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Author Topic:   Y.E.C. Model: Was there rapid evolution and speciation post flood?
bluegenes
Member (Idle past 2477 days)
Posts: 3119
From: U.K.
Joined: 01-24-2007


Message 60 of 518 (808491)
05-11-2017 8:01 AM
Reply to: Message 58 by Percy
05-11-2017 7:43 AM


Re: The YEC model requires ...
Percy writes:
This is better for your scenario because now people have to demonstrate at least five alleles for a gene before they can claim any arose through mutation, and then they still have to show they produced new function.
In the MHC, there are plenty of examples of more than five in small samples, like 100 individuals. There can be more than five at a 5% rate or more in the sample. That's impossible from Adam and Eve in 300 generations by drift alone. It requires positive selection of novelty, and it is Faith (although she doesn't realise it) who needs new function and positive selection for her model.

This message is a reply to:
 Message 58 by Percy, posted 05-11-2017 7:43 AM Percy has replied

Replies to this message:
 Message 61 by Percy, posted 05-11-2017 8:27 AM bluegenes has replied

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


Message 66 of 518 (808524)
05-11-2017 11:14 AM
Reply to: Message 61 by Percy
05-11-2017 8:27 AM


Re: The YEC model requires ...
Percy writes:
I agree, but I think more argument and clarification is needed for your position. Why is a (restating) "5% rate of occurrence or more in the sample for at least five MHC alleles" impossible in 300 generations by drift alone?
Here's a group of 120 Cubans and 1 MHC gene.
Table 1 HLA-A, allele frequencies in
Cuban individuals with a dengue 2 virus infection history.
HLA GF (%)
A*02- 22.7
A*30- 10.6
A*24- 9.5
A*68- 8.0
A*03- 7.0
A*29- 6.5
A*23- 5.5
A*01- 5.5
A*31- 4.5
A*74- 3.5
A*33- 3.0
A*32- 2.5
A*34- 2.0
A*36- 2.0
A*25- 1.5
A*26- 1.5
A*66- 1.5
A*11- 1.0
A*80- 1.0
HLA human leukocyte antigen; GF allele frequency (as percentage
The easiest way to explain this might be to look at ourselves as individuals. On the YEC model, we are ~15,000 mutations away from Adam and Eve on the whole genome. That would give us ~ 180 mutational hits on the small part that is coding genes, most of them falling on different genes, so we have new alleles on ~1% of the total of ~18,000.
So, if we take 120 people as above, what would we expect on a given gene in purely neutral evolution. The four original alleles dominating, and perhaps 1, 2 or 3 exceptions.
Now look at the chart, and what do we see? If the YEC model, then signals of very strong selection on lots of new alleles.
Percy writes:
I was browsing through the Wikipedia article on Major histocompatibility complex and see some of what you've said, for instance (going from memory) that some genes of the MHC complex have nearly 1000 alleles or more. A simple question is how so many alleles could have arisen and spread through a population in only 300 generations. Which you may have asked at least once already?
With a population this size, if 1000 alleles can be tolerated, they'll be there. 100 million births gives you all the point mutations and more. So, it depends on the size of the group you're looking at.
Edited by bluegenes, : nothing of note
Edited by bluegenes, : removed mistake in chart

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 Message 61 by Percy, posted 05-11-2017 8:27 AM Percy has replied

Replies to this message:
 Message 72 by Percy, posted 05-11-2017 2:06 PM bluegenes has replied
 Message 124 by Faith, posted 05-12-2017 2:17 PM bluegenes has not replied

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


Message 74 of 518 (808579)
05-11-2017 2:17 PM
Reply to: Message 70 by Faith
05-11-2017 1:35 PM


Re: The YEC model requires beneficial mutations and strong positive selection.
Faith writes:
I don't see what selection or drift or even number of generations has to do with any of this. I guess I'm just not getting your whole frame of reference.
See if Message 66 makes it any clearer to you. Particularly, concentrate on the point that we would only have mutations (new alleles) on ~1% of our coding genes as individuals. The rest would be identical to the four in Adam and Eve. So, take a random gene and examine it on 100 people, and you'd expect the original 4 alleles + perhaps 1 individual with a new one on average.

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 Message 70 by Faith, posted 05-11-2017 1:35 PM Faith has replied

Replies to this message:
 Message 77 by Faith, posted 05-11-2017 2:57 PM bluegenes has replied

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


Message 76 of 518 (808581)
05-11-2017 2:44 PM
Reply to: Message 72 by Percy
05-11-2017 2:06 PM


Re: The YEC model requires ...
Basically, if we all differ from Adam and Eve on just 1% of our coding genes, then take one gene, examine it in 100 people, they should mostly have the original 4 alleles, but we might expect 1 or 2 exceptions.
So, if we see something completely different, then, as serious YEC scientists, we need an explanation. For the HLA genes, very strong positive selection is the only one!
This, I love.
At first sight, it seems to pose serious theological problems. The new mutant alleles are taking over from the original designs. However, I can think of a way around that. It's actually diversity itself which is being selected for in the immune system.
Is it plausible that the MHCs that we see in mammals could arise in a young earth scenario? Actually, no, but I'm giving it a good try.
With other things, like the Y-chromosome, it's not worth bothering. Not only Noah, but Adam as well gets himself easily falsified.
I'll try to bring some animals and their Ark bottleneck into the discussion.

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


Message 85 of 518 (808590)
05-11-2017 3:14 PM
Reply to: Message 77 by Faith
05-11-2017 2:57 PM


Re: The YEC model requires beneficial mutations and strong positive selection.
Faith writes:
But you think we NEED mutations to get new alleles and I don't, so how many there are on a gene doesn't tell me much; all I can say is the fewer the better.
???What PaulK asked above. And as for the fewer the better, didn't you understand that paper on the MHC i showed you?

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 Message 88 by Faith, posted 05-11-2017 3:17 PM bluegenes has replied

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


Message 97 of 518 (808603)
05-11-2017 3:28 PM
Reply to: Message 88 by Faith
05-11-2017 3:17 PM


Re: The YEC model requires beneficial mutations and strong positive selection.
Faith writes:
I gave an answer to that paper, that's all I know.
ABE: You claim different functions for all those alleles, but haven't shown it. As I suggested they could all be neutral mutations that don't change the function but continue to do what the original allele did.
Variety itself makes the immune system stronger. But that's not the point. They cannot be there in such high percentages in a young earth scenario unless they are positively selected.
And they are there. So, what's your conclusion? Positive selection, or older earth, older life?
It has to be one or the other.

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 Message 88 by Faith, posted 05-11-2017 3:17 PM Faith has replied

Replies to this message:
 Message 99 by Faith, posted 05-11-2017 3:38 PM bluegenes has replied

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


Message 104 of 518 (808610)
05-11-2017 3:58 PM
Reply to: Message 99 by Faith
05-11-2017 3:38 PM


Re: The YEC model requires beneficial mutations and strong positive selection.
Faith writes:
Mutations are random accidents of replication, yes? Most of them are neutral as to function, right:? That is, the mutated allele continues to do what the original allele did, right?: That being the case why should there be any selection involved at all? The immune system from what you've said appears to be particularly prone to mutations.
No. It's no more prone than anywhere else.
Faith writes:
Why should there be any other reason for that than its proneness to frequent random accidents of replication to explain the rate at which they occur?
It isn't prone to these, and the alleles that are present as a measurable percentage are certainly highly functional, otherwise they would be selected out quickly.
They face positive selection because two different ones working in tandem is better than an identical pair.
There's no explanation for their survival other than positive selection. They are like soldiers with slightly different arms.

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 Message 99 by Faith, posted 05-11-2017 3:38 PM Faith has replied

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 Message 108 by Faith, posted 05-11-2017 4:26 PM bluegenes has replied

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


Message 133 of 518 (808779)
05-13-2017 2:00 AM
Reply to: Message 108 by Faith
05-11-2017 4:26 PM


Re: The YEC model requires beneficial mutations and strong positive selection.
Faith writes:
They can be functional simply by not doing anything different than the original allele did, which is what "neutral" mutations do.
Yes, but they (new human immune system alleles) wouldn't be present in the proportions that they are after 300 generations on neutral evolution alone. Only positive selection on new variants would give that effect.
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.
It will be the same for other animals after the Ark bottleneck, particularly those species (or kinds) that only had two members present. When we look at them now, lots of variants in the MHC will be present at proportions that are too high for neutral evolution (drift) to account for, as they could only have a maximum of 4 after the flood.
So, we have to put positive selection on MHC mutant alleles as part of any plausible YEC model.
If, like the folk at Answers in Genesis, you see "kind" at somewhere around the level of family, you will need positive selection during post flood speciation and niche filling as well, even if you argue that the genes/alleles were all present on the original Ark pair genomes.

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 Message 108 by Faith, posted 05-11-2017 4:26 PM Faith has replied

Replies to this message:
 Message 145 by Faith, posted 05-13-2017 1:34 PM bluegenes has replied

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


Message 134 of 518 (808780)
05-13-2017 2:49 AM
Reply to: Message 130 by NosyNed
05-12-2017 3:08 PM


Re: From Someone Less Knowlegable
NosyNed writes:
So the remaining question is:
Are the mutations neutral or beneficial?
If they are neutral they are, by definition, not selected for or against so they only spread through the population by random drift.
So the issue of whether there are any beneficial mutations can be settled by examining if there are any alleles other than the original handful that are spread more widely than drift can do in a few 1,000 years.
As I understand the discussion so far the answer to that is - yes.
Therefore the conclusion is that the human genome has acquired beneficial mutations since the flood or the flood was much longer ago than a few 1,000 years.
That's pretty much it, but not just the flood, Adam and Eve as well.
NNed writes:
If there have been beneficial mutations then the original genome was not "perfect".
Well, there's a twist to that so far as the HLA alleles are concerned. Adam and Eve, like everyone else, would have had two copies at each locus, and if they had two different complimentary variants on each HLA gene, then they are as perfect as possible.
From then on, it's downhill at first, because with only 4 possible alleles, it's a one in three chance of someone having two of the same alleles on any given locus which, for these codominant alleles, is usually a disadvantage, because variety in immune system weaponry is the spice of life.
That's where new functional mutants can help, because every added one decreases the chances of a matching pair. So, it is not that the new alleles are more perfect than the original. Variety itself is facing positive selection, so the YECs needn't necessarily have a theological objection to this.

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 Message 130 by NosyNed, posted 05-12-2017 3:08 PM NosyNed has not replied

Replies to this message:
 Message 136 by jar, posted 05-13-2017 7:03 AM bluegenes has replied

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


(1)
Message 135 of 518 (808782)
05-13-2017 6:51 AM
Reply to: Message 127 by Faith
05-12-2017 2:53 PM


Re: The model in more detail
Faith writes:
Adam and Eve had the genes to produce every skin color there is. Depending on how many children they had they could have produced the entire range in one generation, but certainly produced quite a large range of them in any case. The rest would have appeared in subsequent generations.
And 80 generations later, all the original diversity was still present in Noah's sons and their wives?
Faith writes:
What makes a skin color or any other trait characteristic of a population or race is some form of selection of the color or few colors, and the selection as I've been arguing is in most cases random, a matter of migration of individuals that possess a particular portion of the gene pool ending up as an isolated population in some new place, where they develop a characteristic skin color through generations of inbreeding. That's all it takes for there to be hundreds of different populatios with different characteristics. It's all in the original genome, brought to visible expression by random seleciton and reproductive isolation.
By "random selection" do you mean drift (neutral evolution-no selection involved)?
Faith writes:
And each new race or population develops its characteristic traits by LOSING all the genetic material for other traits, many of which become characteristic of other populations. The original genome for each Kind had tremendous genetic diversity that in various combinations produced all the separate populations or "species" of all Kinds, but each new species has its characteristic phenotypes as a result of losing the genetic material for all the others.
So the ancestral bear kind on the Ark would have contained all the genes/alleles necessary to make a polar bear and a panda?
Even if so, surely natural selection on these would be necessary to produce things like the Arctic adaptations of the Polar?
Research on 59 Alpine Chamois found 19 alleles on one locus, and this level of polymorphism is turning out to be widespread, so I think you have to bring mutation and positive selection into your model, because mutation + drift from an Ark bottleneck doesn't fit what we see.
Evolution defeats Evolution.
We shall see!
I think YECs need to become super-selectionists in order to fit the genetics and the niche adaptations within kinds.

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 Message 127 by Faith, posted 05-12-2017 2:53 PM Faith has not replied

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


Message 138 of 518 (808790)
05-13-2017 7:59 AM
Reply to: Message 136 by jar
05-13-2017 7:03 AM


Re: From Someone Less Knowlegable
jar writes:
bluegenes writes:
Well, there's a twist to that so far as the HLA alleles are concerned. Adam and Eve, like everyone else, would have had two copies at each locus, and if they had two different complimentary variants on each HLA gene, then they are as perfect as possible.
But Eve was a clone of Adam so would that be possible?
Yes, they're diploid. They could be the same as each other and still have two different variants on each gene. However, if they were clones, that's not very good design from the point of view of their descendants.
I don't see why you can't make any genes out of a rib if you can from dirt, anyway.

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


Message 139 of 518 (808795)
05-13-2017 8:14 AM
Reply to: Message 137 by Tangle
05-13-2017 7:03 AM


Tangle writes:
I assume on 'kind' would be marsupial?
No. Some YECs go as far as family, but certainly not class or sub-class. So kangaroos and wallabies might be lumped, but not marsupials.
If someone's mentioned class on this thread, it'll be a typo!
It has partly to do with hybrids being possible, partly to do with limited space on the Ark, and partly a reaction to genetics and directly observable adaptations/evolution, I think.
Anyway, species immutability is out (unless you're in the Davidjay camp), but "kind" or family immutability is definitely still in.

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


Message 142 of 518 (808811)
05-13-2017 9:43 AM
Reply to: Message 141 by jar
05-13-2017 9:16 AM


Re: The YEC model requires beneficial mutations and strong positive selection.
jar writes:
Yet we know for a fact that everyone has a different set of genes which is why DNA testing can identify a specific individual.
Coding genes (~1% of DNA) aren't any use for that. It's the "junk" that mutates quickly without restraint, like micro-satellites, that gets used because it's highly variant. It's also used for approximate dating, and shows that many "kinds" split into species a long, long time before the Ark.
The earliest splits in the giraffe kind, for example, come in at over 1 million years, and far more if we include the Okapi.

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


Message 144 of 518 (808813)
05-13-2017 9:48 AM
Reply to: Message 143 by Percy
05-13-2017 9:43 AM


Re: The YEC model requires beneficial mutations and strong positive selection.
Percy writes:
What Faith is saying is that everyone has the same genes but with potentially a variety of different alleles, and that the current alleles are the only ones that aren't deleterious. Any mutations in existing alleles would be deleterious.
I don't think so. Her posts here certainly seem to accept "neutral". But I'm sure she'll clarify.

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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

  
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