Y.E.C. Model: Was there rapid evolution and speciation post flood?

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I can't offer an explanation for an increase in frequency I don't think even exists.

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Since each mutation appears in a single individual, it is rather hard for an allele to appear in even 1% of the population without an increase in its frequency.See Message 66

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I already gave an answer to this. It's meaningless if the "new" alleles do not change the function of the original.

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And I have already explained why that is very badly wrong.

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That paper actually says that all the variations are a good thing because they vary the product. Not so if they are "neutral" mutations that DON'T vary the product despite the sequence variation. In fact the statement is a very strange assertion, even nave.

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And the paper is right. It is neither strange nor naive if you understand what the genes do. Which is explained in the paper.

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It seems to me all the answers to my simple YEC model are nothing but unnecessary complications based on standard ToE assumptions that treat mutations as normal.

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You can consider the facts to be "unnecessary complications" if you like. But if you do so you prefer a simplistic fantasy world to reality.

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Even assuming that a difference in DNA sequence means a difference in product? That's really a sort of heresy.

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What makes you think that the paper makes that assumption ? Or that it is even relying on DNA sequences rather than the protein sequences ?

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No. what I mean is that scientists are operating under a false paradigm that won't tell them what is really going on because they have false assumptions to begin with.

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That "false paradigm" is looking at what the genes actually do instead of relying on an abstract theoretical model that ignores those facts. That is where the complications come from.

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Treating what is really a disease process as if it were normal is not going to show you "what is really going on."

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Life is just a disease then ? Seriously. The complications come from looking at what the genes do. Looking at how skin colours are actually produced, looking at the functions of the proteins produced by the genes, looking at how the actual genes correspond to skin colour. All things that Gary Parker didn't do. At all.

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Such an "increase in frequency" is absolutely meaningless if it does the same thing the original allele did.

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Wrong. Because we still have to explain how it happened, even then.

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It simply won't be lost, it will be passed on, and it should be passed on at the same rate the original and the other versions of it are passed on, which would look like an increase according to your reckoning but that's an illusion.

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If you think that NOT increasing in frequency would somehow create the illusion of an increase in frequency then you are going to have to explain why. But that is what you just said.

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No, they ARE "relying on an abstract theoretical model" by treating mutations as normal variations. That's the problem.

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It's not an "abstract theoretical model" and they aren't relying on it. The only "problem" is that - unsurprisingly - reality is more complicated Gary Parker's simplistic model. Which is only a problem for you.

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Mutations are a disease, even when they are "neutral." Treating them as normal modes of variation cannot have good consequences in the end either.

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That sounds like a call for eugenics.

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Sounds good but what if it's an illusion under due to the assumptions of the ToE?

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It obviously isn't. How could it be ? The genes do what they do, and the melanocytes do what they do whether they evolved or not.

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There is something really absurd about the idea that a change in the sequence of a part of a gene that is clearly accidental explains how any trait is normally produced.

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And by "absurd" you mean that you don't like it. Too bad for you.

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The theory that is guiding the investigation is actually crucial to finding out "what is really going on.

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In terms of the actual genetics of eye colour it doesn't matter whether the variant allele is a mutation or not, does it?

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An increase in the frequency of a particular mutation, a mistake in replication that changes the sequence of a particular allele, is an illusion if the mutated sequence does what the original allele did. In that case it is NOT really a new allele at all and its increase is utterly meaningless.

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Even if it didn't make any difference then obviously the observed frequency is real and not an illusion. Saying otherwise is insane.

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You count it as a separate allele and that's what makes it seem to have increased in frequency

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The frequency is observed. It is a fact. Of course we have to count the alleles as different in some way to actually count them. But since they are different that isn't a problem. Ignoring the differences to pretend that they don't exist would be a problem.

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but since it takes selection to bring about an increase in frequency, and that means that it has to have a positive impact on the organism, a very positive impact, which wouldn't happen with eye color or skin color or even immune system protection unless it imporoved health enormously, and certainly won't happen at all if it's a neutral mutation, there is no increased frequency. Most likely it is a neutral mutation that should be counted with all the other versions of the allele. Counting it separately from the other versions of the allele simply creates an illusion and apparently scientists fall for it

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Scientists are "making the mistake" of telling the truth instead of inventing stupid excuses to ignore it. Surely you can do better than this crap,

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there is no increase in frequency if the mutation does the same thing as the original allele.

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Of course there is. So long as there is a visible difference we can count the alleles. And if we count them we can measure the frequencies.Assuming that there is no difference in the products is silly enough. Assuming that measured frequencies are an "illusion" for a reason that makes no sense is raving insanity. This is your brain on creationism.

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It's the same allele.

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Obviously it is distinct, since it can be counted.

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It does the same thing.

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That is your assumption - and one that is almost certainly false.

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Increased frequency implies selection. That's the whole point.

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Over a relatively short timescale, and for significant increases in frequency, that is so.

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Selection works on function, not "looks."

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Selection selects for improved fitness of some sort.

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And there is nothing to disagree with there, but...

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There is no difference in fitness; it's the same allele.

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That is your assumption. In reality there is almost certainly selection for diversity in these genes.

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The increased frequency is an illusion.

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So when reality contradicts your assumptions you jump,to the conclusion that reality is wrong. Even if the assumption is almost certainly false and you cannot think of any way that your conclusion could even possibly be correct.Even if you believe such nonsense, why should anyone else ?

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You can't just say it must be functionally different without any proof whatever when neutral mutations are the most common and they do not change the function.

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It doesn't matter to the argument - and you have already made the case for selection, and therefore different function. Moreover, as you admit other points have been made in favour of different function.If you want to insist that the frequencies are illusory you need to do better than rely on assumptions.

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There is no selection happening and I have not accepted that there is

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That is your assumption. The fact that your argument works against your assumption is inconvenient for you, but still a - very obvious - fact.

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Being passed on over a few generations looks like an increase if you are counting it separately as a mere different sequence, but it should be counted with all the other versions of the allele. This is truly an illusion created by the assumption based on the ToE that it is a functioning allele instead of the usual neutral mutation.

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Of course the frequencies are observed fact. You just want them covered up - on obviously fallacious grounds because you don't like that fact.

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Note the title of this series of posts: The YEC model requires beneficial mutations and strong positive selection. I went back and skimmed through earlier posts where it is clear that the mere appearance of mutations, meaning different DNA sequences at a particular locus, is counted as an allele, assuming a changed function

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The original point was that the frequencies are strong evidence of selection, given YEC assumptions. (And I would add when you have genes which are very unusually diverse and where that diversity is itself an advantage it is rather hard to avoid the conclusion that something is going on that favours diversity)

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I'm sure you can follow this logic; the question is why you are so adamantly resisting it and calling me names about it.

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Sure I can follow the logic. That doesn't make it any less silly. Can't you understand that facts trump assumptions ? And pointing out the absurdity of your argument is not calling you names.

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The main problem for me, I think, is that you are assuming there is such a thing as "new alleles" that perform necessary functions for the immune system. This is really the same problem I've been having all along on this subject.

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There are a large number of alleles for these genes and there certainly seems to be a use for them. They don't have to be that new unless you assume that YEC is true.

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I don't have a problem with these genes being polymorphous or with the idea that the alleles differ very slightly and that "they are necessarily different in how they function" as long as I assume that they are built in and not mutations.

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How can you get from your assumed two alleles to over a hundred without mutation ?

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This article actually sounds like it assumes that beneficial mutations practically appear as needed

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Certainly not. The article is speaking about the advantage of variety, not of preplanning. Populations that are too similar are vulnerable (look into the history of banana cultivation sometime)

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Homozygosity occurs after many generations of selection as I thinki of it, or by founder effect. But if a gene's function can be illustrated by a Mendel square there's no need for homozygosity to develop rapidly. This shouldn't occur with the skin color or eye color genes that function according to the Mendel square. If these genes you are talking about can be expressed in a Mendel square I'd like to see it.

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Homozygosity is a disadvantage in these genes. And you are being silly with the Mendel squares. You could draw squares for all the combinations like the squares for your imaginary genes for skin and eye colour. But what would be the point ? When there are multiple genes with many alleles that would be a lot of squares that don't tell you anything.

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But it's probably that you've chosen a case that is too difficult for me to think through, and since it involves only a few genes I don't think it's very useful for a debate about the YEC model, which seems to me to be able to account for the vast majority of genes, and probably these too but if I'm unable to think it through it isn't a good example for this debate.

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It doesn't seem to be very difficult. The actual genetics of eye or skin colour would probably be harder to understand.

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And again, I'm going with two, not four, alleles, per Adam and Eve's genes.

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If God was going to give Adam and Eve an immune system, then why make it less effective than it could be ?

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By realizing that they are mutations, most of which are neutral, not genuine alleles.

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There is a difference between "realizing" and making a false assumption. However I note that you concede that mutation is the cause of the variants.

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The idea that any trait needs hundreds of alleles is in itself ludicrous.

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I suggest that you try to understand what these genes do, and remember that there is a genuine problem that the variety helps to counter. To refer back to your earlier post the variety is needed because we cannot count on the "right" mutation conveniently turning up. By keeping a wide variety of alleles present, at least we stand a good chance that some of us will have alleles that are effective against any disease organism that turns up.

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You get enormous variation with only two per gene, with a few genes per trait.

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Two per gene would be less than ideal in this case since 1/4 of the population would be homozygous.

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Since most mutations are known to be neutral, others deleterious and very very few very iffily beneficial, it ought to be common sense to provide evidence that any mutation is beneficial, but no, all these on this thread are ASSUMED to be beneficial

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Unfortunately for you we are not speaking of mutations, but of alleles that are extant in the population (some of which include multiple mutations). It is very likely that these have already undergone a degree of selection which would change the proportions.In the specific case you are talking about Tag already said that the conclusion that they were beneficial was based on evidence that the alleles had been positively selected. It was not an assumption that they were beneficial.

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I can't call a mutation a mutation, I have to call it an allele, so I can't point out that mutations are usually neutral, second deleterious...

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Because selection will bias the distribution - and because you need positive selection to account for the frequencies given your assumed timescales.

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...so I can't dispute the argument that I have to account for alleles that Adam and Eve didn't have on the ground that they are just neutral mutations;

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Because the evidence is against it.

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and I can't suggest that what is being called an increase in frequency due to positive selection isn't that if these are really neutral mutations, it's an illusion caused by counting new sequences, which are really mutations, as alleles.

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And you can't dismiss the evidence with pathetic excuses that don't even make sense.If there is evidence for positive selection then that overrides your unevidenced assumption of neutrality. And that's the part that is least nonsensical.

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Faith doesn't accept that a high frequency means selection. She thinks all these alleles code for mostly the same proteins and so don't provide any additional benefit beyond the two she believes were contributed by Adam and Eve.

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The question then is how does the frequency increase ? Faith resorts to - her word - flimflam - to try to cover up the frequencies but never honestly addresses the issue.

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One potential problems I see for the MHC example is that MHC is a complex of genes, not a single gene. When the article refers to "more than 200 alleles" it means across all the genes of the complex.

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No. It specifically states: It pretty clearly refers to individual genes - "some genes" can hardly mean the whole of the complex.Edited by PaulK, : No reason given.