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Author | Topic: Y.E.C. Model: Was there rapid evolution and speciation post flood? | |||||||||||||||||||||||||||
Faith  Suspended Member (Idle past 1470 days) Posts: 35298 From: Nevada, USA Joined: |
The basic argument is simple. There are many common alleles of these genes. Meaning there are many "alleles" with different DNA sequences (i.e. mutations) that so far remain in the population.
Under your views there are only four original alleles Two
Every one of these other alleles must have occurred as a mutation and spread significantly If they don't change the function of the original allele they would continue to occur in the population as the original allele would.
You have only 6000 years for the mutations to occur and spread from their original occurrence 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.
This is highly unlikely without strong positive selection. Note that knowing what the different alleles do is not even relevant to the argument. I still don't get what is "highly unlikely" about this.
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Faith  Suspended Member (Idle past 1470 days) Posts: 35298 From: Nevada, USA Joined: |
What Faith is saying is that everyone has the same genes but with potentially a variety of different alleles, and that the current alleles are the only ones that aren't deleterious. Any mutations in existing alleles would be deleterious. --Percy 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.
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Faith  Suspended Member (Idle past 1470 days) Posts: 35298 From: Nevada, USA Joined: |
Two Given that heterozygosity is an advantage in these genes I think you should go for four in this case. 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.
If they don't change the function of the original allele they would continue to occur in the population as the original allele would. You haven't even bothered to find out what these genes do, have you ? I don't even know how to find this out, I have to rely on whatever comes up here.
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. If they don't offer any advantage then - on average - they won't increase in frequency at all. That is pretty basic. "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.
I still don't get what is "highly unlikely" about this How do the extra alleles spread so quickly ? 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.
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Faith  Suspended Member (Idle past 1470 days) Posts: 35298 From: Nevada, USA Joined: |
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.
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Faith  Suspended Member (Idle past 1470 days) Posts: 35298 From: Nevada, USA Joined: |
WHAT exactly has "increased in frequency?" The mutant alleles of course. As I said. 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.
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Faith  Suspended Member (Idle past 1470 days) Posts: 35298 From: Nevada, USA Joined: |
[qs]
Taq writes: Ran across this paper: A Three–Single-Nucleotide Polymorphism Haplotype in Intron 1 of OCA2 Explains Most Human Eye-Color Variation - PMC... It lists multiple alleles for the OCA2 gene, and those alleles are not equal in function. Different combinations of alleles produces different eye colors. This is an example of more than 2 alleles for the same gene 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?
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Faith  Suspended Member (Idle past 1470 days) Posts: 35298 From: Nevada, USA Joined: |
Taq writes: Ran across this paper: A Three–Single-Nucleotide Polymorphism Haplotype in Intron 1 of OCA2 Explains Most Human Eye-Color Variation - PMC... It lists multiple alleles for the OCA2 gene, and those alleles are not equal in function. Different combinations of alleles produces different eye colors. This is an example of more than 2 alleles for the same gene 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?
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Faith  Suspended Member (Idle past 1470 days) Posts: 35298 From: Nevada, USA Joined: |
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.
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Faith  Suspended Member (Idle past 1470 days) Posts: 35298 From: Nevada, USA Joined: |
I can't offer an explanation for an increase in frequency I don't think even exists.
Expression of MHC alleles is codominant, with the protein products of both the alleles at a locus being expressed in the cell, and both gene products being able to present antigens to T cells. The extensive polymorphism at each locus thus has the potential to double the number of different MHC molecules expressed in an individual and thereby increases the diversity already available through polygeny 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.
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Faith  Suspended Member (Idle past 1470 days) Posts: 35298 From: Nevada, USA Joined: |
I think you mean that the "problem" is that scientists try to find out what is really going on ... 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."
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Faith  Suspended Member (Idle past 1470 days) Posts: 35298 From: Nevada, USA Joined: |
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. 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.
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Faith  Suspended Member (Idle past 1470 days) Posts: 35298 From: Nevada, USA Joined: |
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. No, they ARE "relying on an abstract theoretical model" by treating mutations as normal variations. That's the problem.
Treating what is really a disease process as if it were normal is not going to show you "what is really going on." Life is just a disease then ? Mutations are a disease, even when they are "neutral." Treating them as normal modes of variation cannot have good consequences in the end either.
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. Sounds good but what if it's an illusion Edited by Faith, : No reason given. Edited by Faith, : change "under" to "due to" for clarity
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Faith  Suspended Member (Idle past 1470 days) Posts: 35298 From: Nevada, USA Joined: |
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.
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Faith  Suspended Member (Idle past 1470 days) Posts: 35298 From: Nevada, USA Joined: |
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.
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Faith  Suspended Member (Idle past 1470 days) Posts: 35298 From: Nevada, USA Joined: |
there is no increase in frequency if the mutation does the same thing as the original allele.
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