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Author Topic:   Y.E.C. Model: Was there rapid evolution and speciation post flood?
Faith
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Posts: 24845
From: Nevada, USA
Joined: 10-06-2001
Member Rating: 1.1


Message 226 of 301 (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.


This message is a reply to:
 Message 224 by Percy, posted 05-16-2017 1:16 PM Percy has responded

Replies to this message:
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Faith
Member
Posts: 24845
From: Nevada, USA
Joined: 10-06-2001
Member Rating: 1.1


Message 227 of 301 (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 responded

Replies to this message:
 Message 228 by Taq, posted 05-16-2017 5:55 PM Faith has responded
 Message 230 by NosyNed, posted 05-16-2017 8:10 PM Faith has not yet responded
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Taq
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Posts: 6428
Joined: 03-06-2009
Member Rating: 4.3


Message 228 of 301 (809185)
05-16-2017 5:55 PM
Reply to: Message 227 by Faith
05-16-2017 5:47 PM


Re: alleles: sequence and function
Faith writes:

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).

Where is the evidence that they have the same function?

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.

Do all chimp genes function exactly the same as human genes, in your model?


This message is a reply to:
 Message 227 by Faith, posted 05-16-2017 5:47 PM Faith has responded

Replies to this message:
 Message 229 by Faith, posted 05-16-2017 5:59 PM Taq has responded

  
Faith
Member
Posts: 24845
From: Nevada, USA
Joined: 10-06-2001
Member Rating: 1.1


Message 229 of 301 (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:
 Message 228 by Taq, posted 05-16-2017 5:55 PM Taq has responded

Replies to this message:
 Message 231 by PaulK, posted 05-17-2017 12:24 AM Faith has not yet responded
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NosyNed
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Posts: 8774
From: Canada
Joined: 04-04-2003
Member Rating: 5.1


Message 230 of 301 (809195)
05-16-2017 8:10 PM
Reply to: Message 227 by Faith
05-16-2017 5:47 PM


Re: alleles: sequence and function
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.

For some of them that is the claim indeed. However, to keep this simple let's go one step at a time. We already have the terms you are looking for and you used it. A change of allele that does nothing can be called neutral and if it does something and is harmful it is deleterious and if it does something different and helps then it is beneficial. I think there is a word for a set of alleles that all produce the same protein but I don't know it. Neutral can do us for now don't you think?

If you don't want to use the word allele (which most of the world uses) what would you like to use ? "different sequence" That is ok too.

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.

Until someone supplies us with the official terms let us use "effectively different sequence". That is, one that has an external effect.

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.

So while using different terms than the rest of the world uses you and I agree that there are different sequences in the DNA now. That is mutations are changing things and have been for 4 to 6 thousand years.

Whether they are a good thing or not when they are an "effectively different sequence" (different allele to the rest of the world isn't determined yet.

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.

An increase in different sequences (alleles) is something we agree on then. We don't have much choice since they are measured so this is a simple fact. That doesn't have anything with effectively different sequences being beneficial or not yet. So far we agree that they are just there.

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.

Something we agree on then. What effect they might have we can look at next.


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 Message 227 by Faith, posted 05-16-2017 5:47 PM Faith has not yet responded

  
PaulK
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Posts: 12686
Joined: 01-10-2003
Member Rating: 2.8


Message 231 of 301 (809200)
05-17-2017 12:24 AM
Reply to: Message 229 by Faith
05-16-2017 5:59 PM


Re: alleles: sequence and function
quote:

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

Unfortunately for you we are not speaking of mutations, but of alleles that are extant in the population (some of which include multiple mutations). It is very likely that these have already undergone a degree of selection which would change the proportions.

In the specific case you are talking about Tag already said that the conclusion that they were beneficial was based on evidence that the alleles had been positively selected. It was not an assumption that they were beneficial.


This message is a reply to:
 Message 229 by Faith, posted 05-16-2017 5:59 PM Faith has not yet responded

    
Percy
Member
Posts: 15616
From: New Hampshire
Joined: 12-23-2000
Member Rating: 4.4


Message 232 of 301 (809212)
05-17-2017 7:47 AM
Reply to: Message 226 by Faith
05-16-2017 5:26 PM


Re: Number of Genes for Eye Color and Skin Color
Faith writes:

I've been arguing that the supposed frequency is an illusion...

This is just factually wrong. The frequency in the population is measured.

...based on their being assumed to be alleles that change the function of the gene,...

According to the Wikipedia article on MC1R there are a number of variants that affect hair and skin color.

...when they are most likely neutral mutations that don't change the function of the gene (or the allele whose sequence they alter).

Since the MC1R variants have an effect, such as black hair/dark skin versus red hair/fair skin versus freckles and so forth, the variants are mostly not neutral.

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.

This is a fair challenge. Let's see what evidence of different functions for different alleles can be mustered for you.

--Percy


This message is a reply to:
 Message 226 by Faith, posted 05-16-2017 5:26 PM Faith has not yet responded

    
bluegenes
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Posts: 3086
From: U.K.
Joined: 01-24-2007
Member Rating: 3.6


(1)
Message 233 of 301 (809214)
05-17-2017 7:52 AM
Reply to: Message 206 by Faith
05-16-2017 10:39 AM


Re: The YEC model requires beneficial mutations and strong positive selection.
Faith writes:

bluegenes writes:

Faith writes:

The main problem for me, I think, is that you are assuming there is such a thing as "new alleles" that perform necessary functions for the immune system. This is really the same problem I've been having all along on this subject.

Not "assuming". Observing.

Well nothing yet has shown anything actually observed, that I have seen.

Didn't you read the paper? The major histocompatibility complex (MHC) and its functions. NCBI

Faith writes:

It's all assumed.

Ah! Either you didn't read it all, or didn't understand all of it.

Faith writes:

These are assumed to be "alleles" for starters, and since alleles are alternative forms of a gene it is assumed that they do something to alter the gene's product in a beneficial way.

They are alleles by definition, and it is not assumed that all those present are beneficial, it is concluded that many are because of an understanding of how variety in the MHC works, and how the variant proteins function physically.

Faith writes:

There isn't even a discussion of the fact that they are mutations, which are known to be predominantly neutral, they're just called "alleles." I've had to keep bringing that up. It's a major problem for this whole idea.

Variation in the MHC is definitely advantageous, not neutral.

Faith writes:

bluegenes writes:

Faith writes:

I don't have a problem with these genes being polymorphous or with the idea that the alleles differ very slightly and that "they are necessarily different in how they function" as long as I assume that they are built in and not mutations.

They have to be mutations, except for an original maximum of 4 alleles per gene.

Yes they do have to be mutations, meaning they are not alleles according to my YEC model, and it still has to be shown that they ARE alleles as claimed. And please start noting that I'm using the idea of two alleles per gene for Adam and Eve, considering them to have had identical genomes -- not the presumed maximum of 4.

They're alleles by definition, and there are far more than "slight" differences on them.

Faith writes:

I keep suggesting that the "high frequency" is an illusion if the alleles are neutral mutations that don't change the function of the original allele. In that case they would be passed on to the next generations, and if you are counting them separately from other forms of the same allele they may look like they have high frequency when it's nothing but their continued existence in the population because there's no reason for them to be selected out.

A 6,500yr young earther shouldn't be saying that. You won't get many new neutral alleles present in a sample of 120 people (see my Cuban example) on any genes on that time scale, and you certainly can't get the pattern of variance we see on the HLA genes, with so many of them at >2%..

Faith writes:

You assume selection because they persist at all, and count any degree of persistence as increase in frequency when they are not increasing at any greater rate than all the other forms of the same allele, because they are essentially the same allele. This argument I keep making needs to be addressed.

We can observe a level of frequency impossible in a 300 generation neutral evolution model, and we can observe why having lots of different protein products in the MHC is advantageous.

I'm suggesting that it is you YECs who require particularly strong selection in order to explain what can be observed.

Faith writes:

bluegenes writes:

But relatively rare advantageous mutations can occur, then their frequency (the percentage of the population which has them) can increase via positive selection. Your model requires this, as only four alleles per. gene can be there 300 generations ago.

No, let's get this much sorted out please.
1) There are TWO alleles and two only, per gene, in my YEC model.
2) YOU are calling these mutations "alleles," and I am denying that they are alleles, at least saying that you have not shown that they do anything different than the original allele did.

As I hope you now understand from the paper, they are are there because of their difference in function.

Faith writes:

3) YOU are saying that they are positively selected, and I am saying that is an illusion as explained above.

Then your YEC model must be false. It (the YEC model) requires rapid strong positive selection to explain what we see in the MHC.

Faith writes:

4) Therefore the YEC model I'm using does not have to accept any of this. They aren't alleles, they aren't positively selected.

Your model has no obligation to be true, certainly.

Faith writes:

bluegenes writes:

Bear in mind that there are several of these very polymorphous genes, and that if the Adam & Eve maximum of 4 alleles was all that was available to us, then homozygosity would be common (1/4 of the population on each gene, and most people on at least one).

Homozygosity in individuals at particular loci occurs at that rate, but not in the whole population unless those individuals get reproductively isolated among themselves. I'm a bb, my father was a bb, my mother and siblings are all Bb. This is a pretty common situation. The original Scandinavians may have been so predominantly bb that even a Bb was rare, but that's the result of migration and reproductive isolation.

In any case I'm not sure I'm getting your point about the immune system. If the genes are codominant you aren't going to get homozygosity anyway, are you?

If you have the same allele for one gene, yes. Codominant means that, if you have two alleles at the locus, you always get two immune products for the price of one, a better bargain, certainly. The more alleles available, the less chance of individuals ending up with the same ones anywhere, and the better equipped the group or species is to survive a threatening attack.


This message is a reply to:
 Message 206 by Faith, posted 05-16-2017 10:39 AM Faith has not yet responded

Replies to this message:
 Message 235 by Percy, posted 05-17-2017 8:36 AM bluegenes has responded

  
Percy
Member
Posts: 15616
From: New Hampshire
Joined: 12-23-2000
Member Rating: 4.4


(1)
Message 234 of 301 (809218)
05-17-2017 8:18 AM
Reply to: Message 227 by Faith
05-16-2017 5:47 PM


Re: alleles: sequence and function
Faith writes:

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.

NosyNed is trying to accommodate your objection to the definition to "allele", but I believe it will just cause confusion. "Allele" has a definition and you can't change it. An allele is any unique nucleotide sequence for a gene. Some alleles produce different proteins and functions, some don't, but they're all alleles.

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.

Just to emphasize the point, this is an incorrect definition of allele. An allele is any unique nucleotide sequence at a gene locus. It does not need to code for a different protein to be a different allele. When a mutation causes a new and unique nucleotide sequence then it is a new allele, whether it codes for a new protein or not.

The nucleotide sequence of an allele is divided into nucleotide triplets called codons. Each 3-nucleotide codon codes for an amino acid that will be added in sequence to the protein as it is constructed. This table from Wikipedia shows which codons create which amino acids (it's big and very legible if you expand it):

It's false to call it an allele if it only does what all the others do at that locus despite its different sequence.

Since you've said it one more time I want to emphasize one more time that this is incorrect. A different nucleotide sequence is a different allele, whether it produces a different protein or not.

mutations are KNOWN to be predominantly neutral.

Because most of the genome is non-coding, most mutations occur in non-coding regions and are therefore neutral. But mutations that occur in coding regions are *not* "predominantly neutral." As you can see in the chart above, most single nucleotide mutations will result in different amino acids and therefore different proteins.

--Percy


This message is a reply to:
 Message 227 by Faith, posted 05-16-2017 5:47 PM Faith has not yet responded

    
Percy
Member
Posts: 15616
From: New Hampshire
Joined: 12-23-2000
Member Rating: 4.4


Message 235 of 301 (809219)
05-17-2017 8:36 AM
Reply to: Message 233 by bluegenes
05-17-2017 7:52 AM


Re: The YEC model requires beneficial mutations and strong positive selection.
bluegenes writes:

Didn't you read the paper? The major histocompatibility complex (MHC) and its functions. NCBI

I tried to read this paper but found it outside my pay grade. It might help if you could boil the paper down into something less technically dense.

As I hope you now understand from the paper, they are are there because of their difference in function.

I don't think this diagram will be understood without some provided background about what "peptide antigen binding" is and so forth. I kind of get it because I slogged through the first quarter or so of that paper, but I could do with some clarification, too.

--Percy


This message is a reply to:
 Message 233 by bluegenes, posted 05-17-2017 7:52 AM bluegenes has responded

Replies to this message:
 Message 236 by bluegenes, posted 05-17-2017 9:29 AM Percy has responded

    
bluegenes
Member
Posts: 3086
From: U.K.
Joined: 01-24-2007
Member Rating: 3.6


Message 236 of 301 (809227)
05-17-2017 9:29 AM
Reply to: Message 235 by Percy
05-17-2017 8:36 AM


Re: The YEC model requires beneficial mutations and strong positive selection.
Percy writes:

I tried to read this paper but found it outside my pay grade. It might help if you could boil the paper down into something less technically dense.

What did you make of the first extract I posted way back in the thread? It explains how we can express a great variety of antigen (toxic foreign substances) presenters (they identify and "present" the antigens to xenophobic killer cells) because of the many-gened, many-alleled nature of the system. If it sounded like Greek to you, that's partly because some of it is, but I'm sure you can get what's important.

quote:

Because of the polygeny of the MHC, every person will express at least three different antigen-presenting MHC class I molecules and three (or sometimes four) MHC class II molecules on his or her cells. In fact, the number of different MHC molecules expressed on the cells of most people is greater because of the extreme polymorphism of the MHC and the codominant expression of MHC gene products.

The term polymorphism comes from the Greek poly, meaning many, and morphe, meaning shape or structure. As used here, it means within-species variation at a gene locus, and thus in its protein product; the variant genes that can occupy the locus are termed alleles. 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. So there is only a small chance that the corresponding MHC locus on both the homologous chromosomes of an individual will have the same allele; most individuals will be heterozygous at MHC loci. The particular combination of MHC alleles found on a single chromosome is known as an MHC haplotype. 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


Then we can go from there. Important to this thread is that, although Adam and Eve could have the many gened part, they are limited in how many alleles they could have (4 maximum per loci) and now there are loads of functioning alleles in the system, certainly an advantage in dealing with the range of constantly mutating pathogens, and a massive mutational increase in positive functional information since creation, I might add!


This message is a reply to:
 Message 235 by Percy, posted 05-17-2017 8:36 AM Percy has responded

Replies to this message:
 Message 242 by Percy, posted 05-17-2017 1:38 PM bluegenes has responded

  
Taq
Member
Posts: 6428
Joined: 03-06-2009
Member Rating: 4.3


Message 237 of 301 (809237)
05-17-2017 10:53 AM
Reply to: Message 229 by Faith
05-16-2017 5:59 PM


Re: alleles: sequence and function
Faith writes:

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.

You can't assume they have the same function, either.

Faith writes:

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.

We don't need to assume that the genetic differences between humans and chimps are beneficial. We can directly observe that they are beneficial in both humans and chimps. Therefore, we know that changes in DNA can and are beneficial. No assumption needed.


This message is a reply to:
 Message 229 by Faith, posted 05-16-2017 5:59 PM Faith has not yet responded

  
Faith
Member
Posts: 24845
From: Nevada, USA
Joined: 10-06-2001
Member Rating: 1.1


Message 238 of 301 (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?


Replies to this message:
 Message 239 by jar, posted 05-17-2017 1:19 PM Faith has not yet responded
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jar
Member
Posts: 28834
From: Texas!!
Joined: 04-20-2004
Member Rating: 3.1


(1)
Message 239 of 301 (809255)
05-17-2017 1:19 PM
Reply to: Message 238 by Faith
05-17-2017 1:10 PM


Re: SUMMATION OF THE USUAL FLIMFLAM
Faith writes:

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.

Actually Faith, you are free to call mutations mutations but not to call an allele a mutation. Alleles are called alleles.

You are free to suggest whatever you want; just understand it is silly to expect folk to agree with the stuff you suggest that is patently false.

Remember that Adam and Eve would have had exactly the same alleles, not two sets of alleles. After all Eve was just a clone of Adam.

quote:
Oh, give me a clone

Of my own flesh and bone

With its Y chromosome changed to X.

And after it's grown,

Then my own little clone

Will be of the opposite sex.

.

.

.

Clone, clone of my own,

With its Y chromosome changed to X.

And when I'm alone

With my own little clone

We will both think of nothing but sex.


Source: Isaac Asimov

Edited by jar, : fix song spacing

Edited by jar, : No reason given.


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 Message 238 by Faith, posted 05-17-2017 1:10 PM Faith has not yet responded

  
PaulK
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Posts: 12686
Joined: 01-10-2003
Member Rating: 2.8


Message 240 of 301 (809256)
05-17-2017 1:34 PM
Reply to: Message 238 by Faith
05-17-2017 1:10 PM


Faith's Flimflam Fails - again.
quote:

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...

Because selection will bias the distribution - and because you need positive selection to account for the frequencies given your assumed timescales.

quote:

...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;

Because the evidence is against it.

quote:

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.

And you can't dismiss the evidence with pathetic excuses that don't even make sense.

If there is evidence for positive selection then that overrides your unevidenced assumption of neutrality. And that's the part that is least nonsensical.


This message is a reply to:
 Message 238 by Faith, posted 05-17-2017 1:10 PM Faith has not yet responded

    
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