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Author Topic:   Y.E.C. Model: Was there rapid evolution and speciation post flood?
Faith 
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Posts: 35298
From: Nevada, USA
Joined: 10-06-2001


Message 222 of 518 (809136)
05-16-2017 11:53 AM
Reply to: Message 216 by NosyNed
05-16-2017 11:27 AM


Re: alleles
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.

This message is a reply to:
 Message 216 by NosyNed, posted 05-16-2017 11:27 AM NosyNed has replied

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Faith 
Suspended Member (Idle past 1465 days)
Posts: 35298
From: Nevada, USA
Joined: 10-06-2001


Message 226 of 518 (809179)
05-16-2017 5:26 PM
Reply to: Message 224 by Percy
05-16-2017 1:16 PM


Re: Number of Genes for Eye Color and Skin Color
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.
I know. But he has not proved that they "all do something uniquely beneficial," what's the proof? I've been arguing that the supposed frequency is an illusion based on their being assumed to be alleles that change the function of the gene, when they are most likely neutral mutations that don't change the function of the gene (or the allele whose sequence they alter). The two false assumptions support each other: He infers changed function from the supposed increase in frequency, but that increase in frequency is an illusion if they are only neutral mutations, since counting the appearances of each new sequence separately would give a false idea of increase if they are only neutral mutations. He needs to show actual positive change in function and I don't know how you do that with the immune system. It could be done with eye color or skin color.
Edited by Faith, : No reason given.
Edited by Faith, : No reason given.

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Faith 
Suspended Member (Idle past 1465 days)
Posts: 35298
From: Nevada, USA
Joined: 10-06-2001


Message 227 of 518 (809184)
05-16-2017 5:47 PM
Reply to: Message 225 by NosyNed
05-16-2017 1:49 PM


Re: alleles: sequence and function
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?
Because the claim is that these "alleles" code for a different protein and different function of the gene than the allele whose sequence they changed, but there is no evidence that they code for anything other than the original allele did (the one at that particular locus whose sequence they changed). A change in sequence that does not change the protein or function is just a neutral mutation. Calling it an allele confuses things.
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.
Its sequence codes for a different protein and different trait than other sequences for the same locus. If it only does what the others do it's a neutral mutation. If you are still stuck on calling it an allele please provide a term that allows for this crucial distinction I'm talking about.
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?
They aren't alleles according to what I say above, they are merely mutations, changes in the DNA sequence that do not code for a new protein or a new trait, and in my model there are lots of mutations occurring all the time, most of them neutral which is why I'm assuming that's what these are, or deleterious. Mutations ARE increasing. In my model they are not true alleles and they are not a good thing for the organism.
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.
That will not do since the different result is crucial to this discussion. It's false to call it an allele if it only does what all the others do at that locus despite its different sequence.
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?
According to this thread there has been an increase in these different sequences and that seems to be treated as synonymous with a change in function of the gene. I wouldn't doubt the increase in changed sequences, which is an increase in mutations, which fits with the YEC model just fine. I disagree with their assumed beneficial change in function: I haven't seen it proved, I've only seen it assumed. A change in sequence happens all the time; it's called a mutation; mutations are KNOWN to be predominantly neutral. Why are these treated as functioning alleles instead.
Taq posted a paper back there somewhere (I'd have to go track it down) which he claims proves a change in function for some mutations or other, but it's too technical for me, and it's hard on my eyes, at least because its being too technical means I have to spend too much time on it. If you or anyone else can translate it into clear nontechnical English so I can read it that would be a great service to this topic.
Edited by Faith, : No reason given.

This message is a reply to:
 Message 225 by NosyNed, posted 05-16-2017 1:49 PM NosyNed has replied

Replies to this message:
 Message 228 by Taq, posted 05-16-2017 5:55 PM Faith has replied
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Faith 
Suspended Member (Idle past 1465 days)
Posts: 35298
From: Nevada, USA
Joined: 10-06-2001


Message 229 of 518 (809186)
05-16-2017 5:59 PM
Reply to: Message 228 by Taq
05-16-2017 5:55 PM


Re: alleles: sequence and function
.
Where is the evidence that they have the same function?
There is no evidence one way or the other, but it needs to be proved and can't be assumed that the function is not the same.
ABE: Since most mutations are known to be neutral, others deleterious and very very few very iffily beneficial, it ought to be common sense to provide evidence that any mutation is beneficial, but no, all these on this thread are ASSUMED to be beneficial.
Edited by Faith, : No reason given.
Edited by Faith, : No reason given.
Edited by Faith, : No reason given.
Edited by Faith, : No reason given.

This message is a reply to:
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Faith 
Suspended Member (Idle past 1465 days)
Posts: 35298
From: Nevada, USA
Joined: 10-06-2001


Message 238 of 518 (809254)
05-17-2017 1:10 PM


SUMMATION OF THE USUAL FLIMFLAM
I can't call a mutation a mutation, I have to call it an allele, so I can't point out that mutations are usually neutral, second deleterious, so I can't dispute the argument that I have to account for alleles that Adam and Eve didn't have on the ground that they are just neutral mutations; and I can't suggest that what is being called an increase in frequency due to positive selection isn't that if these are really neutral mutations, it's an illusion caused by counting new sequences, which are really mutations, as alleles.
Far as I can see the debate is over and the evos won again. So what else is new?

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Faith 
Suspended Member (Idle past 1465 days)
Posts: 35298
From: Nevada, USA
Joined: 10-06-2001


Message 252 of 518 (809321)
05-17-2017 7:29 PM


High frequency / positive selection
Here's the quote that keeps being passed along from bluegenes' post on the MHC genes:
There are more than 200 alleles of some human MHC class I and class II genes, each allele being present at a relatively high frequency in the population.
What I would like to know is what constitutes a "relatively high frequency in the population?"
There are, what, about seven billion of us now?
Say a single allele has 1000 variants (not a mere 200). I'm sure they wouldn't be evenly distributed in the population, but if they were neutral mutations one of the variants could be possessed by seven million* of us. Is that a high frequency?
That would be the average frequency of the occurrence of a neutral mutation in the population if there were a thousand variants that were all neutral mutations. It would vary quite a bit having to do with where it first appeared so you should find higher frequencies in populations in that area, and of course drift.
So, to repeat the question: What constitutes a "relatively high frequency in the population?"
Edited by Faith, : No reason given.
Edited by Faith, : No reason given.
Edited by Faith, : No reason given.
Edited by Faith, : No reason given.
Edited by Faith, : No reason given.
Edited by Faith, : No reason given.
Edited by Faith, : No reason given.

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Faith 
Suspended Member (Idle past 1465 days)
Posts: 35298
From: Nevada, USA
Joined: 10-06-2001


Message 258 of 518 (809402)
05-18-2017 10:38 AM
Reply to: Message 257 by bluegenes
05-18-2017 10:30 AM


Re: On Adam & Eve?
Faith's going for two alleles, but God might not have used standard cloning procedures, and presumably could have used genetic modification.
I arrived at two based partly on the fact that all we can inherit from our parents is one from each, and DNA and therefore a gene is after all two strands wound together. But the Biblical fact that Eve according to Adam is "bone of my bone and flesh of my flesh" is a good reason too.
d, considering the sub thread, wonder why he gave them an immune system pre-fall, couldn't we?
Yes, I wonder those things too, but I suppose we might as well also wonder why we have a blood clotting system or a wound healing system as well.
Edited by Faith, : No reason given.

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Faith 
Suspended Member (Idle past 1465 days)
Posts: 35298
From: Nevada, USA
Joined: 10-06-2001


Message 260 of 518 (809422)
05-18-2017 11:38 AM
Reply to: Message 259 by jar
05-18-2017 11:28 AM


Re: On Adam & Eve?
they don't look identical to me:

This message is a reply to:
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Faith 
Suspended Member (Idle past 1465 days)
Posts: 35298
From: Nevada, USA
Joined: 10-06-2001


Message 266 of 518 (809457)
05-18-2017 12:43 PM
Reply to: Message 263 by Taq
05-18-2017 12:28 PM


Re: On Adam & Eve?
That's beautiful. And you guys don't believe in intelligent design!

This message is a reply to:
 Message 263 by Taq, posted 05-18-2017 12:28 PM Taq has replied

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Faith 
Suspended Member (Idle past 1465 days)
Posts: 35298
From: Nevada, USA
Joined: 10-06-2001


Message 269 of 518 (809482)
05-18-2017 1:16 PM
Reply to: Message 268 by bluegenes
05-18-2017 1:05 PM


Re: How to understand some but not all. Good grief
Ooooooobviously I understood some of it. Sheesh.
Edited by Faith, : No reason given.

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Faith 
Suspended Member (Idle past 1465 days)
Posts: 35298
From: Nevada, USA
Joined: 10-06-2001


Message 284 of 518 (809733)
05-20-2017 3:19 PM
Reply to: Message 283 by Percy
05-20-2017 8:13 AM


Re: The YEC model requires beneficial mutations and strong positive selection.
Efforts have been to persuade Faith of two things:
That the frequency of the alleles indicates strong selection and therefore different function. Faith rejects this argument, arguing that if the alleles did the same thing as existing alleles then they would also have strong selection.
That there has not been enough time since Adam and Eve to create the distribution of alleles we observe in the human population.
My answer to this, for the record, has been that if they are neutral mutations/alleles there is no limit on how many there would be in a given time frame. I'd also add at this point that the fact that there are so many is evidence in itself that they are neutral mutations according to the YEC framework.
I'm seeking the evidence that proves these two points. It may have been presented already, but not in a form I understand.
It should be pretty clear by now that there isn't any.

This message is a reply to:
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Faith 
Suspended Member (Idle past 1465 days)
Posts: 35298
From: Nevada, USA
Joined: 10-06-2001


Message 293 of 518 (810064)
05-23-2017 10:34 AM
Reply to: Message 292 by Percy
05-23-2017 9:50 AM


Re: The YEC model requires beneficial mutations and strong positive selection.
The binding of something or other to something or other is the evidence. First it would have to be shown that this binding does something beneficial to the immune system. How are they going to prove that? But also it's all about one disease, Dengue fever. What would it prove about different functions of different alleles when it's all about one disease?

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Faith 
Suspended Member (Idle past 1465 days)
Posts: 35298
From: Nevada, USA
Joined: 10-06-2001


Message 299 of 518 (810135)
05-24-2017 1:13 AM
Reply to: Message 298 by NoNukes
05-24-2017 12:52 AM


Re: The YEC model requires beneficial mutations and strong positive selection.
Both the rabbit fur and the blood types came up earlier in the thread. Yes, they are sufficient. End of thread, thank you,.

This message is a reply to:
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Faith 
Suspended Member (Idle past 1465 days)
Posts: 35298
From: Nevada, USA
Joined: 10-06-2001


Message 305 of 518 (810153)
05-24-2017 9:15 AM
Reply to: Message 303 by Percy
05-24-2017 8:27 AM


Re: The YEC model requires beneficial mutations and strong positive selection.
I don't know why Faith answered as she did in Message 299, but the sudden capitulation is inconsistent with the rest of her posts to this thread and I don't think she's saying what she believes.
I'm just tired of fighting it and trying to leave for a while. I can't answer the supposed evidences given so even though I might again try to answer them in the future, not right now. I need a break. Capitulating just means I can't prove my case and am giving up trying.
I don't think either blood type or rabbit fur color proves multiple functional new alleles have come about, because multiple genes must be involved. The Wikipedia article on Blood Type says that "33 blood-group systems have been identified, including the ABO and Rh systems," which implies multiple genes at work. And I couldn't find anything about rabbit fur color earlier in the thread, but I assume it too is governed by multiple genes.
The post about rabbits is Message 23 where bluegenes clearly says the varieties of fur color are from different alleles for one gene. Says it, doesn't prove it, so if you can pin it down to multiple genes more power to you.

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Faith 
Suspended Member (Idle past 1465 days)
Posts: 35298
From: Nevada, USA
Joined: 10-06-2001


Message 332 of 518 (810545)
05-30-2017 5:14 PM


rough ponderings
Just some rough impressions from the Creo point of view.
I'm sticking to my basic idea that there were originally two alleles per gene for the vast majority of traits.
I'm tentatively conceding that there might have been four alleles between Adam and Eve for SOME genes.
I still have the basic idea that the extra alleles are mutations and that mutations are not a normal process but a mistake that usually 1) does not change the phenotype, the "neutral" mutations, 2) often produces disease and 3) sometimes as more of a fluke than anything else produces something that appears to be positive for the phenotype.
What NN posted about the gene with three alleles for blood type, (plus a few other rarer alleles) suggests to me that A and B were the originals and that O is a mutation -- a "frameshift" -- that happens to have a positive enough effect to be considered a true variant, but it's one of those I'd consider to be likely a fluke. In NNs post he describes it as lacking functions that A and B have.
The extra alleles for rabbit fur color are obviously superfluous since the existing genes are certainly sufficient to vary the color in many different ways. So the extras are mutations that are sort of akin to neutral mutations but do produce some difference, just not anything that could be considered necessary.
When someone says that "for all we know such and such an allele might have protected our ancestors from sucn and such a disease" we're deep in evo territory. There are many alleles involved in the immune system some of whose function or phenotypic effect are known, but as Percy's charts point out a lot of them are redundant, doing the same thing. And a lot are unknown. I think this implies that the statement in the article back toward the beginning of the thread that all these alleles are a good thing because they imply the many differences in function needed to protect against the many differences in diseases, isn't really justified.
But as I said these are rough thoughts and I don't claim to be following the argument all that well.

Replies to this message:
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