Apparently not.
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Show your work…
He made two mutually exclusive claims while citing the same papers. This is not compatible with confusion.
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I’m not convinced that @colewd many incoherent and contradictory statements are the result of dishonesty. I think he likely really is just confused by the fact that, as far as he is concerned, he knows that the theory of evolution is wrong and ID is right. If one is convinced of that premise and cannot even contemplate abandoning it, how does one deal with the scientific evidence that contradicts it at every turn? Just because he is better educated then Bill, and better able to form English sentences, does not mean he is any better able to deal with the cognitive dissonance.
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Best thing is Behe & Snoke 2004 basically admit that their paper commits the Texas Sharpshooter fallacy in the discussion(my bolds):
Such numbers seem prohibitive. However, we must be cautious in interpreting the calculations. On the one hand, as discussed previously, these values can actually be considered underestimates because they neglect the time it would take a duplicated gene initially to spread in a population. On the other hand, because the simulation looks for the production of a particular MR feature in a particular gene, the values will be overestimates of the time necessary to produce some MR feature in some duplicated gene. In other words, the simulation takes a prospective stance, asking for a certain feature to be produced, but we look at modern proteins retrospectively. Although we see a particular disulfide bond or binding site in a particular protein, there may have been several sites in the protein that could have evolved into disulfide bonds or binding sites, or other proteins may have fulfilled the same role. For example, Matthews’ group engineered several nonnative disulfide bonds into lysozyme that permit function (Matsumura et al. 1989). We see the modern product but not the historical possibilities.
So Behe & Snoke model a situation in which only a particular set of mutations can yield the function of interest, that no other similarly complex adaptations are possible, requires 2 or more specific mutations (in other words that only 1 out of 20 amino acids are allowed at specific sites), and in which intermediate single mutations are deleterious. And that the novel set of specific mutations must evolve in a gene not under purifying selection before a null mutation occurs. And they assume the majority of mutations cause a null function that renders any subsequent mutations that might have been part of the novel function to be useless because the gene is now broken.
How Behe can admit this much in the very paper, and still go on to pretend his model constitutes some sort of problem for evolution is astounding.
It gets worse. Other absurd features of the model:
In this paper, we report the results of the stochastic simulation of the time to fixation of new MR features by what we consider to be the conceptually simplest route: point mutation in the absence of recombination in a duplicated gene that is free of purifying selection.
And:
The model presented here assumes that newly duplicated genes encode a full-length protein with the signals necessary for its proper expression. It is further assumed that all duplicate genes are selectively neutral.
And:
The pertinent feature of the model is that multiple changes are required in the gene before the new, selectable feature appears. Changes in these nucleotide positions are assumed to be individually disruptive of the original function of the protein but are assumed either to enhance the original function or to confer a new function once all are in the compatible state. Thus, the mutations would be strongly selected against in an unduplicated gene, because its function would be disrupted and no duplicate would be available to back up the function.
These two assumptions, that the individual mutations are deleterious in the functional copy, and that purifying selection is not operating on one of the copies, combine in an extremely restrictive way. Because one of the copies of the gene is assumed to be free of purifying selection, mutations that degrade the original function are not selected away. And these are of course assumed to vastly outnumber the productive mutations that can lead to the new function, so the probability is one of the two copies will sufer a null mutation way before one of the rare novel function-contributing mutations occur.
It’s absurd.
The basic “task” that the model asks a duplicate gene to perform is to accumulate mutations at the correct nucleotide positions to code for a new selectable feature before suffering a null mutation.
And:
However, if several point mutations (indicated by a “+” in the figure) accumulate at specific nucleotide positions (indicated by the three squares outlined in blue in the
figure) in the gene coding for the protein before a null mutation occurs elsewhere in the gene (indicated by a red “X”), then several amino acid residues will have been altered and the new selectable MR feature will have been successfully built in the protein (indicated by the greenshaded area). By hypothesis, the gene is not selectable for the new feature when an intermediate number of mutations has occurred, but only when all sites are in the correct state.
This means Behe & Snoke are modeling a situation where they are demanding a particular set of mutations to evolve to create a new function, with no alternative mutations being able to create a similarly complex function, and that this occurs in one of two copies of a gene where vastly more likely deleterious mutations that render any subsequent mutations invalid, are not purged by selection.
Bill thinks this is a more realistic model of protein evolution.
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His goal is to convince people like @colewd. So mission accomplished. The DI can now claim that there are papers in the literature that support ID. It’s still a lie, but less of a lie than if no papers at all by ID proponents were published.
Maybe the bigger question is how this paper passed peer-review. That it did gives the lie to the ID claim that the scientific elite are conspiring to keep their research out of the literature.
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Yes not only that. Another reason it passed peer-review is that the generalized conclusion that all Darwinian evolution is impossible, or even improbable, is stated nowhere in the paper.
In fact it contains some perfectly reasonable statements about caveats about it’s results, and it is after all a paper that yields a specific result with a model given specific assumptions.
If X, then Y. Here’s how X could be the case, and here’s how X couldn’t be the case. It’s a small section that speaks about caveats, but it is there and in the end also is one among several things that undermines the whole thing. It might even be there because the paper was under review and a reviewer suggested to add it otherwise it’s conclusions could be thought misleading.
What then happens is how the paper is sold in the popular ID press on their blogs, news-websites, and books, where it’s results are presented as if they generalize.
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This is a straw man argument.
There is substitutability in the assumptions. What you have always failed to recognize is that substitutability is little help when dealing with mutating through a sequence. What you have also failed to recognize is when dealing with populations variation to those populations is restricted by the time it takes for fixation to occur.
Lynch’s assumption of equal substitutability is not correct and from your first statement I think you agree with this.
If we want to get a better idea on how close Behe’s assumption is to reality we have a lot more studies available then those cited in an 18 year old paper.
The bigger question is how after 18 years is there no paper that shows gene duplication and divergence is a viable mechanism based on population genetic mathematics? There is also no paper that shows how any mechanism explains life’s diversity based on population genetics mathematics.
At some point without an ideological axe to grind someone might question if the universal common descent king has no clothes 
and stop the generation of papers that assume it is true
Show your work…
Show your work…
Then do the literature review and… show your work.
You’ve admitted it is sufficient. In this thread. You just don’t realize it.
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When all else fails, type a bunch of illiterate gobbledygook. Got to come up with some response, right?
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Oooh I see.
So Bill if my description is correct you then agree that would be an absurd and ridiculous model of evolution, right?
It’s just that you think my description of their models is incorrect, a straw-man. But if it was correct you’d also think it’s a terrible model? I would have a point then, if the model behaved as I described it? My criticisms are valid criticisms of a model that makes those assumptions, you just don’t think their model does that? Do I have that right?
No, I don’t agree with you. There are many sites in known proteins can can do this.
Great. Cite them and show how, with actual math, they are better compatible with Behe’s assumptions.
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None of this has anything to do with universal (or other) common descent. Let us recall that your man Behe agrees with universal common descent. You can get no conceivable support for your separate-creationism from him.
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That’s funny given that Behe says that is the most significant difference between their two models. You’ve quoted him saying as much yourself. Ironically I agree actually with what you say here, that that actually isn’t the most significant problem with Behe’s model(that it is “of little help”). It’s a problem yes, but it’s not the one that has the largest effect on why Behe and Snoke’s estimate is so utterly ridiculous.
There is. It’s Lynch 2005. Perfectly reasonable
The two most fundamental problem with Behe and Snoke 2004, is (1) the Texas Sharpshooter fallacy, which they themselves indirectly admit in the discussion.
Lynch also says as much in his 2005 response paper:
Second, Behe and Snoke assume that only two specific amino acid sites within a protein are capable of giving rise to a new selectable diresidue function. Given that the average protein in most organisms contains between ~300 and 600 amino acids, this assumption is also unrealistic. Increasing the number of participating amino acid sites from n =2 to just 10 can magnify the probability of neofunctionalization by more than 10- fold
That is, if there are 10 alternative positions in the protein that can participate in a new function, rather than just 2, this radically increases it’s probability of evolving.
And of course this would be further amplified by the consideration of the possibility of some function in some gene, rather than a specific function in a specific gene as Behe and Snoke affirms.
And (2) That their duplicate genes are assumed to be completely unlinked, such that purifying selection is initially absent until such a time that the 800 times more likely null mutation renders one of the copies nonfunctional. Which it would be expected to do 800 times more frequently than it would gain just one of the 2, 3, or more, novel function-creating mutations. When one such null mutation occurs in one of the copies, which is basically inevitable given their assumptions, this then instantly puts the other gene under purifying selection so that the novel function creating mutations, which are assumed to be individually deleterious, are purged away in that one. Now neither gene can evolve towards the new function. Because one has been irrecoverably destroyed by a null mutation, and the other has come under purifying selection against the novel deleterious mutations required in sets of 2 or more before they take functional effect.
The whole thing is rigged to fail. And the above is in fact an absolutely 100% accurate characterization of the model.
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Again you fail to recognize the distinction between UCD and the mechanisms of evolution. Even if B&S are correct, this only shows that the currently-understood mechanisms of evolution are insufficient; it doesn’t show that UCD, which is based on mountains of evidence, is false.
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