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

I don't know if I'm tired, burning out on this topic, unable to make sense of the technical language or what, but I can't get anything out of what you are saying.I see mutations as mistakes. Great if sometimes they don't destroy something. Haven't seen any evidence that all these alleles do anything new, so I assume they just do whatever the original alleles did for any given gene.Time since Adam and Eve is irrelevant since things started over with the Flood and that's where counting alleles would have to begin I suppose. How could we know if any of the indiviudals on the Ark had mutant alleles anyway? All that's needed to create all the known diversity since the Ark is two alleles per gene shared by all individuals.If there are too many mutations to have occurred in the last 4500 years since the Ark, what can I do but assume that for some reason they occurred a lot faster than usual since then, at least in the immune system which appears to be unusual for its great number.You don't need selection to increase the number of a certain allele in the population if it does the same thing as the original alleles or SOME original allele somewhere in the original system. Anything that actually functions is going to be passed on no matter what because there's no reason for it not to be.But I think I'm burned out on this topic.Edited by Faith, : No reason given.

Which turns out to be one of the two questions asked in the title of this discussion. I don't think there is anything wrong with that view. The theory of evolution does not consider those mutations to be purposeful, and what is being said in this thread is that mutations are copying errors. Sigh.
1) Selection does nothing of the sort. That is not a mechanism for increasing alleles or genetic diversity.
2) We don't need to make excuses for something that actually exists. We know that some genes have multiple alleles. So what original gene provides protection against malaria so that there is no need for a mutation? Again you seem to be describing some kind of purposeful action when you know that mutations are errors/mistakes. That thinking is not logical.

You seem to have missed the point given by bluegenes and others that selection is what causes the proliferation of a mutant allele, that is, causes its "relatively high frequency" in a population. I don't know. I don't know if anybody knows. All that's being discussed on this thread is the mutant alleles. The only "purposeful action" here is whatever the original allele did. All the immune system genes have specific functions directed against specific diseases. If a mutant allele does nothing more than produce the same phenotype there is no need for it, it would be better that there be no mutants since all they do is scatter the effects.

You are correct. I misread your statement. When you said "You don't need selection to increase the number of a certain allele in the population" you were correct that selection is what is claimed to be responsible the increasingAnd you are also correct that things that are not really selection can do the same. Anything that makes a subset of a population could have a random affect on the distribution including events for which phenotype plays no role at all. The problem is that such subsetting cannot explain traits produced by multiple allele genes and there are at least some example of those. There is also the point that any resulting phenotype changes not based on selection are totally random. That is because the existence of mutant alleles is central to the topic. Presumably any number of alleles greater than two for a location means a mutant allele. The significant idea here is that evidence has been provided for mutation providing new, functionality; something that Creations have denied even being possible in past discussions.I take it that you don't have any examples of the malaria resistance other than that provided by mutant alleles. But even if there were, if it does not use the same mechanism as the ones we know about, then the mutant alleles still have a novel functionality. Edited by NoNukes, : No reason given.Edited by NoNukes, : No reason given.

Of course they're mistakes. As NoNukes said, they're copying errors. The most common adjective for "mutation" is "random", as in random mutation. Yes you have. You've been presented the examples of blood type, rabbit fur color, and the human immune system. All of these have alleles with new functions beyond the original two. In the case of the human immune system there are hundreds of alleles with new functions that couldn't have arisen in the number and frequencies that we observe in the short time available since Adam and Eve, not at currently observed mutation rates. The time since Adam and Eve is all that is relevant, since that is when you claim to know how many alleles there were. This is a new claim. When you say "two alleles per gene shared by all individuals" are you saying there were still only two alleles per each gene in the human population, just as with Adam and Eve? Or are you trying to say that each individual contributed two unique alleles per gene to the human population? A far higher mutation rate is required by your scenario, and there's no evidence of this higher rate. The large number of alleles in the human immune system also require a long period of strong selection in order to appear at their high frequencies in the population. There hasn't been near enough time since Adam and Eve for that to happen. In the human immune system we know the alleles perform different functions because the MHC molecules they produce bind to different antigens.--Percy

I was talking in the context of the immune system, and since I don't recall anything about what the originals do there's no way of knowing if the changes do anything new. Again, the original function needs to be known and I don't recall that being identified. If it was I missed it. Please repeat it or link to it.And obviously I have to assume that the mutation rate was faster in the past. What evidence could there possibly be? If all the alleles do is what original alleles did there wouldn't be any selection. The function doesn't have to be the same as the original gene, just the same as any of the original alleles in the system, which is possible if the coding sequences are similar. Different from each other, yes, but unknown if different from the original alleles.However, I'll concede the point anyway since I can't prove anything for my side, all I can do is guess about it. So the point has been made that there are more alleles than could have arisen in the time since Adam and Eve. I'm still going with two alleles per gene at the Creation so I'll still be trying to prove it.Edited by Faith, : No reason given.

This statement is nonsense. ABO Blood type is completely specified by the three alleles. Nothing else is a factor.Beyond that, it does not matter if there is another gene or genes that can offer the same gross functionality. The hereditary patterns are going to be completely different if the mutant alleles are added. This requirement is literally an attempt to deny the mutant alleles are real alleles for no good reason. Wrong. It is correct that there could not be selection between identical phenotypes. However, there can be selection between the particular patterns that lead to a disease immunity from ones that don't. For example, if the original pattern was recessive, while the new mutant is dominant, then disease immunity of the overall population can be increased.Beyond that, this requirement for brand new functionality has been met with at least the blood type allele and the sickle cell allele. okay...

quote:

---

So the point has been made that there are more alleles than could have arisen in the time since Adam and Eve.

---

That's true even if the new alleles are functional but mimic functions of other gene combinations. There is absolutely no basis for your requirement. Why not four? How many alleles per gene for humans after the Flood? Isn't that just as rigorous a test?

Just as a matter of fact, all the genes in the immune system are codominant. It's possible there were mutant alleles on the Ark, but otherwise I'd expect them to have all the same genes with two alleles each just like Adam and Eve.Why only two? Because it's elegant and it's sufficient to produce all the known diversity. Keep in mind there are usually multiple genes for each trait in this system, perhaps always. Multiple alleles are not needed and as I've argued are far less efficient. It's possible the immune system is an exception, but I doubt it.Edited by Faith, : No reason given.Edited by Faith, : No reason given.

Let me phrase the question in the terms framed by the title of this thread. There were eight folks on the ark of which three were sons of Noah and his wife. Even including mutant alleles, would there be enough mutant alleles to account for what we see today. That means more alleles to start with, but less time to grow to what we see today. Whether or not two is enough, it has been demonstrated that two alleles alone did not produce the observed diversity in say, blood type as one example. But it is your proposal and not mine. You are welcome to it.

I've conceded this point for now because there is no way to know and all I can do is suppose that the rate of mutation was much greater than the rate assumed to be standard. I don't think any time was needed to "grow," if the mutants for the most part do just what the originals did. The nondeleterious ones would spread in the population from generation to generation without any aid from selective pressures. But again that's the best I can do for now and I'm happy enough to concede the point -- for now. Well, it has NOT been demonstrated that two is not sufficient to produce the vast majority of diversity we see, not even in relation to the immune system since the originals have not been defined. The O blood type is apparently a mutation that lost some of the functions of the A and B types but not the basic function of a blood type as far as I know, but even though it makes it universally usable it seems to be an inferior version and that can't be a good thing. And I don't think albinism is a good thing so the rabbit fur example is at least compromised in its supposed beneficiality.But I really would rather not have to keep putting my guesses forward here.

I cannot let you just hide behind "as far as I know" when your statement is complete nonsense.The Blood Type Diets : Blood Type O

quote:

---

Type O was an early success formula. It is the only blood type that carries two opposing blood type antibodies (one blood type A and another against blood type B). These antibodies undoubtably conveyed some survival advantage, as many of the common diseases that plagued our ancestors possessed markers (antigens) that simulated the other blood types.

---

quote:

---

This blood type has a very well-developed ability to digest meals that contain both protein and fat. This is because two chemicals used by the digestive tract, an enzyme called intestinal alkaline phosphatase, and a lipoprotein called ApoB48 are secreted into the digestive tract in much higher amounts by type O's.

---

So, no O type is not just some debilitated A or B type.I know you want to protect your position against complete destruction, but perhaps doing it by making incorrect guesses is just self-deception. Of course that is not the only result of that five-allele c-gene system, so apparently, this is yet another bad excuse. It is quite easy to put a quite low upper limit on the number of alleles that Noah and his family could possess. Noah's three sons could have only the alleles that his parents had regardless of how many mutated alleles existed up to that point. Then there are the three wives whom I assume you would give credit for at most two alleles each per gene, again regardless of what mutants existed in the folks who did not make it into the ark. Edited by NoNukes, : No reason given.

You would have seen the evidence in some of the material presented had you understood it.What the HLA-B proteins do is bind with peptides (parts of other proteins), and transport them to the surface of cells for inspection by killer T-cells which, if they identify what's presented as foreign, will attack the invader. The different alleles bind to different and sometimes overlapping ranges of peptides, and the intruders will have many peptides, so there's a good chance that an allele can latch onto something in most pathogens.Picture a burglar (HLA-B allele) with a set of skeleton keys (peptide binding repetoire) and many mansions (pathogens) with many locked doors per. mansion (peptides). For most mansions, the burglar can open at least one door, but if he works with a friend who has a different set of skeleton keys, they have more chance of being able to open at least one door (heterozygosity).But the mansion owners keep changing the locks, and sometimes they can come up with a set of locks that cannot be opened by either set of keys. The analogy only goes so far, but what we perceive as regional or global disease epidemics can be when a mutant pathogen doesn't happen to have any peptides that are locked onto efficiently by most of the common alleles. When that happens, the strain is successful and can multiply exploiting our bodies. However, because the intruders have many peptides (locked doors) it's hard for them to avoid all the many alleles/burglars in the neighbourhood on all of their peptides, because of the collective range of all the sets of skeleton keys (binding repetoires/ranges) in the population as a whole.The most succesful pathogen strains will be good at evading common alleles because that's why they have become successful (positive selection for not having matching peptides with common HLA-B alleles). But they won't be likely to have adaptations to all the rare alleles, so any alleles that can deal with the problem face positive selection over time against the more common ones. When they themselves become common, then some successful mutant pathogens may have adapted to avoid them, and off we go on a new cycle of balancing selection. Known diversity? Known to whom? A super high rate of neutral mutations gives a different distribution pattern from the one we see. However, YECs do need to argue for past high mutation rates for many animals, including humans, because the divergence on genomes within "kinds" is so much more than the model would predict on normal rates It's a sub-thread/topic, really. Why not try to address something like the niche filling of the species that evolved (or devolved) from the "kinds" on the Ark? Surely loads of natural selection on phenotypes is required for all this. How can specialists like polar bears and Plasmodium falciparum match their environments so well without it?

The original function of the original alleles doesn't need to be known. We know that the original two alleles bound to at most two different antigens. And we know that today there are hundreds of alleles that bind to hundreds of different antigens. Therefore the different alleles of the modern human immune system have different functions, and many more functions, than the original two. We've sequenced ancient DNA and there is no evidence for your higher mutation rate, for example, Oldest-known human genome sequenced:

quote:

---

A 45,000-year-old leg bone from Siberia has yielded the oldest genome sequence for Homo sapiens on record revealing a mysterious population that may once have spanned northern Asia. The DNA sequence from a male hunter-gatherer also offers tantalizing clues about modern humans’ journey from Africa to Europe, Asia and beyond, as well as their sexual encounters with Neanderthals.

---

They sequenced this ancient human DNA to such a level of detail that they could detect Neanderthal DNA, and yet there is no evidence of the large differences with modern human DNA that would have indicated a high mutation rate sometime between then and now.--Percy

I have to concede on this argument though of course I will be looking for ways to reopen it in the future. At the moment I'm not in a position to argue it.But I will make one point: if all those mutant alleles really contribute to protection against many diseases it's rather odd that we seem (to me anyway) to have a lot more immune deficiency diseases than ever before. I note mention of them here and there, but I also have personal experience of it: A friend of mine suddenly acquired one a few years ago and was dead within six months of his first symptoms, a rare muscle-wasting immune deficiency disease that hit him out of the blue in the midst of what had seemed like a condition of robust health.

It's not redundancy if they do something different. Are the mutations that separate the human and chimp genome redundant? Do chimp genes do the exact same thing as human genes?Obviously, they don't do the same thing. They aren't redundant. If they were redundant then chimps would look and act just like humans. I am explaining the differences between species through differences in DNA sequence. You are claiming that you can't change the sequence of the human genome and get something different and functional. Every single primate genome disproves this claim because they have different sequences that are functional and produce different species. But that's not what humans have. We don't have just two alleles that protect against all known diseases. We have tons of different alleles with different functions that protect against different diseases. Then why are other primate species different from humans if it isn't due to a DNA sequence difference between our genomes? Are you saying that the original humans and original chimps looked and acted identical to one another right after the flood? If not, what are you going on about? Do you think humans and all primate species started out with genomes that were 100% identical to each other? Was there a time when the rhesus monkey genome was 100% identical to the human genome?