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Author Topic:   Y.E.C. Model: Was there rapid evolution and speciation post flood?
PaulK
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Posts: 17822
Joined: 01-10-2003
Member Rating: 2.2


(1)
Message 181 of 518 (808900)
05-14-2017 4:54 PM
Reply to: Message 180 by Faith
05-14-2017 4:48 PM


Re: The YEC model requires beneficial mutations and strong positive selection.
quote:
there is no increase in frequency if the mutation does the same thing as the original allele.
Of course there is. So long as there is a visible difference we can count the alleles. And if we count them we can measure the frequencies.
Assuming that there is no difference in the products is silly enough. Assuming that measured frequencies are an "illusion" for a reason that makes no sense is raving insanity. This is your brain on creationism.

This message is a reply to:
 Message 180 by Faith, posted 05-14-2017 4:48 PM Faith has replied

Replies to this message:
 Message 182 by Faith, posted 05-14-2017 5:25 PM PaulK has replied

  
Faith 
Suspended Member (Idle past 1444 days)
Posts: 35298
From: Nevada, USA
Joined: 10-06-2001


Message 182 of 518 (808902)
05-14-2017 5:25 PM
Reply to: Message 181 by PaulK
05-14-2017 4:54 PM


Re: The YEC model requires beneficial mutations and strong positive selection.
It's the same allele.
It does the same thing.
Increased frequency implies selection. That's the whole point.
Selection works on function, not "looks."
Selection selects for improved fitness of some sort.
There is no difference in fitness; it's the same allele.
The increased frequency is an illusion.

This message is a reply to:
 Message 181 by PaulK, posted 05-14-2017 4:54 PM PaulK has replied

Replies to this message:
 Message 184 by PaulK, posted 05-15-2017 12:30 AM Faith has replied

  
jar
Member (Idle past 394 days)
Posts: 34026
From: Texas!!
Joined: 04-20-2004


Message 183 of 518 (808903)
05-14-2017 5:37 PM
Reply to: Message 180 by Faith
05-14-2017 4:48 PM


Re: The YEC model requires beneficial mutations and strong positive selection.
Faith writes:
there is no increase in frequency if the mutation does the same thing as the original allele.
That is simply not true Faith.
As I pointed out back in Message 169:
quote:
Imagine a pile of US coins that add up to $100.00.
Now imagine that some of those coins are converted to French Francs, British Pounds and Japanese Yen.
The value is still the same but the diversity has increased.
They do the same thing. But diversity, frequency, has increased.
When I buy something I can pay for it in Pounds, Dollars, Francs, Yen. They all serve the same purpose but a Dollar is not a Yen is not a Pound is not a Franc.
You can continue to deny reality all you want but the frequency is still observed.
Maybe what would help would be if instead of denying reality you presented some evidence that supports a Young Earth or Creationism, something no Creationist seems to have ever tried to do.
Edited by jar, : fix quotebox

My Sister's Website: Rose Hill Studios My Website: My Website

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PaulK
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Posts: 17822
Joined: 01-10-2003
Member Rating: 2.2


(1)
Message 184 of 518 (808928)
05-15-2017 12:30 AM
Reply to: Message 182 by Faith
05-14-2017 5:25 PM


Re: The YEC model requires beneficial mutations and strong positive selection.
quote:
It's the same allele.
Obviously it is distinct, since it can be counted.
quote:
It does the same thing.
That is your assumption - and one that is almost certainly false.
quote:
Increased frequency implies selection. That's the whole point.
Over a relatively short timescale, and for significant increases in frequency, that is so.
quote:
Selection works on function, not "looks."
Selection selects for improved fitness of some sort.
And there is nothing to disagree with there, but...
quote:
There is no difference in fitness; it's the same allele.
That is your assumption. In reality there is almost certainly selection for diversity in these genes.
quote:
The increased frequency is an illusion.
So when reality contradicts your assumptions you jump,to the conclusion that reality is wrong. Even if the assumption is almost certainly false and you cannot think of any way that your conclusion could even possibly be correct.
Even if you believe such nonsense, why should anyone else ?

This message is a reply to:
 Message 182 by Faith, posted 05-14-2017 5:25 PM Faith has replied

Replies to this message:
 Message 185 by Faith, posted 05-15-2017 1:01 AM PaulK has replied

  
Faith 
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Posts: 35298
From: Nevada, USA
Joined: 10-06-2001


Message 185 of 518 (808930)
05-15-2017 1:01 AM
Reply to: Message 184 by PaulK
05-15-2017 12:30 AM


Re: The YEC model requires beneficial mutations and strong positive selection.
You can't just say it must be functionally different without any proof whatever when neutral mutations are the most common and they do not change the function. You have to show a difference in function, you can't assume it, and it has not been shown. "Diversity" is not diversity unless there is a diversity of function and not just sequence. Increase in frequency is meaningless unless it's based on a difference in function, that is, positive selection for beneficial function.;
You have to SHOW a difference in function.; There are a couple of posts back a ways that attempt to show that. One of them is too technical for me and my eyes have trouble with it too. Why don't you go back and see if you can make a case for changed function from that or something similar instead of pretending mere changes in sequence imply it, which obviously they don't.
Edited by Faith, : No reason given.

This message is a reply to:
 Message 184 by PaulK, posted 05-15-2017 12:30 AM PaulK has replied

Replies to this message:
 Message 186 by PaulK, posted 05-15-2017 1:09 AM Faith has replied
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PaulK
Member
Posts: 17822
Joined: 01-10-2003
Member Rating: 2.2


Message 186 of 518 (808931)
05-15-2017 1:09 AM
Reply to: Message 185 by Faith
05-15-2017 1:01 AM


Re: The YEC model requires beneficial mutations and strong positive selection.
quote:
You can't just say it must be functionally different without any proof whatever when neutral mutations are the most common and they do not change the function.
It doesn't matter to the argument - and you have already made the case for selection, and therefore different function. Moreover, as you admit other points have been made in favour of different function.
If you want to insist that the frequencies are illusory you need to do better than rely on assumptions.

This message is a reply to:
 Message 185 by Faith, posted 05-15-2017 1:01 AM Faith has replied

Replies to this message:
 Message 187 by Faith, posted 05-15-2017 1:19 AM PaulK has replied

  
Faith 
Suspended Member (Idle past 1444 days)
Posts: 35298
From: Nevada, USA
Joined: 10-06-2001


Message 187 of 518 (808932)
05-15-2017 1:19 AM
Reply to: Message 186 by PaulK
05-15-2017 1:09 AM


Re: The YEC model requires beneficial mutations and strong positive selection.
There is no selection happening and I have not accepted that there is. What is mistaken for selection is a mere normal passing on of the allele because it is neutral. Being passed on over a few generations looks like an increase if you are counting it separately as a mere different sequence, but it should be counted with all the other versions of the allele. This is truly an illusion created by the assumption based on the ToE that it is a functioning allele instead of the usual neutral mutation.
Note the title of this series of posts: The YEC model requires beneficial mutations and strong positive selection. I went back and skimmed through earlier posts where it is clear that the mere appearance of mutations, meaning different DNA sequences at a particular locus, is counted as an allele, assuming a changed function. Changed function is assumed in that article bluegenes posted where it's even said that slight changes in sequence are beneficial because slight changes in function are beneficial to the immune system. It's assumed, it is not shown. And it's odd that it is assumed when surely neutral mutations are well known.
I'm sure you can follow this logic; the question is why you are so adamantly resisting it and calling me names about it.

This message is a reply to:
 Message 186 by PaulK, posted 05-15-2017 1:09 AM PaulK has replied

Replies to this message:
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PaulK
Member
Posts: 17822
Joined: 01-10-2003
Member Rating: 2.2


(1)
Message 188 of 518 (808933)
05-15-2017 1:50 AM
Reply to: Message 187 by Faith
05-15-2017 1:19 AM


Re: The YEC model requires beneficial mutations and strong positive selection.
quote:
There is no selection happening and I have not accepted that there is
That is your assumption. The fact that your argument works against your assumption is inconvenient for you, but still a - very obvious - fact.
quote:
Being passed on over a few generations looks like an increase if you are counting it separately as a mere different sequence, but it should be counted with all the other versions of the allele. This is truly an illusion created by the assumption based on the ToE that it is a functioning allele instead of the usual neutral mutation.
Of course the frequencies are observed fact. You just want them covered up - on obviously fallacious grounds because you don't like that fact.
quote:
Note the title of this series of posts: The YEC model requires beneficial mutations and strong positive selection. I went back and skimmed through earlier posts where it is clear that the mere appearance of mutations, meaning different DNA sequences at a particular locus, is counted as an allele, assuming a changed function
The original point was that the frequencies are strong evidence of selection, given YEC assumptions. (And I would add when you have genes which are very unusually diverse and where that diversity is itself an advantage it is rather hard to avoid the conclusion that something is going on that favours diversity)
quote:
I'm sure you can follow this logic; the question is why you are so adamantly resisting it and calling me names about it.
Sure I can follow the logic. That doesn't make it any less silly. Can't you understand that facts trump assumptions ? And pointing out the absurdity of your argument is not calling you names.

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 Message 187 by Faith, posted 05-15-2017 1:19 AM Faith has not replied

  
bluegenes
Member (Idle past 2477 days)
Posts: 3119
From: U.K.
Joined: 01-24-2007


Message 189 of 518 (808939)
05-15-2017 4:47 AM
Reply to: Message 145 by Faith
05-13-2017 1:34 PM


Re: The YEC model requires beneficial mutations and strong positive selection.
Faith writes:
bluegenes writes:
That's why I'm saying that, to get a plausible 6,500yr YEC model, we have to accept positive selection on many of those extra HLA alleles.
Well, I'm just a creationist loony but I would guess there are many variables here you probably haven't taken into account, and if I can't derive your statistic myself I can't very well accept it anyway.
Drift can increase and decrease the frequency of alleles (the percentage of the population in which they are present) but it certainly can't explain what we see with the HLA alleles.
Perhaps it would be easier to explain directly how the new alleles are advantageous, and how they are necessarily different in how they function.
MHC polymorphism extends the range of antigens to which the immune system can respond.
quote:
Most polymorphic genes encode proteins that vary by only one or a few amino acids, whereas the different allelic variants of MHC proteins differ by up to 20 amino acids. The extensive polymorphism of the MHC proteins has almost certainly evolved to outflank the evasive strategies of pathogens.* Pathogens can avoid an immune response either by evading detection or by suppressing the ensuing response. The requirement that pathogen antigens must be presented by an MHC molecule provides two possible ways of evading detection. One is through mutations that eliminate from its proteins all peptides able to bind MHC molecules. The Epstein-Barr virus provides an example of this strategy. In regions of south-east China and in Papua New Guinea there are small isolated populations in which about 60% of individuals carry the HLA-All allele. Many isolates of the Epstein-Barr virus obtained from these populations have mutations in a dominant peptide epitope normally presented by HLA-All; the mutant peptides no longer bind to HLA-All and cannot be recognized by HLA-All-restricted T cells. This strategy is plainly much more difficult to follow if there are many different MHC molecules, and the presence of different loci encoding functionally related proteins may have been an evolutionary adaptation by hosts to this strategy by pathogens.
In large outbred populations, polymorphism at each locus can potentially double the number of different MHC molecules expressed by an individual, as most individuals will be heterozygotes. Polymorphism has the additional advantage that individuals in a population will differ in the combinations of MHC molecules they express and will therefore present different sets of peptides from each pathogen. This makes it unlikely that all individuals in a population will be equally susceptible to a given pathogen and its spread will therefore be limited. That exposure to pathogens over an evolutionary timescale can select for expression of particular MHC alleles is indicated by the strong association of the HLA-B53 allele with recovery from a potentially lethal form of malaria; this allele is very common in people from West Africa, where malaria is endemic, and rare elsewhere, where lethal malaria is uncommon.**
Similar arguments apply to a second strategy for evading recognition. If pathogens can develop mechanisms to block the presentation of their peptides by MHC molecules, they can avoid the adaptive immune response. Adenoviruses encode a protein that binds to MHC class I molecules in the endoplasmic reticulum and prevents their transport to the cell surface, thus preventing the recognition of viral peptides by CD8 cytotoxic T cells. This MHC-binding protein must interact with a polymorphic region of the MHC class I molecule, as some allelic variants are retained in the endoplasmic reticulum by the adenoviral protein whereas others are not. Increasing the variety of MHC molecules expressed therefore reduces the likelihood that a pathogen will be able to block presentation by all of them and completely evade an immune response.
*"The extensive polymorphism of the MHC proteins has almost certainly evolved to outflank the evasive strategies of pathogens. That should make sense to you (post Fall).
**"That exposure to pathogens over an evolutionary timescale can select for expression of particular MHC alleles is indicated by the strong association of the HLA-B53 allele with recovery from a potentially lethal form of malaria; this allele is very common in people from West Africa, where malaria is endemic, and rare elsewhere, where lethal malaria is uncommon." Undeniable natural selection, surely.
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 homozygousity would be common (1/4 of the population on each gene, and most people on at least one).
Note also the first sentence in yellow. The new alleles are significantly different, and do not arrive easily by a single point mutation.
So, these new arrivals being different is important, and they are certainly beneficial.
Therefore, I repeat the title of the sub-thread:
The YEC model requires beneficial mutations and strong positive selection.
I think you'll agree if you understand the information in the paper.

This message is a reply to:
 Message 145 by Faith, posted 05-13-2017 1:34 PM Faith has replied

Replies to this message:
 Message 191 by Faith, posted 05-15-2017 1:59 PM bluegenes has replied

  
Taq
Member
Posts: 9973
Joined: 03-06-2009
Member Rating: 5.6


Message 190 of 518 (809016)
05-15-2017 1:43 PM
Reply to: Message 159 by Faith
05-14-2017 7:46 AM


Re: Multiple Alleles of OCA2 Produce a Wide Variety of Human Eye Colors
Faith writes:
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.
It isn't an assertion. It is the conclusion of the paper as backed by the facts presented in the article. Sorry, but a handwave won't make this evidence go away.
Faith writes:
Different combinations of alleles at one locus? What do you mean? What's combining with what? How many different eye colors?
Alleles are defined as different gene sequences at the same locus, so yes, at the same locus. There is more than two allele for the OCA2 gene, and those multiple alleles have different functions meaning that there is more than 2 functions for that gene. This runs counter to your model.

This message is a reply to:
 Message 159 by Faith, posted 05-14-2017 7:46 AM Faith has replied

Replies to this message:
 Message 192 by Faith, posted 05-15-2017 2:04 PM Taq has replied

  
Faith 
Suspended Member (Idle past 1444 days)
Posts: 35298
From: Nevada, USA
Joined: 10-06-2001


Message 191 of 518 (809019)
05-15-2017 1:59 PM
Reply to: Message 189 by bluegenes
05-15-2017 4:47 AM


Re: The YEC model requires beneficial mutations and strong positive selection.
Perhaps it would be easier to explain directly how the new alleles are advantageous, and how they are necessarily different in how they function.
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.
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.
...two possible ways of evading detection. One is through mutations that eliminate from its proteins all peptides able to bind MHC molecules. The Epstein-Barr virus provides an example of this strategy. In regions of south-east China and in Papua New Guinea there are small isolated populations in which about 60% of individuals carry the HLA-All allele. Many isolates of the Epstein-Barr virus obtained from these populations have mutations in a dominant peptide epitope normally presented by HLA-All; the mutant peptides no longer bind to HLA-All and cannot be recognized by HLA-All-restricted T cells. This strategy is plainly much more difficult to follow if there are many different MHC molecules, and the presence of different loci encoding functionally related proteins may have been an evolutionary adaptation by hosts to this strategy by pathogens.
Understanding this by my YEC model the idea would be that the necessary alleles were already present and then selected.
This article actually sounds like it assumes that beneficial mutations practically appear as needed, such as here:
The extensive polymorphism of the MHC proteins has almost certainly evolved to outflank the evasive strategies of pathogens.*
[and this is footnoted] "The extensive polymorphism of the MHC proteins has almost certainly evolved to outflank the evasive strategies of pathogens. That should make sense to you (post Fall).
I would expect that somehow the solution to the problem has to be already present in the system and then it's selected. That is, it was created to function as it does, it didn't evolve for that purpose.
Mutations don't just occur as needed but that's how this sounds.
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 homozygousity would be common (1/4 of the population on each gene, and most people on at least one).
Homozygosity occurs after many generations of selection as I thinki of it, or by founder effect. But if a gene's function can be illustrated by a Mendel square there's no need for homozygosity to develop rapidly. This shouldn't occur with the skin color or eye color genes that function according to the Mendel square. If these genes you are talking about can be expressed in a Mendel square I'd like to see it.
But it's probably that you've chosen a case that is too difficult for me to think through, and since it involves only a few genes I don't think it's very useful for a debate about the YEC model, which seems to me to be able to account for the vast majority of genes, and probably these too but if I'm unable to think it through it isn't a good example for this debate.
And again, I'm going with two, not four, alleles, per Adam and Eve's genes.

This message is a reply to:
 Message 189 by bluegenes, posted 05-15-2017 4:47 AM bluegenes has replied

Replies to this message:
 Message 193 by PaulK, posted 05-15-2017 2:40 PM Faith has replied
 Message 204 by bluegenes, posted 05-16-2017 8:35 AM Faith has replied

  
Faith 
Suspended Member (Idle past 1444 days)
Posts: 35298
From: Nevada, USA
Joined: 10-06-2001


Message 192 of 518 (809020)
05-15-2017 2:04 PM
Reply to: Message 190 by Taq
05-15-2017 1:43 PM


Re: Multiple Alleles of OCA2 Produce a Wide Variety of Human Eye Colors
If I can't grasp the argument for whatever reason there is no debate. I believe eye color is based on genes with two alleles whose function can be expressed in a Mendel's square. I think the belief in mutations as the source of functioning alleles is false, not demonstrable in reality, just an artifact of the ToE.
Edited by Faith, : No reason given.

This message is a reply to:
 Message 190 by Taq, posted 05-15-2017 1:43 PM Taq has replied

Replies to this message:
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PaulK
Member
Posts: 17822
Joined: 01-10-2003
Member Rating: 2.2


Message 193 of 518 (809028)
05-15-2017 2:40 PM
Reply to: Message 191 by Faith
05-15-2017 1:59 PM


Re: The YEC model requires beneficial mutations and strong positive selection.
quote:
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.
There are a large number of alleles for these genes and there certainly seems to be a use for them. They don't have to be that new unless you assume that YEC is true.
quote:
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.
How can you get from your assumed two alleles to over a hundred without mutation ?
quote:
This article actually sounds like it assumes that beneficial mutations practically appear as needed
Certainly not. The article is speaking about the advantage of variety, not of preplanning. Populations that are too similar are vulnerable (look into the history of banana cultivation sometime)
quote:
Homozygosity occurs after many generations of selection as I thinki of it, or by founder effect. But if a gene's function can be illustrated by a Mendel square there's no need for homozygosity to develop rapidly. This shouldn't occur with the skin color or eye color genes that function according to the Mendel square. If these genes you are talking about can be expressed in a Mendel square I'd like to see it.
Homozygosity is a disadvantage in these genes. And you are being silly with the Mendel squares. You could draw squares for all the combinations like the squares for your imaginary genes for skin and eye colour. But what would be the point ? When there are multiple genes with many alleles that would be a lot of squares that don't tell you anything.
quote:
But it's probably that you've chosen a case that is too difficult for me to think through, and since it involves only a few genes I don't think it's very useful for a debate about the YEC model, which seems to me to be able to account for the vast majority of genes, and probably these too but if I'm unable to think it through it isn't a good example for this debate.
It doesn't seem to be very difficult. The actual genetics of eye or skin colour would probably be harder to understand.
quote:
And again, I'm going with two, not four, alleles, per Adam and Eve's genes.
If God was going to give Adam and Eve an immune system, then why make it less effective than it could be ?

This message is a reply to:
 Message 191 by Faith, posted 05-15-2017 1:59 PM Faith has replied

Replies to this message:
 Message 194 by Faith, posted 05-15-2017 3:06 PM PaulK has replied

  
Faith 
Suspended Member (Idle past 1444 days)
Posts: 35298
From: Nevada, USA
Joined: 10-06-2001


Message 194 of 518 (809034)
05-15-2017 3:06 PM
Reply to: Message 193 by PaulK
05-15-2017 2:40 PM


Re: The YEC model requires beneficial mutations and strong positive selection.
How can you get from your assumed two alleles to over a hundred without mutation
By realizing that they are mutations, most of which are neutral, not genuine alleles.
The idea that any trait needs hundreds of alleles is in itself ludicrous.
You get enormous variation with only two per gene, with a few genes per trait.

This message is a reply to:
 Message 193 by PaulK, posted 05-15-2017 2:40 PM PaulK has replied

Replies to this message:
 Message 195 by PaulK, posted 05-15-2017 3:18 PM Faith has not replied
 Message 196 by Tanypteryx, posted 05-15-2017 3:21 PM Faith has replied

  
PaulK
Member
Posts: 17822
Joined: 01-10-2003
Member Rating: 2.2


Message 195 of 518 (809036)
05-15-2017 3:18 PM
Reply to: Message 194 by Faith
05-15-2017 3:06 PM


Re: The YEC model requires beneficial mutations and strong positive selection.
quote:
By realizing that they are mutations, most of which are neutral, not genuine alleles.
There is a difference between "realizing" and making a false assumption. However I note that you concede that mutation is the cause of the variants.
quote:
The idea that any trait needs hundreds of alleles is in itself ludicrous.
I suggest that you try to understand what these genes do, and remember that there is a genuine problem that the variety helps to counter. To refer back to your earlier post the variety is needed because we cannot count on the "right" mutation conveniently turning up. By keeping a wide variety of alleles present, at least we stand a good chance that some of us will have alleles that are effective against any disease organism that turns up.
quote:
You get enormous variation with only two per gene, with a few genes per trait.
Two per gene would be less than ideal in this case since 1/4 of the population would be homozygous.

This message is a reply to:
 Message 194 by Faith, posted 05-15-2017 3:06 PM Faith has not replied

  
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