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Author Topic:   Y.E.C. Model: Was there rapid evolution and speciation post flood?
Taq
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Posts: 6428
Joined: 03-06-2009
Member Rating: 4.3


Message 241 of 301 (809257)
05-17-2017 1:37 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;

No one is stopping you from saying that some alleles are detrimental, so I really don't understand what the problem is.

If you want to plant your flag on the hill labeled "mutations don't happen", go for it. However, such a position is rather hard to defend being that we can directly observe mutations happening. Alleles is just another way of saying that mutations happen. If you don't object to the observation that mutations happen, then why object to the observation that mutations produce new alleles?


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

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


Message 242 of 301 (809258)
05-17-2017 1:38 PM
Reply to: Message 236 by bluegenes
05-17-2017 9:29 AM


Re: The YEC model requires beneficial mutations and strong positive selection.
Putting my ignorance on full display, I found this paragraph particularly difficult:

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.

If I hadn't just looked it up earlier this morning I wouldn't remember what the MHC complex was - we've talked about several different genes, and to me they're still just alphabet soup. The terms polygeny and antigen are unfamiliar. I don't know what "class I" and "class II" molecules are.

I think the sentence you emphasized contains the information Faith questions most:

quote:
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.

Faith doesn't accept that a high frequency means selection. She thinks all these alleles code for mostly the same proteins and so don't provide any additional benefit beyond the two she believes were contributed by Adam and Eve. She thinks it's just assumed that these alleles code for different proteins, not observed. Do you have any evidence that the alleles code for different proteins?

One potential problem I see for the MHC example is that MHC is a complex of genes, not a single gene. When the article refers to "more than 200 alleles" it means across all the genes of the complex. How many genes is that? Looking this up in Wikipedia (Major histocompatibility complex) I see that its chromosome region contains 240 genes, half of which have "known immune functions." Half of 240 is 120, and since each gene has two alleles, one from each parent, that's 240 potential different alleles. Since Adam and Eve contributed two alleles for each of these 120 genes, that's more than enough to account for the "more than 200 alleles" that are currently observed.

--Percy


This message is a reply to:
 Message 236 by bluegenes, posted 05-17-2017 9:29 AM bluegenes has responded

Replies to this message:
 Message 243 by PaulK, posted 05-17-2017 1:44 PM Percy has responded
 Message 244 by Taq, posted 05-17-2017 2:02 PM Percy has responded
 Message 255 by bluegenes, posted 05-18-2017 9:53 AM Percy has responded

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


Message 243 of 301 (809260)
05-17-2017 1:44 PM
Reply to: Message 242 by Percy
05-17-2017 1:38 PM


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

Faith doesn't accept that a high frequency means selection. She thinks all these alleles code for mostly the same proteins and so don't provide any additional benefit beyond the two she believes were contributed by Adam and Eve.

The question then is how does the frequency increase ? Faith resorts to - her word - flimflam - to try to cover up the frequencies but never honestly addresses the issue.

quote:

One potential problems I see for the MHC example is that MHC is a complex of genes, not a single gene. When the article refers to "more than 200 alleles" it means across all the genes of the complex.

No. It specifically states:


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.

It pretty clearly refers to individual genes - "some genes" can hardly mean the whole of the complex.

Edited by PaulK, : No reason given.


This message is a reply to:
 Message 242 by Percy, posted 05-17-2017 1:38 PM Percy has responded

Replies to this message:
 Message 245 by Percy, posted 05-17-2017 3:35 PM PaulK has responded

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


(1)
Message 244 of 301 (809261)
05-17-2017 2:02 PM
Reply to: Message 242 by Percy
05-17-2017 1:38 PM


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

If I hadn't just looked it up earlier this morning I wouldn't remember what the MHC complex was - we've talked about several different genes, and to me they're still just alphabet soup. The terms polygeny and antigen are unfamiliar. I don't know what "class I" and "class II" molecules are.

The Major Histocompatibility Complex (MHC) is a complex of over 200 separate genes. That is, there is a region in your genome made up of over 200 genes that produce all of your MHC proteins. Think of it like a car manufacturer that makes over 200 different models. These models can be grouped into about 3 main categories: cars, pickups, and SUV's. Those are like the 3 MHC groups, of which MHC I and MHC II have been studied the most. They are grouped into these classes due to the type of immunity they are involved in, be it bacterial pathogens (MHC II) or cancer (MHC I).

The wide variety of MHC molecules allow them to bind to many different foreign and misformed proteins/molecules and present them on the outside of the immune cell. This allows T-cells to interact with the presented antigen and respond accordingly, either releasing cytokines to amp up the immune system to fight off infection or killing of a cell that is presenting the wrong proteins (cancer/tissue rejection).

When the article refers to "more than 200 alleles" it means across all the genes of the complex.

That's not accurate. For any single gene in the complex there can be hundreds or even thousands of alleles. For example, one of the genes in the complex is HLA-DRB1. Again, that is just a single gene. For that single gene there are hundreds if not thousands of different alleles.


This message is a reply to:
 Message 242 by Percy, posted 05-17-2017 1:38 PM Percy has responded

Replies to this message:
 Message 246 by Percy, posted 05-17-2017 3:38 PM Taq has responded

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


Message 245 of 301 (809266)
05-17-2017 3:35 PM
Reply to: Message 243 by PaulK
05-17-2017 1:44 PM


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

quote:

One potential problems I see for the MHC example is that MHC is a complex of genes, not a single gene. When the article refers to "more than 200 alleles" it means across all the genes of the complex.

No. It specifically states:


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.

It pretty clearly refers to individual genes - "some genes" can hardly mean the whole of the complex.

Good point, but can more consistent figures be nailed down? Taq just responded that some genes of the complex "have hundreds or even thousands of alleles" all by themselves.

--Percy


This message is a reply to:
 Message 243 by PaulK, posted 05-17-2017 1:44 PM PaulK has responded

Replies to this message:
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Percy
Member
Posts: 15616
From: New Hampshire
Joined: 12-23-2000
Member Rating: 4.4


Message 246 of 301 (809267)
05-17-2017 3:38 PM
Reply to: Message 244 by Taq
05-17-2017 2:02 PM


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

When the article refers to "more than 200 alleles" it means across all the genes of the complex.

That's not accurate. For any single gene in the complex there can be hundreds or even thousands of alleles. For example, one of the genes in the complex is HLA-DRB1. Again, that is just a single gene. For that single gene there are hundreds if not thousands of different alleles.

How do you reconcile "more than 200 alleles" across MHC I and MHC II with possibly "hundreds or even thousands" for a single gene?

--Percy


This message is a reply to:
 Message 244 by Taq, posted 05-17-2017 2:02 PM Taq has responded

Replies to this message:
 Message 249 by Taq, posted 05-17-2017 4:18 PM Percy has acknowledged this reply

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


Message 247 of 301 (809268)
05-17-2017 3:46 PM
Reply to: Message 245 by Percy
05-17-2017 3:35 PM


Re: The YEC model requires beneficial mutations and strong positive selection.
"More than two hundred" is sufficient for "hundreds". The "thousands" could conceivably be more recent and accurate figures.
This message is a reply to:
 Message 245 by Percy, posted 05-17-2017 3:35 PM Percy has acknowledged this reply

Replies to this message:
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Taq
Member
Posts: 6428
Joined: 03-06-2009
Member Rating: 4.3


Message 248 of 301 (809270)
05-17-2017 4:15 PM
Reply to: Message 245 by Percy
05-17-2017 3:35 PM


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

Good point, but can more consistent figures be nailed down? Taq just responded that some genes of the complex "have hundreds or even thousands of alleles" all by themselves.

The genomic region has been sequenced and you can find the map here:

http://www.nature.com/...v401/n6756/fig_tab/401921a0_F1.html

Excel spreadsheet containing all 224 genes here:

http://www.nature.com/...01/n6756/extref/401921a0.table1.xls

If you look at the function column you will notice that not all of the genes code for actual MHC proteins (i.e. antigen presenting proteins). There are a few chaperone and and protein modifying proteins in there, such as heat shock proteins and kinases. So not all of the genes in the MHC region are directly related to immunity.

We can pick one of the MHC II molecules at random from the Excel list: HLA-DPB1. If you do a search for that molecule at Uniprot you get this page:

http://www.uniprot.org/uniprot/P04440

If you scroll down to polymorphisms, it lists about 120 known alleles for the gene, at least by my quick count.


This message is a reply to:
 Message 245 by Percy, posted 05-17-2017 3:35 PM Percy has responded

Replies to this message:
 Message 254 by Percy, posted 05-18-2017 8:05 AM Taq has responded

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


Message 249 of 301 (809271)
05-17-2017 4:18 PM
Reply to: Message 246 by Percy
05-17-2017 3:38 PM


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

How do you reconcile "more than 200 alleles" across MHC I and MHC II with possibly "hundreds or even thousands" for a single gene?

Using our car manufacturing analogy from before, the MHC region is analogous to a single car manufacturer. Each gene in the region is a single vehicle model. Each vehicle model can have different trim packages, paint color, and so on. Each variant of the single type of vehicle is an allele in the analogy.

There are 224 car models in the MHC region. Each car model can possibly have just a few different variants, but some are known for having hundreds to thousands of variants.

Does this make sense?

Edited by Taq, : No reason given.


This message is a reply to:
 Message 246 by Percy, posted 05-17-2017 3:38 PM Percy has acknowledged this reply

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jar
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Posts: 28834
From: Texas!!
Joined: 04-20-2004
Member Rating: 3.1


Message 250 of 301 (809272)
05-17-2017 4:29 PM
Reply to: Message 249 by Taq
05-17-2017 4:18 PM


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

Using our car manufacturing analogy from before, the MHC region is analogous to a single car manufacturer. Each gene in the region is a single vehicle model. Each vehicle model can have different trim packages, paint color, and so on. Each variant of the single type of vehicle is an allele in the analogy.

There are 224 car models in the MHC region. Each car model can possibly have just a few different variants, but some are known for having hundreds to thousands of variants.

Does this make sense?

Following along with that analogy, some car models were sold fully equipped and with very few options. Other models from the same maker were marketed at the basic functionality level with a very long list of additional options that could be selected. In the latter case it was almost possible for each car sold to be unique.


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

This message is a reply to:
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Taq
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Posts: 6428
Joined: 03-06-2009
Member Rating: 4.3


Message 251 of 301 (809273)
05-17-2017 4:31 PM
Reply to: Message 247 by PaulK
05-17-2017 3:46 PM


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

"More than two hundred" is sufficient for "hundreds". The "thousands" could conceivably be more recent and accurate figures.

The most up to date resource I could find is this one:

http://hla.alleles.org/nomenclature/stats.html

For HLA-DRB1 they have 2,058 alleles listed.


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


Message 252 of 301 (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.


Replies to this message:
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PaulK
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Posts: 12686
Joined: 01-10-2003
Member Rating: 2.8


Message 253 of 301 (809361)
05-18-2017 12:22 AM
Reply to: Message 252 by Faith
05-17-2017 7:29 PM


Re: High frequency / positive selection
quote:

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?

As I said earlier the frequency should tend to remain about the same for neutral drift. By chance some alleles will become more frequent but slowly.

The absolute numbers would tend to track population change - starting when the mutation occurred.

So even 1% would be quite surprisingly high - even allowing for multiple generations. You would need a very small population when the original mutation occurred for that to be the original frequency.


This message is a reply to:
 Message 252 by Faith, posted 05-17-2017 7:29 PM Faith has not yet responded

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


Message 254 of 301 (809372)
05-18-2017 8:05 AM
Reply to: Message 248 by Taq
05-17-2017 4:15 PM


Re: The YEC model requires beneficial mutations and strong positive selection.
I'll reply to your Message 248 and Message 249 in this single message.

quote:
The genomic region has been sequenced and you can find the map here:

http://www.nature.com/...v401/n6756/fig_tab/401921a0_F1.html


Here's the image for reference:

About this from the comment beneath the figure:

quote:
As will be the case for the rest of the human genome, the MHC reference sequence is a composite of different haplotypes.

What is a haplotype? The Wikipedia article on Haplotype offers several definitions.

What does the little symbol between curly braces mean?

quote:
However, in regions with known differences in gene content...

Does this mean that for some loci different people can have different genes instead of different alleles?

Excel spreadsheet containing all 224 genes here:

http://www.nature.com/...01/n6756/extref/401921a0.table1.xls

96 of the 224 genes are actually pseudogenes, which Wikipedia defines as disabled or only partially functioning.

We can pick one of the MHC II molecules at random from the Excel list: HLA-DPB1. If you do a search for that molecule at Uniprot you get this page:

http://www.uniprot.org/uniprot/P04440

If you scroll down to polymorphisms, it lists about 120 known alleles for the gene, at least by my quick count.

Here's the list of alleles:

quote:
Polymorphismi
The following alleles of HLA-DPB1 are known: DPB1*01:01, DPB1*01:02, DPB1*02:01, DPB1*02:02, DPB1*02:03, DPB1*03:01, DPB1*03:02, DPB1*04:01, DPB1*04:02, DPB1*04:03, DPB1*05:01, DPB1*05:02, DPB1*06:01, DPB1*06:02, DPB1*08:01, DPB1*08:02, DPB1*09:01, DPB1*09:02, DPB1*10:01, DPB1*10:02, DPB1*11:01, DPB1*11:02, DPB1*13:01, DPB1*13:02, DPB1*14:01, DPB1*14:02, DPB1*15:01, DPB1*15:02, DPB1*16:01, DPB1*16:02, DPB1*17:01, DPB1*17:02, DPB1*18:01, DPB1*18:02, DPB1*19:01, DPB1*19:02, DPB1*20:01, DPB1*20:02, DPB1*21:01, DPB1*21:02, DPB1*22:01, DPB1*22:02, DPB1*23:01, DPB1*24:01, DPB1*24:02, DPB1*25:01, DPB1*25:02, DPB1*26:01, DPB1*26:02, DPB1*27:01, DPB1*28:01, DPB1*29:01, DPB1*30:01, DPB1*31:01, DPB1*32:01, DPB1*33:01, DPB1*34:01, DPB1*35:01, DPB1*36:01, DPB1*37:01, DPB1*38:01, DPB1*39:01, DPB1*40:01, DPB1*41:01, DPB1*44:01, DPB1*45:01, DPB1*46:01, DPB1*47:01, DPB1*48:01, DPB1*49:01, DPB1*50:01, DPB1*51:01, DPB1*52:01, DPB1*53:01, DPB1*54:01, DPB1*55:01, DPB1*56:01, DPB1*57:01, DPB1*58:01, DPB1*59:01, DPB1*60:01, DPB1*62:01, DPB1*63:01, DPB1*65:01, DPB1*66:01, DPB1*67:01, DPB1*68:01, DPB1*69:01, DPB1*70:01, DPB1*71:01, DPB1*72:01, DPB1*73:01, DPB1*74:01, DPB1*75:01, DPB1*76:01, DPB1*77:01, DPB1*78:01, DPB1*79:01, DPB1*80:01, DPB1*81:01, DPB1*82:01, DPB1*83:01, DPB1*84:01, DPB1*85:01, DPB1*86:01, DPB1*87:01, DPB1*88:01, DPB1*89:01, DPB1*90:01, DPB1*91:01, DPB1*92:01, DPB1*93:01, DPB1*94:01, DPB1*95:01, DPB1*96:01, DPB1*97:01, DPB1*98:01 and DPB1*99:01. The sequence shown is that of DPB1*04:01.

There are 118 (good "quick count" by you).

Faith is asking how we know which alleles produce unique proteins that do something different.

--Percy


This message is a reply to:
 Message 248 by Taq, posted 05-17-2017 4:15 PM Taq has responded

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


Message 255 of 301 (809386)
05-18-2017 9:53 AM
Reply to: Message 242 by Percy
05-17-2017 1:38 PM


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

Putting my ignorance on full display, I found this paragraph particularly difficult:

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.


Translation: Because there are several genes that produce different molecules that detect, bind to, and "present" foreign bodies (to killer T-cells or other killers which get rid of them) in both classes (the difference in the classes doesn't matter for our discussion), at least 6 or 7 different such molecules will be expressed in the cells of all people. In fact, the number (of different foreign body detecting + presenting molecules) expressed in the cells of most people is greater because of the very large amount of different alleles (coding sequences) on most of these genes (meaning the two copies of each gene per. individual are very likely to be different =heterozygosity) and the fact that all alleles are codominant (the products of both are expressed - neither is recessive).

Better? Or worse?

The variance in alleles on the same genes is advantageous (it increases the range of foreign bodies that can be detected), so variance itself is under positive selection.

Percy writes:

If I hadn't just looked it up earlier this morning I wouldn't remember what the MHC complex was - we've talked about several different genes, and to me they're still just alphabet soup. The terms polygeny and antigen are unfamiliar. I don't know what "class I" and "class II" molecules are.

There are several genes (polygeny) that produce the proteins that detect and present "poisonous" foreign bodies (antigens) to anti-bodies. (Forget classes for now).

Percy writes:

I think the sentence you emphasized contains the information Faith questions most:

quote:

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.

Faith doesn't accept that a high frequency means selection. She thinks all these alleles code for mostly the same proteins and so don't provide any additional benefit beyond the two she believes were contributed by Adam and Eve. She thinks it's just assumed that these alleles code for different proteins, not observed. Do you have any evidence that the alleles code for different proteins?

Yes. It does actually state that indirectly in the second sentence of the bit you quoted above.

quote:

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.

I quoted another extract from the same paper (actually, a book) in Message 189

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.


Don't worry about things like the disgusting sounding "endoplasmic reticulum", but I hope you get the gist. The "T cells" are pathogen killers which act on signals from these varying alleles. It's the famous "evolutionary arms race" that's being described.

Percy writes:

One potential problem I see for the MHC example is that MHC is a complex of genes, not a single gene. When the article refers to "more than 200 alleles" it means across all the genes of the complex.

No. It means more than 200 on some individual genes.

Percy writes:

How many genes is that? Looking this up in Wikipedia (Major histocompatibility complex) I see that its chromosome region contains 240 genes, half of which have "known immune functions." Half of 240 is 120, and since each gene has two alleles, one from each parent, that's 240 potential different alleles. Since Adam and Eve contributed two alleles for each of these 120 genes, that's more than enough to account for the "more than 200 alleles" that are currently observed.

No. There are more than 200 on some individual genes. Adam and Eve: maximum possible 4.

Drift on neutral alleles might give anything from 0 to 4 more in a sample of 100 individuals on any given gene (modern individuals would differ from A&E on about 1% of all coding loci) giving a likely maximum of 8 (average 5 if A&E had 4). These would typically differ by a single point mutation from A&E originals.

The sample of 120 Cubans I posted earlier had 19 different alleles on HLA -A (one gene).

So, are you beginning to understand why I'm saying that the YECs need to include mutation and positive selection into their model?


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 Message 256 by jar, posted 05-18-2017 10:00 AM bluegenes has responded
 Message 272 by Percy, posted 05-19-2017 9:09 AM bluegenes has responded

  
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