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Author | Topic: Y.E.C. Model: Was there rapid evolution and speciation post flood? | |||||||||||||||||||||||||||||||||||||||
PaulK Member Posts: 17828 Joined: Member Rating: 2.3
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quote: 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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Faith  Suspended Member (Idle past 1473 days) Posts: 35298 From: Nevada, USA Joined: |
It's the same allele.
It does the same thing. Increased frequency implies selection. That's the whole point. Selection works on function, not "looks." Selection selects for improved fitness of some sort. There is no difference in fitness; it's the same allele. The increased frequency is an illusion.
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jar Member (Idle past 423 days) Posts: 34026 From: Texas!! Joined: |
Faith writes: there is no increase in frequency if the mutation does the same thing as the original allele. That is simply not true Faith. As I pointed out back in Message 169:
quote: They do the same thing. But diversity, frequency, has increased. When I buy something I can pay for it in Pounds, Dollars, Francs, Yen. They all serve the same purpose but a Dollar is not a Yen is not a Pound is not a Franc. You can continue to deny reality all you want but the frequency is still observed. Maybe what would help would be if instead of denying reality you presented some evidence that supports a Young Earth or Creationism, something no Creationist seems to have ever tried to do. Edited by jar, : fix quotebox
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PaulK Member Posts: 17828 Joined: Member Rating: 2.3
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quote: Obviously it is distinct, since it can be counted.
quote: That is your assumption - and one that is almost certainly false.
quote: Over a relatively short timescale, and for significant increases in frequency, that is so.
quote: And there is nothing to disagree with there, but...
quote: That is your assumption. In reality there is almost certainly selection for diversity in these genes.
quote: 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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Faith  Suspended Member (Idle past 1473 days) Posts: 35298 From: Nevada, USA Joined: |
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. You have to show a difference in function, you can't assume it, and it has not been shown. "Diversity" is not diversity unless there is a diversity of function and not just sequence. Increase in frequency is meaningless unless it's based on a difference in function, that is, positive selection for beneficial function.;
You have to SHOW a difference in function.; There are a couple of posts back a ways that attempt to show that. One of them is too technical for me and my eyes have trouble with it too. Why don't you go back and see if you can make a case for changed function from that or something similar instead of pretending mere changes in sequence imply it, which obviously they don't. Edited by Faith, : No reason given.
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PaulK Member Posts: 17828 Joined: Member Rating: 2.3 |
quote: 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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Faith  Suspended Member (Idle past 1473 days) Posts: 35298 From: Nevada, USA Joined: |
There is no selection happening and I have not accepted that there is. What is mistaken for selection is a mere normal passing on of the allele because it is neutral. 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.
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. Changed function is assumed in that article bluegenes posted where it's even said that slight changes in sequence are beneficial because slight changes in function are beneficial to the immune system. It's assumed, it is not shown. And it's odd that it is assumed when surely neutral mutations are well known. 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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PaulK Member Posts: 17828 Joined: Member Rating: 2.3
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quote: That is your assumption. The fact that your argument works against your assumption is inconvenient for you, but still a - very obvious - fact.
quote: Of course the frequencies are observed fact. You just want them covered up - on obviously fallacious grounds because you don't like that fact.
quote: 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)
quote: 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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bluegenes Member (Idle past 2506 days) Posts: 3119 From: U.K. Joined: |
Faith writes: bluegenes writes: That's why I'm saying that, to get a plausible 6,500yr YEC model, we have to accept positive selection on many of those extra HLA alleles. Well, I'm just a creationist loony but I would guess there are many variables here you probably haven't taken into account, and if I can't derive your statistic myself I can't very well accept it anyway. Drift can increase and decrease the frequency of alleles (the percentage of the population in which they are present) but it certainly can't explain what we see with the HLA alleles. Perhaps it would be easier to explain directly how the new alleles are advantageous, and how they are necessarily different in how they function.
MHC polymorphism extends the range of antigens to which the immune system can respond. quote: *"The extensive polymorphism of the MHC proteins has almost certainly evolved to outflank the evasive strategies of pathogens. That should make sense to you (post Fall).
**"That exposure to pathogens over an evolutionary timescale can select for expression of particular MHC alleles is indicated by the strong association of the HLA-B53 allele with recovery from a potentially lethal form of malaria; this allele is very common in people from West Africa, where malaria is endemic, and rare elsewhere, where lethal malaria is uncommon." Undeniable natural selection, surely. Bear in mind that there are several of these very polymorphous genes, and that if the Adam & Eve maximum of 4 alleles was all that was available to us, then homozygousity would be common (1/4 of the population on each gene, and most people on at least one). Note also the first sentence in yellow. The new alleles are significantly different, and do not arrive easily by a single point mutation. So, these new arrivals being different is important, and they are certainly beneficial. Therefore, I repeat the title of the sub-thread:
The YEC model requires beneficial mutations and strong positive selection. I think you'll agree if you understand the information in the paper.
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Taq Member Posts: 10085 Joined: Member Rating: 5.1 |
Faith writes: I can't read the paper, it's too technical and it's hard on my eyes as well, and your summary is nothing but an assertion. It isn't an assertion. It is the conclusion of the paper as backed by the facts presented in the article. Sorry, but a handwave won't make this evidence go away.
Faith writes: Different combinations of alleles at one locus? What do you mean? What's combining with what? How many different eye colors? Alleles are defined as different gene sequences at the same locus, so yes, at the same locus. There is more than two allele for the OCA2 gene, and those multiple alleles have different functions meaning that there is more than 2 functions for that gene. This runs counter to your model.
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Faith  Suspended Member (Idle past 1473 days) Posts: 35298 From: Nevada, USA Joined: |
Perhaps it would be easier to explain directly how the new alleles are advantageous, and how they are necessarily different in how they function. 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. 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.
...two possible ways of evading detection. One is through mutations that eliminate from its proteins all peptides able to bind MHC molecules. The Epstein-Barr virus provides an example of this strategy. In regions of south-east China and in Papua New Guinea there are small isolated populations in which about 60% of individuals carry the HLA-All allele. Many isolates of the Epstein-Barr virus obtained from these populations have mutations in a dominant peptide epitope normally presented by HLA-All; the mutant peptides no longer bind to HLA-All and cannot be recognized by HLA-All-restricted T cells. This strategy is plainly much more difficult to follow if there are many different MHC molecules, and the presence of different loci encoding functionally related proteins may have been an evolutionary adaptation by hosts to this strategy by pathogens. Understanding this by my YEC model the idea would be that the necessary alleles were already present and then selected. This article actually sounds like it assumes that beneficial mutations practically appear as needed, such as here:
The extensive polymorphism of the MHC proteins has almost certainly evolved to outflank the evasive strategies of pathogens.* [and this is footnoted] "The extensive polymorphism of the MHC proteins has almost certainly evolved to outflank the evasive strategies of pathogens. That should make sense to you (post Fall). I would expect that somehow the solution to the problem has to be already present in the system and then it's selected. That is, it was created to function as it does, it didn't evolve for that purpose. Mutations don't just occur as needed but that's how this sounds.
Bear in mind that there are several of these very polymorphous genes, and that if the Adam & Eve maximum of 4 alleles was all that was available to us, then homozygousity would be common (1/4 of the population on each gene, and most people on at least one). 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. 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. And again, I'm going with two, not four, alleles, per Adam and Eve's genes.
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Faith  Suspended Member (Idle past 1473 days) Posts: 35298 From: Nevada, USA Joined: |
If I can't grasp the argument for whatever reason there is no debate. I believe eye color is based on genes with two alleles whose function can be expressed in a Mendel's square. I think the belief in mutations as the source of functioning alleles is false, not demonstrable in reality, just an artifact of the ToE.
Edited by Faith, : No reason given.
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PaulK Member Posts: 17828 Joined: Member Rating: 2.3 |
quote: 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.
quote: How can you get from your assumed two alleles to over a hundred without mutation ?
quote: 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)
quote: 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.
quote: It doesn't seem to be very difficult. The actual genetics of eye or skin colour would probably be harder to understand.
quote: 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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Faith  Suspended Member (Idle past 1473 days) Posts: 35298 From: Nevada, USA Joined: |
How can you get from your assumed two alleles to over a hundred without mutation By realizing that they are mutations, most of which are neutral, not genuine alleles. The idea that any trait needs hundreds of alleles is in itself ludicrous. You get enormous variation with only two per gene, with a few genes per trait.
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PaulK Member Posts: 17828 Joined: Member Rating: 2.3 |
quote: 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.
quote: 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.
quote: Two per gene would be less than ideal in this case since 1/4 of the population would be homozygous.
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