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

Meaning there are many "alleles" with different DNA sequences (i.e. mutations) that so far remain in the population. Two If they don't change the function of the original allele they would continue to occur in the population as the original allele would. 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. I still don't get what is "highly unlikely" about this.

No, what I'm saying is that everyone has the same genes but not originally with a variety of different alleles, originally with only two alleles per gene. This refers only to the original alleles. From what is being said here, the "current" alleles, insofar as they show a variety of different DNA sequences, are mostlymutations ("mostly" assuming some have the same sequence as the original allele) but not deleterious ones since they persist in the population.As bluegenes said in response to this, I recognize that there may be a lot of neutral mutations -- mutations that don't change the function of the original allele -- its sequence is different but not its function -- it still makes the same protein and still produces the same trait as the original --ONLY the sequence was changed by the mutation. As long as they function just as the original allele did the changed sequence doesn't make any difference in the condition of the trait or the organism positive or negative.(There may even be some cases where ALL the "alleles" for a particular gene in a population are mutations and none of the originals even continue to exist. That's occurred to me although it hasn't been brought up before. The only way we'd know they do what the original allele did is that the trait continues in the population as usual.Edited by Faith, : No reason given.

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. Even with no more genes with their two alleles contributing to eye color, subsequent generations will continue to have more Bb heterozygous brown eye color than the homozygous bb and BB.Even when you get populations that become completely homozygous BB or bb there is no disadvantage over many generations. What eventually can threaten the genetic makeup is mutations that kill one of the alleles and therefore kill the trait in an individual. This would have to be a seriously lethal change in the sequence, and I don't know what it would do to the trait itself, do you? In reality the other genes for the trait would probably kick in anyway, but I'm trying to stick to the example of the one gene Bb. (If the mutations are neutral the trait will continue as always of course).The point is that it takes a lot to kill a gene and a trait, it can take a long time of deleterious mutations attacking genes for a disease process to result and then be passed on. Homozygous genes are most vulnerable, could even be completely disabled by one lethal mutation, but unless it's lethal to the organism, to the individual, it can get passed on but while that would be a disease process spreading through the population it won't threaten the population itself. It would take a lot of these occurrences in a lot of genes to do that. That has happened in heavily inbreeding populations like the Amish and the Inuit. But unless a lot of genetic disease occurs frequently throughout the population it won't take a toll on the species itself for a long time. Of course since each individual has -- what? -- hundreds of mutations of his/her/its own, the odds aren't negligible, and they get more problematic with each generation, and not being lethal, get passed on to the next.Homozygosity for one gene is likely to be accompanied by homozygosity for many, since it's usually the result of reduced numbers of individuals in the founding population, the Amish, the Inuit, being cases in point for human beings. The larger the population grows from that point the safer it will be from a genetic problem due to the homoygosity, but once it is established it's going to be passed on unless it actually kills the organism. I may not be saying this as well as I'd like, but I think I'm in the ballpark. I don't even know how to find this out, I have to rely on whatever comes up here. "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. The same way the original allele would spread, nothing unusual, just according to the principles of the Mendelian square.Edited by Faith, : No reason given.

I've responded a few times to the message you suggest I respond to.Please answer this question: WHAT exactly has "increased in frequency?"and how can you know when (how long ago) a particular mutation occurred and how "quickly" it spread?Edited by Faith, : No reason given.

this should really be answered by bluegenes who posted that information. He might be more informative.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.I don't know what link you were talking about so I seem to have missed it. And if it's a link that goes to a long white page I won't be able to read it carefully anyway.

[qs] 1) 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.Different combinations of alleles at one locus? What do you mean? What's combining with what? How many different eye colors?

1) 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.Different combinations of alleles at one locus? What do you mean? What's combining with what? How many different eye colors?

You say I can't extrapolate from one gene to the entire genome. Seems to me if one gene can be understood in terms of a Mendel square many others ought to be as well. Even more complicated situations such as codominance can be expressed in those terms.The problem with standard genetics seems to be that mutations are treated as normal events and that's why it's all so complicated. A bunch of random accidents of replication complicates things enormously if you're trying to discover a lawful pattern there, and explain things like variation in eye color as in the previous post.And it's so unnecessary if eye color is governed simply by some number of genes with two alleles each. Extra alleles are redundant at best in such a system.

I can't offer an explanation for an increase in frequency I don't think even exists. I already gave an answer to this. It's meaningless if the "new" alleles do not change the function of the original. 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.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. Even assuming that a difference in DNA sequence -- produced by a mutation -- means a difference in product? That's really a sort of heresy. Edited by Faith, : No reason given.

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

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

No, they ARE "relying on an abstract theoretical model" by treating mutations as normal variations. That's the problem. Mutations are a disease, even when they are "neutral." Treating them as normal modes of variation cannot have good consequences in the end either. Sounds good but what if it's an illusion under due to the assumptions of the ToE?. The article that purports to be "looking at how [eye] colors are actually produced" is looking at a mutation in a gene that happens to have some effect on eye color, based on the assumption that mutations produce all new variation, when all that you are looking at is one aberrant way eye color may continue to be produced even with a change in an allele's sequence. 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. The theory that is guiding the investigation is actually crucial to finding out "what is really going on."Edited by Faith, : No reason given.Edited by Faith, : change "under" to "due to" for clarity

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.Edited by Faith, : No reason given.

You count it as a separate allele and that's what makes it seem to have increased in frequency, 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.Edited by Faith, : No reason given.

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