basepair/generation is mutations/(basepair/generation) which would be mutations*generations/basepair
      whereas it is really (mutations/basepair)/generation which would be mutations/(basepair*generation). So the ambiguity of the expression a/b/c seems to have led Charley astray.

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    2. True. I have the 1998 edition of Gillespie's textbook, where he defines the mutation rate as follows:

      "The probability that a mutation appears in a gamete at the locus under study is u, which is called the mutation rate even though mutation probability would be a more accurate term."

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  2. Wait wait. Isn't the most insane part of the below simply that they are ignoring the fact that the human 2N genome is 1000+ times bigger than the typical E. coli genome, and thus would accumulate thousands of times more mutations even if neutral mutation rates were equal? Then they ignore that, unlike E. coli, most of the human genome is junk and therefore a much greater proportion of random mutations will be neutral.

    ==================
    In the passage cited above, Professor Moran referred to Lenski’s results with E. coli bacteria: a mere 35 fixations after 60,000 generations. That’s about 0.0006 fixation events per generation, for the population as a whole.

    By contrast, the fixation rate which Professor Moran claims for human beings (130 per generation) was 200,000 times faster than the rate which Lenski observed for his bacteria. That’s a difference of over five orders of magnitude! This difference in fixation rates requires an explanation. Do we agree on this point, Professor Moran?
    ==================

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    1. @NickM
      No, the most insane part is that they sincerely believe they have caught Larry with his trousers down, rather than realising they made a silly mistake...again.

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    2. I'm not sure that "insane" isn't dignifying this too much. Something as dramatic as insanity isn't needed for an explanation. It's more prosaic - just a bunch of people who can't manage to get the math right, repeatedly.

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    3. Then they ignore that, unlike E. coli, most of the human genome is junk and therefore a much greater proportion of random mutations will be neutral

      Ah, but they don't believe that! So despite 60-130 mutations occuring per zygote without apparent harm, they can't actually be occurring at that rate!

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    4. Either that, or they're all being personally created by Baby Jesus, as part of his ongoing Intelligent Desigining project. I wonder, then, while we don't see every one of them getting fixed in the genome.

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    5. This is most peculiar. Commenter wd400 over at UD (who deserves a medal) has pointed out the flaw of ignoring the enormous difference in genome size between humans and E. coli. To this Vincent Torley answered:
      Hi wd400, Thank you for your post. I had anticipated your criticism: [...] I was waiting for Professor Moran to come out and say something like that. To my surprise, he didn’t.
      To which wd400 replied:
      Then why did you not correct your error in conflating the E coli results and human-chimp differences?
      Good question.

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    6. And Larry, in effect, does say that. Just not so directly that Torley is not able to somehow miss it. If Larry tailored his writing to the comprehension level of the average IDiot, this would be a very tedious blog.

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    7. Torley might also consider that a 'generation' for E.Coli involves one genome replication. For a human it averages out at a couple of hundred.

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    8. "Then why did you not correct your error in conflating the E coli results and human-chimp differences?"

      It is always the human-chimp issue. Those folks just do NOT want to admit that they share an ancestor with chimps. They love hyping any 'new discovery' that decreases the chimp-human genome identity, but they will never apply the same criteria to creatures that they claim/allow are related via descent. Golly, I wonder why...

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  3. A side note: I cringe whenever this cargo-cult dummy called Bio-Complexity is referred to as a "journal". How many issues of Bio-C have appeared so far? How many of them appear yearly? How many research articles has this "journal" ever published? Why does, say, a stupid exercise in numerology (Castro Chavez 2012) qualify as a research paper? Was it peer-reviewed? By whom (if not a panel of village idiots)? What sort of impact factor does Bio-C have (or may possibly have in the most distant optimistically foreseeable future)?

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    1. You have to understand the creationist mindset.

      Random creationist with a Ph. D.? No, world's expert.

      Editor of a "journal" with more editors than papers published? Mark of distinction.

      Mediocre philosopher of no repute at all who babbles endlessly about things he doesn't understand? Worth publishing over and over and over.

      Professor of biochem at top Canadian university? Just another dogmatic Darwinist.

      See how creationists think?

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    2. Was it peer-reviewed? By whom (if not a panel of village idiots)?

      Some questions just answer themselves. A panel of IDiots would certainly meet the strict definition of "peers."

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  4. Torley has approximately 3 'pet' scientists: Axe, Gauger and Kozulic. If they say anything at all, Torley sits up. Meanwhile the opinions of the remainder of the scientific community are as the whisperings of a breeze in the tree-tops.

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    1. Torley: It was then that I was contacted by a scientist who wrote to me...

      After such an introduction one might think that the scientist was a sort of disinterested good Samaritan -- a total stranger who by a stroke of luck came to Torley's rescue when Larry Moran had left him badly bruised and half-conscious at the roadside.

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  5. "What Dr. Kozulic rejects is the idea that all these mutations could have been fixed by any undirected process (e.g. random mutations plus natural selection, or plus genetic drift), within the time available, especially when we consider the pattern of fixed mutations."

    So, the AMAZING astounding DR. Kozulic rejects it. Does he explain WHY he rejects it? It doesn't look like it. He just does.

    'Living is easy with eyes closed...'

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  6. Torley and Kozulic have a new (giant) post up. I honestly now can't parse their point, but if you're going to reply, maybe starting by defining some simple terms like population, fixation and variation. They are using "genetics words", but the relationship set out in post makes me think they don't actually comprehend. "

    One question I have--is the assumption that all the identified genetic differences between (what I assume is one reference human genome) and one chimpanzee genome are fixed in both populations actually valid?

    "Since the effective human population size N was 10,000 or less during most of the Paleolithic era, it would follow that N << 1/μ, "leading to a population devoid of variation," as Gillespie states. This runs completely contrary to the scenario Professor Moran is proposing: he maintains that there was sufficient variation to fix 100 mutations in each generation, from five million years ago to the present.)"

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    1. One question I have--is the assumption that all the identified genetic differences between (what I assume is one reference human genome) and one chimpanzee genome are fixed in both populations actually valid?

      Yes, for the most part. That is, if you picked a new random chimp and a new random human to compare, you would find that the great majority of the differences found in the published genomes would still be in the new genomes. They would match in a few places where the published genomes didn't and they would differ in a few places where the published genomes matched. (For values of "a few" probably in the thousands, but still a tiny percentage of the published difference.)

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    2. I do wonder what they imagine would lead to a population devoid of variation, starting from a population with lots of variation. Lots of fixations, perhaps? And they still haven't come to grips with the most basic result of neutral theory, that fixation rate doesn't vary with population size.

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    3. Given the vital importance of population genetics models, we hope Professor Moran will answer all of the above questions. Since he is a biochemist, he can hardly be expected to know all the intricacies of population genetics (and neither would we claim to possess such knowledge), so we would encourage him to consult the textbooks and ask for assistance from his colleagues.

      Hee hee! Non-pop-geneticists Torley and Kozulic have uncovered evolution's most embarrasing secret. It's been known for years, as he'll find out when he consults the experts and they shuffle and discover prior engagements. Or ....

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    4. They are in full Gish gallop mode, dropping plenty of red herrings as they ride along. For example:

      Is Professor Moran a Darwinist, protestations to the contrary notwithstanding?

      (followed by a brand-new definition of "Darwinism").

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    5. I think that "fixation" is the wrong emphasis here. What we have is not definite evidence that 22 million sites are fixed one way in humans and another in chimps. It is that the human reference sequence differs by at least that much from the chimp reference sequence. If there are neutral mutations occurring in both lineages, this can be accounted for if we have a mutation rate that is sufficiently high that along the genealogy of genes going from human down to the common ancestor, and a bit deeper to account for coalescence time, and then back up to chimp, there are the requisite number of mutations.

      They need not be fixed, just present in those genomes. Furthermore, they can also even overlie each other (our computations of distances correct for that, though there will not be many of those events in this case).

      Larry's computation was formulated in terms of "fixation" as were the UD objections. But the computation is the same if one does it in terms of the difference between reference genomes: change at a rate μ per generation in each lineage.

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    6. I just read the post by Torley and Kozulic. I'd love to continue with trying to teach these IDiots some basic evolutionary biology but, frankly, it seems impossible. It would take me ages to wade through that post to try and figure out where they are going wrong.

      Even something as simple as "mutation rate" seems to elude them in spite of the fact I've posted several articles on that topic.

      Has anyone figured out whether there's a point to their objections? I don't see it. The whole issue of population size seems irrelevant to me. Don't they realize that it cancels out of the equation?

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    7. This is so Torley:

      "Hi Nick and wd400,

      Thank you both for your comments. May I remind you that Branko Kozulic, the co-author of this post, is a biochemist who has published about 30 scientific papers and who is the inventor or co-inventor of numerous Patents (18 of which are issued in the USA). He is also well-read in the field of population genetics. "

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    8. He should have thanked both "wd400" and Nick Matzke for their heroic attempts to set him straight. It wasn't their fault that Torley had no clue what the heck they were talking about, and Branko "Numerous Patents" Kozulić, PhD, was engaged elsewhere.

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    9. UD poster 'Andre' has noted that if you add in insertions, deletions and copy number variation, you get much more difference (a fact that is suppressed by the Great Darwinist Conspiracy). Darwinists the world over are stumped. Because of course if you can add or remove multiple bases with each mutational event, 5 million years is nowhere near enough to ... oh hang on, forget I even mentioned it.

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    10. At least one IDiot, by name of TruthCrusader, tries to help Torley out:

      Torley, your intentions are noble, but I suggest you walk away from this issue and pretend it never happened.

      The evidence for evolution on the whole is limited, but population genetics and neutral drift have been established experimentally and mathematically. You, or whoever is advising you has made some basic errors in the above.


      I understand Larry not wanting to continue this increasingly pointless correspondence with Torley. But I hope he'll at least draw attention to this latest UD post with a post of his own. It deserved to be carved in granite as a monument to IDiocy.

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    11. Holy shit! Even Sal Cordova is telling Torley he's way off (comment #39):

      Dr. Torley,

      I’m sorry I must sympathize with Nick Matzke (puke) and WD400 objections, but I feel some obligation to ask you to at least pause and reconsider.

      The YEC Creationist genetics model, Mendel’s Account agrees to great degree with Larry Moran, Nick Matzke, and WD400....


      Hmm, that might actually be the first good reason to doubt whether neutral theory is correct....

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    12. Branko "Numerous Patents" Kozulić, PhD

      May his name never appear without the portion in quotes. :)

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    13. Yeah, my head exploded when Sal Cordova came down on my side.

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  7. This comment has been removed by the author.

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  8. Branko "Numerous Patents" Kozulić has now made a new post at UD worrying about the issue of fixation.

    This is the third time I have said this. No one has paid attention. I know what I am talking about, folks.

    Fixation is not the issue. The issue is whether measured mutation rates, plus the fact that most of those mutations are neutral, fits with the observed degree of difference between the human and chimpanzee reference genomes. It does fit.

    But the observation that we see a G at a position in the human genome, and a C at the same position in the chimpanzee genome, does not mean that all humans have a G there, and all chimps have a C there.

    "Fixation" is not the issue. For some reason you all are fixated on fixation.

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    1. You are absolutely right about fixation not really being the issue here, though "Numerous Patents" manages to be completely wrong about fixation as well.

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  9. Professor Moran,

    Are you suggesting this modest degree of nucleotide divergence is sufficient to explain the extensive phenotypic differences between chimpanzee and human species?

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    1. I don't know what "modest degree" you are referring to. Of the 44 million nucleotide differences I assume that more than 99% of them are neutral. I would guess that most of the observable phenotypic differences are probably due to less than 1000 actual differences in nucleotide sequences. .

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    2. I'm referring to 1.5% difference in protein-coding loci between the species.

      Are you implying that less than a 1000 of actual nucleotide sequences can explain the vast phenotypic differences between the two species? What are your basing it on? I'd like to see some evidence, please professor Moran.

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    3. There is no 1.5% difference in protein-coding loci between the species. It's actually around 0.5% (if, as is not completely clear, you mean the percent difference of homologous sites in protein-coding exons).

      Larry is basing his 1000 differences on a guess, as he said. It's hard to find evidence for a guess. Do you have evidence for your guess, if you have one, or against Larry's?

      And if you think the genetic differences don't explain the phenotypic differences, what do you think does explain them?

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  10. No. I'm going to guess that Larry's guess is just as good as anybody's guess. This is what your science is all about

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  11. Professor Moran,
    Some studies seem to imply that "Junk DNA" either makes human different from chimpanzees or as well as the genome differences.

    "Junk DNA' defines differences between humans and chimps"

    "For years, scientists believed the vast phenotypic differences between humans and chimpanzees would be easily explained -- the two species must have significantly different genetic makeups. However, when their genomes were later sequenced, researchers were surprised to learn that the DNA sequences of human and chimpanzee genes are nearly identical. What then is responsible for the many morphological and behavioral differences between the two species?

    Researchers at the Georgia Institute of Technology have now determined that the insertion and deletion of large pieces of DNA near genes are highly variable between humans and chimpanzees and may account for major differences between the two species.

    The research team lead by Georgia Tech Professor of Biology John McDonald has verified that while the DNA sequence of genes between humans and chimpanzees is nearly identical, there are large genomic "gaps" in areas adjacent to genes that can affect the extent to which genes are "turned on" and "turned off." The research shows that these genomic "gaps" between the two species are predominantly due to the insertion or deletion (INDEL) of viral-like sequences called retrotransposons that are known to comprise about half of the genomes of both species. The findings are reported in the most recent issue of the online, open-access journal Mobile DNA.

    "These genetic gaps have primarily been caused by the activity of retroviral-like transposable element sequences," said McDonald. "Transposable elements were once considered 'junk DNA' with little or no function. Now it appears that they may be one of the major reasons why we are so different from chimpanzees."

    McDonald's research team, composed of graduate students Nalini Polavarapu, Gaurav Arora and Vinay Mittal, examined the genomic gaps in both species and determined that they are significantly correlated with differences in gene expression reported previously by researchers at the Max Plank Institute for Evolutionary Anthropology in Germany.

    "Our findings are generally consistent with the notion that the morphological and behavioral differences between humans and chimpanzees are predominately due to differences in the regulation of genes rather than to differences in the sequence of the genes themselves," said McDonald.

    The current analysis of the genetic differences between humans and chimpanzees was motivated by the group's previously published findings (2009) that the higher propensity for cancer in humans vs. chimpanzees may have been a by-product of selection for increased brain size in humans.
    Story Source:
    Journal Reference:
    1.Nalini Polavarapu, Gaurav Arora, Vinay K Mittal, John F McDonald. Characterization and potential functional significance of human-chimpanzee large INDEL variation. Mobile DNA, 2011; 2: 13 DOI: 10.1186/1759-8753-2-13"

    Original Publication

    Characterization and potential functional significance of human-chimpanzee large INDEL variation

    Would you care to comment?


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    1. Some studies seem to imply that "Junk DNA" either makes human different from chimpanzees or as well as the genome differences.

      It's junk syntax. The sentence makes no sense as it stands. Would you care to rephrase it?

      As for regulatory DNA, it isn't junk. A lot of non-coding DNA isn't junk. Still, most of the typical eukaryote genome (some 90% in humans or chimps) is junk. What's so difficult to understand here?

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    2. Are you professor Moran?

      Where I come from it is impolite to answer when one is not asked to do so especially for someone who is the host. Would you care to sod off mate!

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    3. He doesn't need to be professor Moran to give you an answer. The answer he gives is correct too.

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  12. Also, I've not been able to find any reliable evidence as to what the genome of the ancestor-that human and chimpanzee diverged from-consisted of? What evidence is there to support your notion? Is it based on some calculations I'm not familiar with? Or, is it another guess of yours?

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    1. That's just straight up dumb. A general observation is that our genome is very similar to the chimp genome, so is our anatomy. It is less similar to gorillas, and even less similar to orangutans and so on. This implies a genealogical relationship through change and diversification over time. We have a fossil record that implies we have diverged about 5-7 million years ago from a common ancestor.
      Taking this evidence at face value we can make a number of predictions, which, if we test them, gives us very good reasons to conclude that we really did share a common ancestor.
      One among them is that if we really did share such an ancestor, the number of genetic differences should roughly match how many would have accumulated over that 5-7 million year period. There are also many significant predictions about the specific patterns we should find, that most of the changes should have happened in junk regions, that some mutations are more likely than others due to well-known biochemical events (transition vs transversion bias and all that). That gene duplications should be more frequent at sites more prone to unequal crossing over due to homologous recombination. Given this, if our genomes really did evolve to be slightly different from a common ancestor, we should expect to find a higher frequency of such mutations, at sites that would be expected to be more prone to such mutations, for simple biochemical reasons. All these predictions turn out to be true, the simplest explanation for this fact is that we share a common ancestor approximately 5-7 million years ago.

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