I suspect that the actual quote was in better English. Your rearrangement of it speaks volumes.
Here is the whole quote from the paper.
Based on these observations and in contrast to Behe and Snoke, the following model assumes that the intermediate step toward a two-residue adaptation is nondebilitating with respect to the original function but also effectively neutral, with one caveat noted below. Under this assumption, the first step in the evolutio n of a two-residue function potentially resides at the ancestral locus, where two alternative classes of alleles maybe present prior to duplication: those containing a key amino acid at one of the potentially participating sites (type 2), and those with none (type 1) (Fig. 1
). Assuming that n amino acid sites can potentially participate in the origin of the new function, the expected frequencies of these two allelic classes are obtained by normalizing the first two terms of the Poisson distribution, as loss of the ancestral protein function renders inviable all single-copy alleles with two or more key residues. The expected frequencies of type-1 and type-2 alleles are then 20/(20+n ) and n /(20+n ), respectively, under the assumption that all 20 amino acids are equally substitutable in the intermediate neutral state. As a consequence of random genetic drift and mutation, very small populations will generally be monomorphic for one type of allele, with the nature of that allele varying stochastically over time according to the preceding probabilities. In contrast, larger populations will approach a drift-mutation equilibrium, with the two allelic classes following these respective frequencies. In either case, averaging over a long period of time, when a random gene duplicates, it will be of type 1 with probability 20/(20+n ) and type 2 with probability n /(20+n ). Thus, immediately following gene duplication, there is a single copy of either allelic type 3 or type 5 in the population (Fig. 1
BTW Behe cited the paper you cited along with several other papers.
Look! It’s existing polymorphism, which Behe simplistically assumed didn’t exist.
And the fact that someone cited a paper does not necessarily mean that it supports that someone’s position. Such citations are common in pseudoscience.
And I cited TWO papers, so I don’t know why you’re only referring to one.
A false statement, and still further evidence that you have no idea what an ad hominem fallacy is.
Another vague and unsubstantiated assertion Bill. As such, as worthless as all your other defenses of Michael ‘I’m always wrong – but IDiots listen to me anyway’ Behe and his discredited model.
If you cannot quote exactly where Behe “clearly” states that he is excluding/ignoring “existing variation” (and “why”), then we have every reason to consider this claim to be false.
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If what you were trying to say is that an individual carrying a gene that has accumulated deleterious mutations, and is removed from the population for that reason, is no longer accumulating mutations. Then that is true, but it does not mean there are no other individuals in the population that have genes that are accumulating neutral mutations.
We return to the factors of population size and offspring numbers. With a sufficiently large population, where individuals generally produce more offspring than can survive, there are going to be individuals born every generation with no deleterious mutation in the gene of interest. That’s what the larger numbers ensures in matters of probability. It is those neutral mutations that accumulate, ensured by the large numbers of individuals.
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(I think the circles are much too large).
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Those aren’t the same. Is your misquote a result of incompetence or dishonesty? If the former, why didn’t you correct it?
What’s even stranger is that, in the post immediately preceding yours, he acknowledged his error and thanked @Rumraket for the correction.
It was a cut and paste error. I have no idea how It happened but it had no material impact on the discussion.
Why didn’t you mention the error and correct it when you posted the full paragraph?
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This is true but according to the parameter you offered they (the family) are accumulating neutral mutations at the same rate as deleterious ones. When the selection filter reaches an intolerant level both types of mutations get filtered essentially reducing mutational variation in the population.
We see this with proteins like skeletal muscle alpha actin where over 100 million generations the consensus sequence does not change. This case is by looking at the sequence comparing mice and rats.
If we look at heart muscle alpha actin we see the same issue between species but slight variation with skeletal muscle alpha actin. What Winston is exploring is if this is a design signature.
Why would I need to do anything more then post the correct paragraph? There is no change in content only a sentence out of order.
To explain why your ‘quote’ didn’t match the actual text.
But apparently you don’t care about such things.
I agree as I don’t think why the error occurred is important to the overall discussion.
It really is breathtaking the number of contradictory ideas you can hold in your head without suffering any dissonance. It is almost impressive in a way.
What family? You mean the population?
No Bill, the neutral mutations are not removed at the same rate as the deleterious ones. The deleterious ones, by definition are removed at a much greater rate than the neutral ones. That’s what it means to say one class is deleterious and the other is neutral.
Why can you not fathom this? You have had it directly demonstrated to you with elementary probability.
Try to think. At least try. You can try, can’t you? For the love of anything you might hold dear, please just try to think. Ask for help.
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The near parents and dependents of the organism in question.
Deleterious mutations themselves are not removed necessarily at a much higher rate. They may cause issues with the organism that do not affect the ability to reproduce and live a normal life. When mutations are removed from purifying selection all mutations in that lineage are removed.
By studying alpha actin you will understand this. There are over 70 variants in the human population yet the consensus sequence has not changed in mammals with very high reproductive rates.
@Mercer first brought this idea up when discussing MYH 7.
Then they’re not deleterious. By definition.
Deleterious mutations (see Glossary) **cause loss or alteration of normal gene function, leading to reductions of organismal fitness . While fitness in nature and fitness under domestication often have overlapping criteria, the primary scope of this review concerns fitness under domestication.
Do you disagree with this definition?
I endorse that definition wholeheartedly.
I endorse it because it correctly identifies that the defining attribute of deleterious mutations is their effect on fitness.
That they cause…
reductions of organismal fitness
reductions of organismal fitness
reductions of organismal fitness
reductions of organismal fitness
reductions of organismal fitness
Do I need to call 911? If you give me your address I will make sure you get help. I say this because you might be suffering a clotting issue in the brain this very moment. Do you need help?
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