quote:Originally posted by Mister Pamboli: Interesting stuff. Largely irrelevant, I suspect, but interesting.
I'd be interested in how the graph was arrived at - criteria for defining benefit, how mutations were observed, in what species, that sort of thing.
How would it class say a mutation to greater body weight by the increased adiposity in a mammal? Detrimental - making escape from predators more difficult? Beneficial - better able to survive a harsh winter? Or beneficial today but detrimental tomorrow?
I'm skeptical about graphing a qualitative judgement.
Mr. P: I agree, the graph is interesting. Like you, I would like to know how it was derived.
OTOH, I've always used the following "rule of thumb" in making a relatively objective determination of what constitutes a deleterious, neutral, or beneficial mutation at the gene level:
1. neutral mutation: A neutral mutation would be a change in nucleotide triplet(s) that: a) took place in an intron, and hence had no effect, b) eliminated or modified a redundant codon (again, no effect), or c) produced an alternative form of a gene that made no difference on the efficiency or form of the final product (ex: if the third base in the TCT codon for serine is changed to any one of the other three bases, serine will still be encoded). Since something on the order of 97% of the genome doesn't actually code for anything at all, neutral mutations would tend to be the rule, rather than the exception.
2. deleterious mutation: A deleterious mutation would be a mutation occurring in an exon, an error in the pre-mRNA splicing function, or a translocation that caused loss of function or (damage to) the final protein product. This type of error, if occuring in a somatic cell, will either kill the cell or initiate a tumor. In a germline cell, it will most likely have a negative fitness effect on the zygote.
3. beneficial mutation: A beneficial mutation is a mutation in an exon, or (rarely) a translocation, where the resultant product is either a) more efficient and hence able to perform its metabolic function at lower energy cost; b) create novel genes which allow new opportunties; or c) allow for a new cascade which permits either elimination of now-redundant genes or the co-option of existing cascades to new products.
It should be noted that my definitions are purely genetic. Whereas there are implications in each case for allelic frequency and organism fitness (and ultimately population fitness), the definitions deliberately do NOT discuss the ultimate expression of these changes in an organism. The reason I do it like this is because, once you start talking fitness, the concept can only be empirically understood in the context of the complete environment (biotic and abiotic) in which the particular organism lives. In short, a beneficial mutation in terms of fitness is one that increases the reproductive success of an individual organism in their current environment. A deleterious mutation does the opposite. Worse, any change in the environment may cause an allele that is beneficial to turn deleterious - without any further actual mutation.
This is the bit creationists don't seem to grasp. An individual organism's adaptation to its current environment, and by extension the population of which this individual is a part, is by definition the result of beneficial alleles. If it wasn't, NS would long ago have ruthlessly eliminated it.
For any discussion of mutation rates, fitness, fixation rates, mutational load, etc, etc, to be relevant, it must be done IN CONTEXT of the particular organism and its specific environment. Otherwise you're just playing hypothetical construct and semantic games rather than reality.
quote:Originally posted by Quetzal: 1. neutral mutation: A neutral mutation would be a change in nucleotide triplet(s) that: a) took place in an intron, and hence had no effect, b) eliminated or modified a redundant codon (again, no effect), or c) produced an alternative form of a gene that made no difference on the efficiency or form of the final product (ex: if the third base in the TCT codon for serine is changed to any one of the other three bases, serine will still be encoded). Since something on the order of 97% of the genome doesn't actually code for anything at all, neutral mutations would tend to be the rule, rather than the exception.
One more for the neutrals. A nucleotide substitution that changes the amino acid coded for. If this amino acid makes no difference to the function of the protein, & it looks like a high percentage of any particular protein doesn't mind which amino acid is at a particular location in the sequence, & will therefore be neutral.
------------------ Occam's razor is not for shaving with.
Mark: Yep, I agree. Knew I didn't list all of the possibilities... There are multiple ways for amino acids to code for a given protein, so anything that didn't change the final product would be neutral, by definition.
[This message has been edited by Quetzal, 02-27-2002]
quote:Scott, I would specifically like to see you address the errors I listed in the summary that I've pasted below. Comments from others also welcome.
· Mistakenly claiming that Haldane based his substitution estimate on the observation of peppered moths (Haldane did the opposite, see Haldane 1957, p521)
You sure like p.521. In my copy of Haldane's 1957 paper, on p.521. there is nothing at all about what he based his estimate on. You should notice that on the first page, p. 511, Haldane expends some time explaining the observations seen in peppered moths, and how he will attempt to estimate "the effect of natural selection in depressing the fitness of a species." I committed an error of omission, and should have included the fact that he considered some Drosophila experiments and such as well. However, your claim that he "did the opposite" seems to have no basis in reality.
quote: · Implying that a large population is a bad assumption for evolution (Haldane did the opposite; see Haldane 1960, p351)
You are recklessly misrepresenting me. I claimed no such thing. Quoting from my solid refutation of your original bombast, the times I mentioned population size or Haldane's use of it:
"…premised on unrealistic assumptions (such a s a constant population size), made using observations of phenotypic variation in Peppered moths."
"Williams writes "entire population" for a reason - the connotation of "entire population" is that the population is extremely large, such as the human population of today. This is an unreasonable allusion."
I did, however, say that a constant population size is an unrealistic assumption. But 'constant' does not mean 'large.'
quote: · Claiming that a wild-type allele can still persist in a population even after its mutant allele reaches 100% fixation in the same population!
I see you have trouble with what fixation means, or perhaps are unaware of what a dominat allele is. If 100% of a population has a DOMINANT allele, they can still be heterozygous - the individuals can still have a recessive allele for the same locus, and yet they all would exhibit the dominant phenotype.
quote: · Because of his previous error, reaches the erroneous conclusion that a dominate[sic] allele does not need to be replaced, which implies it has no reproductive cost.
More misrepresentation. If the members of a population are homozygous for the wild type, then the replacement of one allele with a dominant mutant will incur your beloved cost. However, the impact of the cost - under realistic assumptions - is not what you continue to claim it is.
quote: · Claiming that a beneficial mutation will spread through a population in a sexual species "as well" as it would in an asexual species, even given an environment free of deleterious mutations. I wonder if there is even one population geneticist in the world who would agree with him.
I really wish that you would put a lid on your shameless attempts at revisionism. That or learn some common colloquial english:
"If there were no deleterious mutations, then beneficial mutations would by necessity spread throughout a sexual species as well, since those are the only mutations available."
IN RESPONSE TO YOUR HYPOTHETICAL SCENARIO:
"Let's assume an environment where there are no deleterious mutations, just beneficial ones."
I am unsure whether you are purposely trying to be inflammatory, if you simply ignore the context, or that your english really is that poor. Either way, you are not doing your credibility much good.
quote: · Claims that Wu's study dos *not* assume human/simian ancestry in its determination of the substitution rate.
That is a fact. I already provided the source for their comparison's - OLD WORLD monkey genes. You previously stated:
"The authors of the genetics study are arriving at their estimate of 10 generations by first assuming that man and ape share a common ancestor."
Old world monkeys are not apes. Please retract your erroneous claims and your attempt to rewrite your original error. That or provide the exact quotations from their paper pointing out their assumption of human-ape ancestry - as per your ORIGINAL claim - and how it was pivotal in their mutation rate analyses. Wu's group assumes evolution, of course. There is good reason to.
quote: · Re-visits circular reasoning by asking why 620,000 substitutions from the Keightley study is not sufficient to account for simian/human shared ancestry, given the 500,000 he believes Remine set as a minimum.
ReMine did imply that 500,000 is a minimum. Surely, you are familiar with his clumsy prose about making a 'sapien out of a simian'? Of course, here again we have your conundrum - you endearlingly refer the the E-W and K paper, which assumes not just evolution, but human-ape ancestry, and yet you call it 'circular reasoning' to invite you to discuss additional implications of their study! If you think it circular to look at one aspect, you should similarly dismiss the others. That is, if you are to try to appear unbiased and not employ double standards.
quote: The problem is, the Keightley study also arrives at its numbers by first assuming simian/human shared ancestry. Thus, it is circular to use their numbers when contrasting against any arbitrary guestimate of mutations that would separate simian/man.
Well, lets hope that you stop referring to their flawed circular reasoning in your repeated allusions to their deleterious mutation rate.
[This message has been edited by SLP2, 02-27-2002]
quote:Dr Page spends quite a bit of energy in his reply focusing on my “lack of training” in “the biological sciences”. I have never claimed to be an “expert” in “the biological sciences”, but I have read a wealth of material on the subject (particularly genetics) and am quite capable of identifying obvious inconsistencies with evolution. I should note that Dr Page has admitted to me in the past that population genetics is not his area of expertise (you'll soon see this is the case, in glaring fashion), yet he insists on making a formal education on the topic an issue.
From SLP`s web page: [QUOTE]PUBLICATIONS
Goodman, M., Czelusniak, J., Page, S.L., and Meireles, C. Where DNA Sequences Place Homo sapiens in a Phylogenetic Classification of Primates. In: Humanity from African Naissance to Coming Millenia. P.V. Tobias, (ed.). Firenze University Press, Florence, Italy, pp. 279-289. 2001.
Goodman, M., McConkey, E, and Page, S.L. Reconstructing Human Evolution in the Age of Genomic Exploration. In: New Perspectives in Primate Evolution & Behavior, B. Sherwood, (ed.),Westbury Publishing Co. in press.
Page, S.L., and Goodman, M. Catarrhine Phylogeny: Noncoding DNA Evidence for a Diphyletic Origin of the Mangabeys and for a Human-Chimp Clade. Mol Phylogenet Evol. 2001 Jan;18(1):14-25
Page, S.L., Chiu, C-H., and Goodman, M. Molecular phylogeny of Old World monkeys (Cercopithecidae) as inferred from gamma-globin DNA sequences. Mol Phylogenet Evol. 1999 Nov;13(2):348-59.
Chaves, R., Sampaio, I., Schneider, M. P., Schneider, H., Page, S. L., and Goodman, M. The place of Callimico goeldii in the callitrichine phylogenetic tree: evidence from von Willebrand factor gene (vWF) intron II sequences. Mol Phylogenet Evol. 1999 Nov;13(2):392-404.
Goodman, M., Page, S.L., Meireles, C.M., and Czelusniak, J. Primate phylogeny and classification elucidated at the molecular level. In: Evolutionary Theory and Processes: Modern Perspectives, S.P. Wasser (ed.), Kluwer Academic Publishers b.v., Dordrecht, The Netherlands, pp. 193-212, 1999.
Goodman, M., Porter, C.A., Czelusniak, J., Page, S.L., Schneider, H., Shoshani, J., Gunnell, G., and Groves, C.P. Toward a phylogenetic classification of primates based on DNA evidence complemented by fossil evidence. Mol. Phylogenet. & Evol. 9:585-598, 1998.
Meireles, C.M., Czelusniak, J., Page, S.L., Gumucio, D.L., Schneider, M.P.C., and Goodman, M. Testing a model of the fetal recruitment of gamma-globin genes in callitrichine New World monkeys. Blood Cells, Molecules, and Diseases 24:491, 1998.
Porter, C.A., Page, S.L., Czelusniak, J.C., Schneider, H., Schneider, M.P.C., Sampaio, I., and Goodman, M. Phylogeny and evolution of selected primates as determined by sequences of the epsilon-globin locus and 5' flanking regions. International Journal of Primatology 18:261-295, 1997. [/b][/QUOTE]
If you don`t mind me asking what published papers have you authored on evolution? Also a lot of these papers seem to have to do with the genetics of a population....
Let's be fair, though. Fred hasn't been here in a couple months, and any delay likely means he simply isn't checking this site any more. We all of us cycle in and out of different discussion boards, there's no crime in that.
Maybe someone would like to send Fred a note that there's been a couple posts to a thread he started here.
Also, do you really want to call it the concluding post? I've never seen one of those in this debate.
This is only my opinion, but I think the discussion between you and Scott becomes impenetrable to anyone but yourselves when you focus so much attention on the other person rather than the actual issues. There were a few earlier posts that you weren't here for urging Scott to stay focused on the technical issues.
quote:do you really want to call it the concluding post? I've never seen one of those in this debate.
Good point. My intentions that it will be the concluding post may be short-sighted indeed!
quote:This is only my opinion, but I think the discussion between you and Scott becomes impenetrable to anyone but yourselves when you focus so much attention on the other person rather than the actual issues. There were a few earlier posts that you weren't here for urging Scott to stay focused on the technical issues.
Thanks, I did see your comments. However, I do think our latest debate does invite outside dialog. For example, Page’s first citation was a backfire, as it is clearly evidence against evolution. This is an exciting point for creationists and should be enticing for evolutionists to try to challenge.
Only in the wacky world of creationism does a research paper that provides evidence for the benefits of sexual reproduction and another one that demonstrates the failure of one of the linchpins of antievolutinism become evidence against evolution.
Fred's latest argument via repeated assertion - hardly a refutation of anything - will be dealt with in due time.
Here again is the relevant passage from the citation Page thought supported his cause:
The genomic deleterious mutation rate in humans was previously estimated to be at least 1.6 on the basis of an estimate that 38% of amino acid mutations are deleterious. The genomic deleterious mutation rate is likely much larger given our estimate that 80% of amino acid mutations are deleterious and given that it does not include deleterious mutations in noncoding regions, which may be quite common. [emphasis mine]
A straight extrapolation yields a mutation rate of U=3.4. Using a Poisson distribution from statistics 101, the required offspring per breeding couple to produce a pair without a new defect is B=2e^u. Plug in the mutation rate, and you end up with a requirement of 60 offspring per breeding couple!!! This number is actually extremely conservative as many other factors are ignored. When more realistic (and still conservative) numbers are used, the number exceeds 200!
Evolutionists have no explanation for this. Creationists do. My recommendation to evolutionists? Stop determining the mutation rate by comparing simians to humans. The number of nucleotide differences are clearly demonstrating that we are not related.
A response to the rebuttal posted by Fred Williams at his website phrased in the same manner would not be acceptable here at the EvC Forum. For this discussion only I will rewrite any posts that violate forum guidelines. Here is a rewrite of Fred's rebuttal:
This is my concluding response to Dr Page's latest rebuttal. Dr Page's latest comments appear in maroon, my response in black, and any original comments from a prior post in blue.
Hairsplitting and semantics games
In my opening rebuttal, I mistakenly used “ape” instead of “monkey” when I wrote “The authors of the genetics study are arriving at their estimate of 10 generations by first assuming that man and ape share a common ancestor”.Page made note of this in his first rebuttal: “Chimpanzees ('ape') are not Old World monkeys”. I instead used the term “simian” (a more encompassing term). Note Page’s argument when he writes:
“First, Williams refers to Old World monkeys as apes in his original rebuttal. I point out that Old World monkeys are not apes. Williams then re-writes his original 'challenge' and presents it as he did above, using the word 'simian' instead of ape. Old World monkeys are, at least by laymen, considered to be simians. Williams has reworded his claim so as to prevent it from being rendered moot and shown to be inaccurate, and now bases his 'new' argument on this reformulated claim.”
I did not “re-formulate” my argument. I simply changed one word, ape, to “simian”. Whether or not the simian used in the study was an ape or a monkey has no bearing on whether or not your use of the citation was circular reasoning.”
Next, Dr. Page calls my use of the term “analogous” instead of “homologous” a “fundamental error”. This is quite an exaggeration. From a creationist perspective the sequences could be called analogous because creationists do not believe “simians” are related to humans via decent. Nevertheless, to speak in evolutionary terms “homologous” would indeed be the appropriate term.
Equivocation of the word "evolution"
I originally wrote:
This fixation rate is in stark contrast to Haldane's calculation of 300 generations, so that's why Dr. Page cites this study. But Haldane's cost argument is a mathematical model that is not based on the assumption that simian/man ancestry (or any other form of large-scale evolution) is true.
Page replies with:
“Williams is incorrect. Haldane assumed evolution when he formulated his model. If Haldane had simply set out to produce a purely mathematical model, devoid of evolutionary assumptions and constraints, as Williams suggests (insists?), then one should be curious as to why the formulae employed by Haldane contain a variable called the selection coefficient. For, what good is the concept of selection except in an evolutionary context?”
Here Dr. Page is equivocating on the definition of ‘evolution’ (see my article on this). In my preceding comment that he responded to, I explicitly stated that Haldane’s model is not based on the assumption that simian/man ancestry (or any other form of large-scale evolution) is true. I am not referring to population genetics (also called evolutionary biology) where concepts such as selection coefficients are used. Creationists have no problem with natural selection, and in fact proposed selection before Darwin1. So I ask Dr. Page yet again, to provide any evidence whatsoever that Haldane’s model requiresthe assumption that simian/man ancestry (or any other form of large-scale evolution) is true.
Red Herrings Galore
Following are several Red Herrings that have nothing to do with our debate:
Williams' continued claims that Haldane's model contradicts human/ape ancestry is premised on his personal disbelief that 1667 fixed beneficial mutations can account for human evolution from an ape-like ancestor. Willaims has never been able to provide evidence that that position has merit.
Our debate is not on the merits of Haldane’s Dilemma. As I stated in my previous post, even if Haldane’s model is wrong, it still doesn’t rescue Dr Page from his circular reasoning error.
Page then provides the weak chimp-bonobo example, which does not bear on the debate.
But Dr Page expands his chimp-bonobo example by offering several lengthy citations regarding non-random mutations, again, unrelated to the debate?
Revisiting Dr Page's Core Error
I cited the Genetics paper as recent data-based evidence that the rate of change is much faster than originally estimated by Haldane (1957). Williams expends a considerable amount of energy trying to convince the reader that 1. the authors engaged in circular reasoning (an assumption of common descent), and so 2. my citation of it and use of it is also circular and 'faulty logic.'
I actually accused you of circular reasoning. It is you who tried to apply a study that requires the assumption of simian/human ancestry, to a mathematical model (Haldane) that does not require the assumption of simian/human ancestry. If the assumption of simian/human ancestry is wrong, then the Genetics study is useless. To apply such a study to a mathematical model void of assumptions about human/simian ancestry is faulty logic.
More Population Genetics Errors by Dr Page
Page: Williams then writes that all those lacking the mutation and all of their descendants had to be removed from the population. As worded – and probably as understood by Williams – it sounds as though all non-mutation holding organisms must be literally removed. This is incorrect.
Me: No, it is entirely correct, unless you believe our ancestors are all still alive!
Page: How ridiculous. I was clearly referring to a time-dependant explanation.
Check Futuyma, Evolutionary Biology, p 299. When an allele becomes fixed, it becomes monomorphic, its frequency is 1 (100%). That means the wild type is GONE, and ALL prior descendants who had the wild type (did not receive the new allele) over time had to be removed from the population.
In a 'harmful mutation environment', reducing the number of them that become fixed in the population, via whatever means, is a benefit, no matter how you look at it.
But a harmful mutation environment is itself an obvious and huge disadvantage to evolution! J
Page: I presented it [Rice study] as evidence that the typical claims of harmful mutations accumulating fast enough to prevent evolution – as is often implied by Williams and his ilk – is in error. And in this it succeeds.
No, it does not succeed. The Rice study is misleading, because it has surely misled you into believing something that is not true. The Rice study merely shows the advantage of recombination when contrasted with an asexual species in a harmful mutation environment, period. It does nothing to reduce the mutation problem. Here is my article on the mutation rate problem. Please explain to the audience how the Rice study has any impact whatsoever on this problem.
Dr Page's Response to List of Errors I Presented Him
(my original claim is in blue)
* [Me] Mistakenly claiming that Haldane based his substitution estimate on the observation of peppered moths (Haldane did the opposite, see Haldane 1957, p521)
Page: In my copy of Haldane's 1957 paper, on p.521. there is nothing at all about what he based his estimate on. You should notice that on the first page, p. 511, Haldane expends some time explaining the observations seen in peppered moths, and how he will attempt to estimate "the effect of natural selection in depressing the fitness of a species." I committed an error of omission, and should have included the fact that he considered some Drosophila experiments and such as well. However, your claim that he "did the opposite" seems to have no basis in reality.
On page 521 Haldane writes: "...This represents, in my opinion fairly intense selection, of the order of that found in Biston betularia [peppered moth]... I doubt if such high intensities of selection have been common in the course of evolution. I think n=300...is a more probable figure". It is quite clear that Haldane did NOT base his substitution rate on the peppered moth observation (which you now implicitly admit above), and in fact did the opposite (low intensity as opposed to high intensity selection).
* [Me] Implying that a large population is a bad assumption for evolution (Haldane did the opposite; see Haldane 1960, p351)
Page: I claimed no such thing. Quoting from my refutation, the times I mentioned population size or Haldane's use of it: "…premised on unrealistic assumptions (such a s a constant population size), made using observations of phenotypic variation in Peppered moths." "Williams writes "entire population" for a reason - the connotation of "entire population" is that the population is extremely large, such as the human population of today. This is an unreasonable allusion." I did, however, say that a constant population size is an unrealistic assumption. But 'constant' does not mean 'large.'
Why did you write that an extremely large population is an "unreasonable allusion"? It sounds to me that you believe its a bad (unfavorable) assumption for evolution, or you would not have wrote "unreasonable allusion". It is clear you were unaware that Haldane believed it was a favorable assumption for evolution (1960, p 351).
* [Me] Claiming that a wild-type allele can still persist in a population even after its mutant allele reaches 100% fixation in the same population!
Page: I see you don't understand what fixation means, or perhaps are unaware of what a dominant allele is.
I again reference Futuyma, Evolutionary Biology, p 299. You may also check his glossary: "Fixation: Attainment of a frequency of 1 (ie. 100%), by an allele in a population, which thereby becomes monomorphic for the allele" [emphasis in original].
Page continues: If 100% of a population has a DOMINANT allele, they can still be heterozygous - the individuals can still have a recessive allele for the same locus, and yet they all would exhibit the dominant phenotype.
This a very bad argument because, using your new explanation, if 100% of the population has the dominant allele, it is extremely likely that any remaining recessive alleles are by now virtually extinct, at a frequency very near zero.
* [Me] Because of his previous error, reaches the erroneous conclusion that a dominate[sic] allele does not need to be replaced, which implies it has no reproductive cost.
Page: If the members of a population are homozygous for the wild type, then the replacement of one allele with a dominant mutant will incur your cost. However, the impact of the cost - under realistic assumptions - is not what you continue to claim it is.
Wrong again! Perhaps this figure from Futuyma, p 298 will help:
The diagram above should help illustrate that a new allele from a mutated wild-type, be it recessive or dominant, will have to incur reproductive costs over the life of the fixation. Haldane assumed ALL of his mutations were dominant, since the cost of recessive mutation is exponentially higher.
* [Me] Claiming that a beneficial mutation will spread through a population in a sexual species "as well" as it would in an asexual species, even given an environment free of deleterious mutations.
Page: By "as well" I meant the common definitino "in addition".
I take Dr Page at his word about his intended use, so I hereby retract my original claim (stated above in blue).
* [Me] Claims that Wu's study does *not* assume human/simian ancestry in its determination of the substitution rate.
Page: Please provide the exact quotations from their paper pointing out their assumption of human-ape ancestry - as per your original claim - and how it was pivotal in their mutation rate analyses.
I already did, in my previous post in this debate. I'll copy it here:
Let’s look at an important passage from the study, emphasis mine. Particularly note the word “divergence”, which refers to the monkey/man split, and “positive selection” which is derived from the “divergence” data:
A common test for positive selection is a comparison of the A/S ratio of polymorphism and divergence (MCDONALD and KREITMAN 1991 ; SAWYER and HARTL 1992 ; TEMPLETON 1996 ). Since mutations under positive selection spread through a population quickly, they are not well represented in polymorphism but should have a cumulative effect on divergence. The A/S ratio from divergence is estimated from 182 orthologous human and old world monkey genes (Table 1). To avoid the confounding effects of deleterious mutations, which do not contribute to divergence but do make a significant contribution to polymorphism, the A/S ratio from divergence is compared to that of common SNPs (Table 1). The difference in the A/S ratio of common SNPs combined from both surveys compared to divergence is significant (2 = 8.14, P < 0.01) and can be explained by positive selection, assuming the average constraint on the divergence and polymorphism genes is the same.
The large number of amino acid substitutions suggests a high rate of adaptive evolution in primates. The expected number of amino acid substitutions is 2382 (4151 x 70/122) based on the A/S ratio of common polymorphism and the excess is 1278. Therefore, a large proportion, 35%, of amino acid substitutions between humans and old world monkeys are estimated to have been driven by positive selection. Extrapolating this proportion to the total amount of coding DNA in the genome (5 x 107 bp) yields an estimate of up to 1 advantageous substitution every 200 years since humans separated from old world monkeys 30 million years ago (LI 1997 ).
If Dr Wu has arrived at this substitution rate of 1 per 200 years without contrasting DNA between old-world monkeys and humans, as Dr Page is essentially saying, then Dr. Wu needs to re-write his study. But I suspect he will not need to re-write it, because he is indeed contrasting simian/human DNA, and hence assuming simian/man ancestry to arrive at this rate.
You may be in error here. Dr. Wu clearly states that simian/man ancestry is an important assumption in the study!
To conclude, I have clearly shown in this debate that Dr. Page was mistaken to cite the Genetics study (Wu, et al) and the Science article (Rice, et al) as implied refutations of Haldane’s Dilemma. In the Genetics study he clearly engaged in circular reasoning. The study actually worsens the mutational cost problem! (required offspring per breeding couple increases to at least 60 instead of 40; see first post in debate, and my article on the mutation problem for evolution). In the Rice study, Page admitted that the evolutionary "benefit" described by the study pertains to a "harmful mutation environment", which by its very description is a huge disadvantage to evolution!
I believe Dr Page's citations are not valid weapons against the Haldane substitution problem, nor do they support the theory of evolution in any way (as I mentioned earlier, the Wu study in fact provides evidence against evolution). Certainly the authors of these studies did not think their findings had a bearing on such an important issue as Haldane's Dilemma, or you would think they would have mentioned it.
1. Evolutionist Stephen Jay Gould notes that many creationists before Darwin advocated natural selection. S.J. Gould, "Darwinism and the Expansion of Evolutionary Theory, Science, 1982, Vol 216, p 380 (original source: Modern Creation Trilogy, Vol II, 1996, p 34).