That’s not Behe. Behe agrees that all life is related by common descent, while Bill is now shown to think that each species is independently created from nothing. And the data prove that in some inexplicable fashion. No, this is Bill’s own butt talking.
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Hi Ron
This is an assertion which does not take the population genetic models that show sever limitations of this mechanism. Are you not able to see the problem here?
Yes, not. Are you able to articulate the problem? Again, show your work.
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Amazing
I do not agree there is a problem. I agree with others here that Behe’s reasoning is flawed.
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Have you studied his model? What is wrong with it? I think this is group denial at this point.
I was wondering what their definition of “gene family” was. Turns out it’s inapplicable in Bill’s world:
(From the supplementary methods file.)
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So the answer to my question was “no”?
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You like many of your colleagues are stuck in a paradigm and impeding scientific progress. The single origin model is broken.
Until this is acknowledged you are stuck making assertions and defending what has become dogma.
How is this relevant to a request for you to articulate your claims and to show your work?
Silly notion. I’m defending what the data show. Can you explain why rodents form a nested hierarchy?
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The work is to show that gene duplication and divergence can account for these patterns. It’s been 5 years and you are the professional. Where is the model?
If after 5 years your claim has not gone beyond gene gain and loss is it possibly time to question the single origin model?
No, Bill, you said you had mathematically excluded those mechanisms. Show your work!
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No, the work (which you claim to have done) is to show that they can’t. Where is that work?
It’s possible to question anything, but to do so credibly you have to present some kind of evidence. You claim to have that evidence, but you haven’t shown anything. My claim doesn’t have to go beyond gene gain and loss because those do explain the data. You claim there’s more gain and loss than expected or credible. But you provide no evidence or calculations.
(Also, pro forma, I will note that even if natural processes couldn’t explain the magnitude of gains and losses, this would not support separate creation of species.)
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Behe has been done to death on this forum. No response I could craft would persuade you.
That’s fine. It’s still a free country.
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Reminder, we have (1), and a partial answer to (2). Now it’s time for @colewd to provide the per generation rate for the process he has named. Shocking that he refuses.
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When you do not have a model that shows gene gain and loss can account for the pattern you have a speculation and not an explanation.
The Behe model shows severe limitations to gene duplication and variation. This supports my claim that novel complex gene patterns are very unlikely supported by this mechanism.
We do not have real support for the single origin model. If we want to claim this model is viable it needs a reproductive mechanism that can support its viability.
The model is that normal processes happen at observed rates. That is, by all evidence, sufficient to explain everything you have presented.
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The fact that would persuade is a convincing mathematical model that explains the pattern. We have been discussing this for five years and there is zero progress. Not due to lack of effort but due to the severity of the problem.
Behe’s model shows severe limitations to the mechanism. So does Lynch’s model which does not take pre duplicated gene deleterious mutations into account. There has been a lot of non substantive noise generated but no model exists that explains these gene Venn diagrams that support a single point of origin for vertebrates.
Why not try to develop a competing model?
Again:
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The two most fundamental problems with Behe and Snoke 2004, is (1) the Texas Sharpshooter fallacy, which they themselves indirectly admit in the discussion.
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.
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.
That is, the novel function is modeled as a multi-residue replacement function for the old one, rather than an additional function in one of the copies.
The whole thing is rigged to fail. And the above is in fact an absolutely 100% accurate characterization of the model.
And none of Behe’s model has anything to do with Howe et al in any case, as there’s zero evidence any of the gene gains in the venn diagram have replaced their ancestral functions in a manner concocted by Behe.
There are more problems, but the above two are definitely the worst. Still significant is also the fact that his model ignores recombination. All eukaryotes do recombination, definitely all sexually reproducing animals.
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