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

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Not if they are all neutral or deleterious mutations.

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I have to say that that is a bizarre answer. Neutral and deleterious mutations only spread by drift, and deleterious mutations have selection working against them. So they should not be any easier to find.Did you mean "not if they are all strongly beneficial mutations" ?

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The evidence is all in the reasoning. The fact that you can get two different eye colors from one gene with two alleles, and eight different skin colors from two genes with two alleles each. Any traits governed by more than one gene would have a lot of variability with only two alleles per gene. And greater heterozygosity (genes with two different alleles) in former times along with a larger number of functioning genes (before they died and became "junk DNA") would produce a LOT of variation down the generations from there.

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You do realise that all that is pure abstract theorising which doesn't take into account what the genes actually do ? In reality skin colour - and eye colour - are not that simple. Your ideas about what might be needed can't overrule what is actually there.

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Tis indeed all abstract, but so is the ToE, so is the claim that mutations are the source of variation, and in that case not just abstract but pure wishful thinking.

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Aside from the fact that we KNOW of variations produced by mutation ? And given the difficulty of proving that, there must be many more that are not provable. That is not abstract theorising, and certainly not wishful thinking.

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There is no need to conjure with all the complications and details of genetic inheritance, Mendel demonstrated how it works just fine, which applies to eye color and skin color just fine.

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I see there is no need to actually investigate the facts. Abstract theorising and wishful thinking are the way to go.That is really a very impressive - and obvious - example of the standard creationist trick of falsely attributing their flaws to their opponents.

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But you think we NEED mutations to get new alleles and I don't, so how many there are on a gene doesn't tell me much; all I can say is the fewer the better.

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So where do you think new alleles come from if not mutations ?

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We don't need new alleles. All new phenotypes are the product of new combinations of the existing alleles.

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Faith, the alleles exist. Whether they are "needed" or not. The question is how do you explain where the additional alleles come from. You say that is is not mutation. Then what is it ?(And I would suggest that simplistic Mendelian genetics without regard to what the genes really do is hardly a good way to judge what is "needed" - especially when we are talking about the immune system)

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Where did I said it's not mutations?: Of course it's mutations. Is the problem that I don't regard mutations as viable alleles then?

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When you said: it certainly seemed to indicate that you felt that new alleles could appear without mutation. And in fact that is the sensible reading in context.

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The "additional alleles" are mutations which are not really viable alleles even though most of them may not change the function of the allele they displaced so the original function is not disturbed

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That is just confused and almost certainly wrong - and makes it very difficult to explain why we actually find so many alleles if Adam and Eve are literally true and lived only 6000 years ago.

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the problem is nobody has SAID what all those alleles DO

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The first thing to understand is that genes are not simple switches that turn traits on and off. They are a representation of a protein sequence. In the immune system they are going to code for proteins that can help us resist diseases. By having a wide variety of defences it is less likely that a single disease could wipe us all out.

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OK I'll try to be clearer: I don't think we need mutations OR new alleles.

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Whether we need them or not they are there. And some of them are far more common than seems reasonable given YEC timescales - unless they are strongly advantageous. That is the fact that needs to be explained. Saying that we don't "need" them just looks like making an excuse to stick your head in the sand and ignore the facts. It certainly isn't relevant, nor does it address any point in the post you were replying to.

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There is no problem explaining a bazillion mutations if they are damaged/changed/mutated alleles

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I certainly didn't expect you too give up on your YEC beliefs that easily!Because if YEC is true there shouldn't be that many that are common enough to get noticed. As I pointed out a little while back neutral and deleterious mutations won't spread quickly.

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Yes so when I ask if they actually DO anything I mean do they actually produce a protein that really does something NEW to protect the immune system?

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Then you still don't understand what I said. The point is not that some are inherently better or worse. The point is that disease organisms vary. Some of them - like the influenza virus can vary very quickly. With vaccines doctors try to predict which flu strains will be dangerous in the coming winter and prepare for those. our bodies can't do that. But, if our immune systems are different some of us will (probably) be resistant to whatever nature throws at us.

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Yes, that's the assumption, what is the actual known fact? What DO they actually code for? If they are neutral mutations they will code for the same protein the unmutated original allele coded for with the same effect on the immune system.

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I very much doubt that synonymous mutations would be counted. Even if the alleles were identified by genetic analysis rather than the proteins themselves (which used to be the main method before gene sequencing took off)

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But the question is whether the extra alleles actually contribute variety to the immune system. What if they ARE "neutral" mutations that simply don't change the original function of the allele?

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I'm sure that they aren't, not least because there would be no advantage in having such variety (and that they almost certainly wouldn't be counted - or even noticed - and it would be bizarre for it not to be mentioned if there were hundreds of synonymous variations of a gene - that weirdness deserves to be mentioned)Also see Message 26 in this thread. And since heterozygosity is a distinct advantage having more distinct alleles helps there, too.Edited by PaulK, : Added reference to earlier and very relevant postEdited by PaulK, : ...And an important implication of the information there

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So the fact that "they are there" doesn't mean much. They are just random mutations, they don't change anything, so they can occur in huge numbers with no problem and certainly without any effect on whatever incomprehensible idea of the YEC model is you all have.

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The fact that they are there means that they have had sufficient time to occur and to spread. Spreading takes a long time by drift. So the observed numbers are extremely surprising assuming YEC timescales. I am sorry that you find it "incomprehensible" that YEC typically allows only 6000 years since Adam and Eve, or 10,000 at most but it is a fact.

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Hardly. It's a way of saying the original genetic code was perfect without any changes whatever, so that changes are an interference, not a benefit, at best not changing the function, at worst producing disease

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How is this relevant to explaining why we find additional alleles at appreciable frequencies ?

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Then please repeat the unaddressed points.

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If you say something completely irrelevant we are supposed to repeat the entire post ? Why ?

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Why not? That's a lot of mutations.

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Because - to repeat the point again - there isn't time for them to spread.

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My understanding of the situation is that the neutral mutations keep occurring, not that they spread. I'm not at the moment thinking of deleterious mutations.

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So, if an allele is found in 5% of the population it will not be a neutral (let alone deleterious) mutation ?

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I did understand that. It's clear in bluegenes' article in Message 26 as well. That article says it helps to have a lot of slightly different sequences to deal with all the different diseases and attributes that function to all the different sequences in all the additional allleles. An example is give of codominant alleles that are both expressed in the cell, assuming that they or one of them is one of those additional alleles. But that is an assumption, nothing is said to show that it is such an additional allele

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Odd then that you would ask what they do since you claim to have already known. And doubly odd since that message mentions that some of those genes have more than 200 known alleles

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My question remains whether these many alleles do anything other than the original allele did, make the same protein for the same function. We're talking about ONE gene are we not?

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So you don't really understand. Yes, they make different proteins. But there are a number of these genes. Let's repeat part of the quote from the earlier message you cited.

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But the sequence can be different but the protein product identical, so what would that prove?

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If you only look at the protein you are only going to find differences in the protein.
And of course if you know the gene sequence you can work out the protein sequence.

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Apparently so is the author of that article bluegenes posted, but it needs to be known not assumed.

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Looks like the author knew it.

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If it's variations in sequences that are being counted I would assume they would be counted. But I keep asking and nobody has said anything about this is actually known; it all appears to be assumed, and it's the same with your remarks.

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It isn't simply assumed. I have given reasons to think that. And the quote explicitly says that the protein sequences differ.

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First it has to be shown that your scenario is more than just an assumption.

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That was done back in Message 26

It's a pretty trivial - in fact inevitable - result.Gary Parker is just engaging in abstract theorising, trying to prop up the (daft) idea that the "races" of human beings come from Noah's three kids and their wives.We don't need such superficial and intellectually empty theorising. But it seems that we do need - or at least have a good use for - far more than two alleles for some genes.

The basic argument is simple.There are many common alleles of these genes.Under your views there are only four original allelesEvery one of these other alleles must have occurred as a mutation and spread significantlyYou have only 6000 years for the mutations to occur and spread from their original occurrenceThis is highly unlikely without strong positive selection.Note that knowing what the different alleles do is not even relevant to the argument.

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Two

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Given that heterozygosity is an advantage in these genes I think you should go for four in this case.

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If they don't change the function of the original allele they would continue to occur in the population as the original allele would.

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You haven't even bothered to find out what these genes do, have you ?

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See above. If they do what the original allele did this whole line of reasoning does not apply. They would "spread" according to the circumstances under which the original allele would spread.

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If they don't offer any advantage then - on average - they won't increase in frequency at all. That is pretty basic.

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I still don't get what is "highly unlikely" about this

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How do the extra alleles spread so quickly ?

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One gene made up of the two alleles B and b, possessed by both parents, produces both blue and brown eyes in the offspring, most of them brown heterozygous Bb's like the parents.

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Instead of rambling on about other genes perhaps you could deal with the specific genes under discussion ?

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I don't even know how to find this out, I have to rely on whatever comes up here

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You could have read the link provided in Message 52

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"Advantage" is a ToE concept that doesn't have much to do with the YEC model, some perhaps but not much. In the YEC model variation is a random thing that follows the principles of the Mendelian square. Some traits may proliferate over others for many reasons but the "advantage" in each case is mostly a random thing too. Random selection such as by migration and geographic isolation of a portion of the larger population is more common than natural selection

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So the YECs don't allow alleles to increase in frequency? Isn't that a bit awkward when you have to explain how these alleles very quickly increased in frequency ?

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The same way the original allele would spread, nothing unusual, just according to the principles of the Mendelian square.

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The Mendelian square doesn't include increases in frequency.This is why it pays to understand what you are talking about.

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I've responded a few times to the message you suggest I respond to

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I didn't suggest that you respond to any message. I suggested that you read a link to understand the function of the genes and why heterozygosity is an advantage.

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Please answer this question: WHAT exactly has "increased in frequency?"

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The mutant alleles of course. As I said.

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and how can you know when (how long ago) a particular mutation occurred and how "quickly" it spread?

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I'm not claiming to know any such thing. Only that in your model the mutations can't occur much more than 6000 years ago, and that they would have to spread very quickly to reach the observed frequencies.

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this should really be answered by bluegenes who posted that information. He might be more informative.

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It's not exactly a difficult concept. As an allele becomes more common in the population it increases in frequency.

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So far I don't have any good reason to think they are something other than neutral mutations that didn't alter the function of the original allele, in which case an increase in frequency means nothing.

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You have been given reasons to think that they differ (although the basic function is the same there are important differences - that is part of the reason why heterozygosity is an advantage).But the increase in frequency IS the big point. I'm still waiting for you to offer any explanation for it that is consistent with YEC.

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I don't know what link you were talking about so I seem to have missed it

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There are times when I think you are just playing at being obtuse. And even if your inability to understand the use of frequency - despite all the context - isn't one of them, being unable to find a link in a post is pretty bad. The major histocompatibility complex (MHC) and its functions. NCBIYou might like to consider this part of the quoted section again

I think you mean that the "problem" is that scientists try to find out what is really going on rather than just settling for a simple theoretical model that you happen to like.And that is just another example of your anti-scientific thinking.