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Author | Topic: Y.E.C. Model: Was there rapid evolution and speciation post flood? | |||||||||||||||||||||||||||||||||||||||
Taq Member Posts: 9973 Joined: Member Rating: 5.7
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Faith writes: Exactly what are these "30 known alleles" and why isn't this discussed? Obviously it's assumed that they ARE alleles, meaning alternative forms of the gene that do different things, presumably in this case varying the eye color. They are OBSERVED to be alleles since we can sequence them. Alleles are defined by their DNA sequence which can be easily determined, allowing scientists to determine which individuals have which alleles. As shown in the previous papers, multiple alleles (i.e. more than two) result in a wide range of eye colors. Two alleles can't do it. It requires more than two alleles to produce the variety of eye color in humans.
But to be bona fide alleles they have to do something different. They do do something different. They produce different eye colors.
This is a gene for eye color we're talking about. Even if the mutated allele did do something new all it could do is produce a new shade of eye color. That is irrelevant to the discussion. Whether the new function increased in frequency due to positive selection or neutral drift does nothing to change the fact that they have different functions.
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Taq Member Posts: 9973 Joined: Member Rating: 5.7
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Faith writes: That is correct, and since it has nothing to do with function you can't claim it's positively selected just based on the sequence, you have to show that it does change the function. The sequence can't be selected, only the function can be selected. To stress this point again, whether the allele increased in frequency due to positive or neutral selection has nothing to do with the fact that there are more than two alleles with more than two functions.
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Taq Member Posts: 9973 Joined: Member Rating: 5.7 |
Faith writes: Well nothing yet has shown anything actually observed, that I have seen. Sticking your head in the sand does not make the facts go away. I have already linked to the peer reviewed paper that contains the very facts you claim don't exist, and you still refuse to address it.
No, let's get this much sorted out please. 1) There are TWO alleles and two only, per gene, in my YEC model. In reality, there are more than two alleles for some genes as defined by function. Your model doesn't match up to reality, so it is rejected.
It is possible to construct a Mendel square for codominance using two genes. It is possible to build a model of our Solar System with just one planet. That doesn't mean there is just one planet in our Solar System. You seem to have a serious problem understanding the difference between reality and models. If I showed you a map of Kansas that had a 10,000 foot mountain range going down the middle of Kansas, which would be wrong, the map or the actual state of Kansas? You seem to be saying that the actual state of Kansas would be wrong because the map shows a mountain range going down the middle of it. Do you see the problem?
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Faith  Suspended Member (Idle past 1445 days) Posts: 35298 From: Nevada, USA Joined: |
Taq writes: Faith writes: That is correct, and since it has nothing to do with function you can't claim it's positively selected just based on the sequence, you have to show that it does change the function. The sequence can't be selected, only the function can be selected. To stress this point again, whether the allele increased in frequency due to positive or neutral selection has nothing to do with the fact that there are more than two alleles with more than two functions. It has to do with the fact that they aren't alleles, period, so they don't affect the model of two alleles per gene. And there is no such thing as "neutral" selection that I know of. As I keep saying, there seems to be an illusion of positive selection based on the assumption that these are in fact alleles, when this hasn't been shown and what they most likely really are is just neutral mutations -- when you count the separate sequences you create the illusion of selection when it's nothing but the mutated being passed on at the same rate as all the other versions of the same allele. By the way I edited the post after you'd answered it:
That is correct, and since it has nothing to do with function you can't claim it's positively selected just based on the sequence, you have to show that it does change the function. The sequence can't be selected, only the function can be selected, and since a neutral mutation would be passed on at the same rate as all the other forms of the same allele, you are most likely counting as an increase in frequency what is nothing but this normal passing on. It's an illusion based on counting the sequences as separate alleles. .
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Taq Member Posts: 9973 Joined: Member Rating: 5.7
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Faith writes: It has to do with the fact that they aren't alleles, period, Why aren't they alleles?
And there is no such thing as "neutral" selection that I know of. A Google search for "neutral selection" finds 78.3 million hits. Have you heard of Google?
As I keep saying, there seems to be an illusion of positive selection based on the assumption that these are in fact alleles, when this hasn't been shown and what they most likely really are is just neutral mutations -- when you count the separate sequences you create the illusion of selection when it's nothing but the mutated being passed on at the same rate as all the other versions of the same allele. You are deluding yourself. Whether these alleles are being selected for or not has nothing to do with the OBSERVATION that they have different functions.
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NosyNed Member Posts: 8996 From: Canada Joined:
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Also, as most board members are of European ancestry, many will have visible phenotype features that owe their existence to mutants of this gene. Well, here's the ToE assumption stated outright: all characteristics are the result of mutations; all alleles were originally mutations. (how original genes and their alleles got created by mutations when there was no DNA for them to alter is a puzzle but anyway...) No, not a ToE assumption.First: it is a requirment of your model. There weren't very many alleles to begin with and now there are more so there, by your model have to have been mutations. Second: The ToE doesn't say what any "original" allele was. You do. (and 3rd you are jumping way out there by suddenly talking about orgination of DNA which doesn't have anything to do with this discussion -- focus!). There is no such thing as a "bona fide" allele. Each allele is just a different pattern of base pairs in the gene they are all equal at that level.
3) But to be bona fide alleles they have to do something different. Why isn't it even discussed whether they do or not? I mean it's common knowledge that most mutations don't, how come it's so easy to assume these do? It is not an assumption and this thread has explained it already. In fact several times. The whole discussion about frequency is because of that. I tried to summarize for you to make it simpler. Did you read that?That's in Message 130
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Faith  Suspended Member (Idle past 1445 days) Posts: 35298 From: Nevada, USA Joined: |
There has been absolutely NO evidence that different functions have been observed.
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14174dm Member (Idle past 1109 days) Posts: 161 From: Cincinnati OH Joined: |
I'm not a biology type so please correct me if I'm wrong.
My understanding of genes and alleles is that when we say this gene controls such, we mean that we found a statistical link between the gene and the effect. We haven't traced the protein and its impacts through every cell and biochemical process. When we see this allele at the gene causing blue eyes, are we also seeing what else it does? For example, adrenaline increases heart rate, opens airways and increases the emotional aspect of memories. Is it possible for eye color to be a side effect of mutation/selection for (random example) enzymes in saliva for digesting grain products?
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Faith  Suspended Member (Idle past 1445 days) Posts: 35298 From: Nevada, USA Joined: |
I can't read that paper for various reasons s I've said. And you can cut the snarky remarks. I'm not sticking my head in the sand or any of the other crass accusations you keep laying on me. I'm debating in good faith and I'll just start ignoring you if you don't cut it out.
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Taq Member Posts: 9973 Joined: Member Rating: 5.7
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Faith writes: I can't read that paper for various reasons s I've said. That doesn't change the fact that it contains the very observations you claim don't exist.
I'm not sticking my head in the sand or any of the other crass accusations you keep laying on me. The very fact that you can't even do a simple Google search for "neutral selection" shows how you are suffering from self imposed ignorance. It isn't that you can't understand it. It's that you don't want to understand it.
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Taq Member Posts: 9973 Joined: Member Rating: 5.7 |
14174dm writes: My understanding of genes and alleles is that when we say this gene controls such, we mean that we found a statistical link between the gene and the effect. We haven't traced the protein and its impacts through every cell and biochemical process. For the specific paper on eye color, this is an accurate description. For some alleles the biochemical and physical interactions are understood at the molecular level.
When we see this allele at the gene causing blue eyes, are we also seeing what else it does? For example, adrenaline increases heart rate, opens airways and increases the emotional aspect of memories. It is entirely possible that the alleles affeting eye color also have functions elsewhere that are being selected for.
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Faith  Suspended Member (Idle past 1445 days) Posts: 35298 From: Nevada, USA Joined: |
Also, as most board members are of European ancestry, many will have visible phenotype features that owe their existence to mutants of this gene. Well, here's the ToE assumption stated outright: all characteristics are the result of mutations; all alleles were originally mutations. (how original genes and their alleles got created by mutations when there was no DNA for them to alter is a puzzle but anyway...)No, not a ToE assumption. First: it is a requirment of your model. There weren't very many alleles to begin with and now there are more so there, by your model have to have been mutations. The alleles that are the subject of this discussion are mutations, which I don't regard as alleles. And as the Mendel squares easily demonstrate, more than two alleles per gene are not needed for all the diversity we see in living things.
Second: The ToE doesn't say what any "original" allele was. You do. Yes, that is MY model, not the ToE; however you will find it expressed this way even in referenced articles by bluegenes and maybe even Taq. It's kind of hard to avoid even though it isn't part of the ToE model.
(and 3rd you are jumping way out there by suddenly talking about orgination of DNA which doesn't have anything to do with this discussion -- focus!). That's why I put it in parentheses. Kind of just occurs in the course of this sort of discussion. Where did all those sequences come from that are being altered by mutations anyway? I don't expect an answer or even want one since it isn't the topic.
There is no such thing as a "bona fide" allele. Each allele is just a different pattern of base pairs in the gene they are all equal at that level. Yes, according to the ToE, but we're trying to have a debate here, right? Or maybe not. I am anyway. So the views of both debaters really should be kept in mind don't you think? By the YEC model I'm trying to keep on the table there is definitely a bone fide allele. I reject the ToE idea that they are the result of mutations. I keep trying to keep this clearly stated too, so there shouldn't be a lot of confusion. If you just want to insist on the ToE there is no debate and so buhbye.
3) But to be bona fide alleles they have to do something different. Why isn't it even discussed whether they do or not? I mean it's common knowledge that most mutations don't, how come it's so easy to assume these do? It is not an assumption and this thread has explained it already. In fact several times. The whole discussion about frequency is because of that. Sorry, I missed it. All I've seen is assumptions and no evidence. They are called "alleles" rather than mutations, that's an assumption. As "alleles" they are said to have increased in frequency. I've said that isn't the case if they are just different sequences with the same function being counted separately, which would create a false increase in frequency.
I tried to summarize for you to make it simpler. Did you read that? That's in Message 130 I don't know if I saw it. Maybe I didn't think it worth checking on. Edited by Faith, : No reason given.
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Taq Member Posts: 9973 Joined: Member Rating: 5.7 |
Faith writes: And as the Mendel squares easily demonstrate, more than two alleles per gene are not needed for all the diversity we see in living things. How so? You seem to just assert this without any backing.
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Percy Member Posts: 22393 From: New Hampshire Joined: Member Rating: 5.2 |
Percy writes: ...but if you add more genes, such as those mentioned by Percy for eye color, and many more for skin color, the number of variations increases enormously. There is really absolutely no need for extra alleles. No one should be arguing that extra alleles beyond two are needed for eye or skin color, since these are both determined by multiple genes. Bluegenes is arguing that the MC1R gene has 30 known alleles that occur at a frequency that indicates positive selection (i.e., they do something uniquely beneficial than other alleles). These 30 alleles had to come from mutation, and there has been insufficient time since Adam and Eve's original 4 (max) for them to arise and spread. --Percy Edited by Percy, : Clarify first sentence.
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NosyNed Member Posts: 8996 From: Canada Joined: |
The alleles that are the subject of this discussion are mutations, which I don't regard as alleles. And as the Mendel squares easily demonstrate, more than two alleles per gene are not needed for all the diversity we see in living things. Then what are they? An allele is any pattern as part of the DNA of an organism marked out as a gene in the DNA. If it is changed by any means at all then it is a new allele. Why do you disagree with this?
Yes, according to the ToE, but we're trying to have a debate here, right? Or maybe not. I am anyway. So the views of both debaters really should be kept in mind don't you think? By the YEC model I'm trying to keep on the table there is definitely a bone fide allele. I reject the ToE idea that they are the result of mutations. I keep trying to keep this clearly stated too, so there shouldn't be a lot of confusion. If you just want to insist on the ToE there is no debate and so buhbye Please define what a 'bona fide' allele is so we can tell it apart from others. We are not talking about the ToE model here, we are talking about your model. Since there were fewer (many fewer) alleles in your model around 4 to 6,000 years ago where did the additional ones come from?
Sorry, I missed it. All I've seen is assumptions and no evidence. They are called "alleles" rather than mutations, that's an assumption. As "alleles" they are said to have increased in frequency. I've said that isn't the case if they are just different sequences with the same function being counted separately, which would create a false increase in frequency. If we are to discuss we'll have to have a common vocabulary. I don't see why we have to have a new word for something that is already defined. An allele is any different sequence whether it has a different result in the phenotype or not. There has been, according to your model, an increase in these different sequences (whatever you want to call them). Are you now saying there aren't more sequences (alleles is the word to everyone else) than there were a few 1,000 years ago?
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