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Author | Topic: Y.E.C. Model: Was there rapid evolution and speciation post flood? | |||||||||||||||||||||||||||||||||||||||
Taq Member Posts: 10081 Joined: Member Rating: 5.1
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Faith writes: It should be pretty clear by now that there isn't any. That is not an honest statement since you have already stated that your religious beliefs require you to reject the evidence that has already been presented.
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bluegenes Member (Idle past 2505 days) Posts: 3119 From: U.K. Joined: |
Percy writes: I guess I must have misunderstood..... Let's simplify it by just looking at one of these highly polymorphic (many alleled) genes. In the HLA class 1 set there are three genes, A,B, and C. I'll pick HLA-B, because it's the most polymorphic. This is one gene on one locus. Humans are diploid, so we all have two copies. As with the other main HLA genes, both copies are expressed in the cell as they are "codominant". There are many different alleles, and they function differently, so we are better off being heterozygous (having two different alleles) than homozygous (having one), because two different alleles cover more immunity ground. This is because the alleles all have different repertoires. They search out and bind onto differing repertoires of the peptides of pathogens, then present these as signals to killer T-cells (anti-bodies) which attack the intruders, and the alleles vary in their effectiveness on different pathogens. One HLA-B allele is known to be excellent at dealing with a lethal form of malaria common in West Africa, and is found at high frequencies in the local population (positive selection) and another HLA-B allele does the job on an East-Asian form of Malaria. Two different HLA-B alleles are particularly effective against HIV, and other variants are quite good at staving of the development of Aids in people infected with HIV for long periods. Heterozygosity itself has been demonstrated to delay the onset of Aids. Other HLA-B alleles are known for being good for other diseases, and there's usually a range of effectiveness. So, if you've got two different alleles, the chances of resisting lethal invaders are better than with the same allele on both copies, and the more there are floating around, the higher the chances of being heterozygous. The more variance in the species as a whole, and in regional sub populations, the better, because there's more chance of a sector of the population being resistant to a serious epidemic. The variety is necessary partly because of the variety of different pathogens that attack us, and partly because of their nasty habit of constantly mutating and producing strains that can avoid the recognition of common HLA-B alleles. When such strains develop regionally, there's a known "rare allele" effect. Individuals with rare alleles can have resistance to successful pathogens that have "learnt" to avoid the more common HLA-B identifiers. If you've grasped all that, you can probably figure out why new functional mutations with new "repertoires" can face positive selection on arrival. The pathogens haven't adapted to them, and, while still rare, they are very unlikely to be paired up with themselves in individuals, so contribute to heterozygosity. All this variance is the product of a type of Darwinian selection known as "balancing selection". If you want to see evidence in this thread for the variance in function of HLA-B, in addition to the original book extracts I presented which mention the malaria example amongst other things, the Dengue fever paper that Taq linked to in Message 270 gives it. In Message 271 I linked to a paper that shows the functional variance in the Class 2 HLA genes. The HLA-B alleles are certainly not neutral variants with identical functions, as Faith wants them to be. Their difference itself is what is selected for, and we're lucky as a species that it's there! Edited by bluegenes, : typo
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bluegenes Member (Idle past 2505 days) Posts: 3119 From: U.K. Joined: |
Taq writes: I presented a paper in post 270 that discusses many different alleles (i.e. much greater than 2) for HLA-A and HLA-B that have different function. Jar and I also discuss the paper in posts 271 and 277. I'm many things, but I'm not "a wide-mouthed cylindrical container made of glass or pottery."
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Taq Member Posts: 10081 Joined: Member Rating: 5.1 |
Not Jar writes: I'm many things, but I'm not "a wide-mouthed cylindrical container made of glass or pottery." My apologies. The previous post has been edited to reflect my mistake.
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Percy Member Posts: 22500 From: New Hampshire Joined: Member Rating: 4.9 |
Taq writes: What they did was chop up proteins from the dengue virus and determine which of these chopped up proteins, called peptides, bound to which allele for both HLA-A and HLA-B. Don't you mean that the peptides bound to the proteins produced by the alleles? I tried to read the paper you referenced in Message 270 (HLA Class I Alleles Are Associated with Peptide-Binding Repertoires of Different Size, Affinity, and Immunogenicity) and found it impenetrable.
HLA-A and HLA-B are antigen presenting proteins, so when they bind different viral peptides it indicates that they differ in function. Each gene has more than two functions spread out over many alleles which directly contradicts Faith's claims. Right. Explaining again, in Faith's view Adam and Eve contributed at most two alleles for each gene, and since creation any new alleles must be neutral and not perform any new function. But since the analysis in the paper reveals many more than two differently functional alleles for each gene, Faith must be wrong. The problem is that I can't understand the paper well enough to see how it supports this point. --Percy
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Percy Member Posts: 22500 From: New Hampshire Joined: Member Rating: 4.9 |
I'm gradually picking up some terminology. Is it correct to say the MHC complex of proteins is produced by the HLA complex of genes?
bluegenes writes: This is because the alleles all have different repertoires. They search out and bind onto differing repertoires of the peptides of pathogens,... Asking the same question I asked Taq, why do you say that the alleles bind to peptides, instead of that proteins produced by the alleles bind to the peptides?
...then present these as signals to killer T-cells (anti-bodies) which attack the intruders, and the alleles vary in their effectiveness on different pathogens. And what we need is evidence that many more that two alleles of the same gene have different functions in that they bind to different pathogen peptides.
So, if you've got two different alleles, the chances of resisting lethal invaders are better than with the same allele on both copies, and the more there are floating around, the higher the chances of being heterozygous. When you say "floating around" I think you mean "floating around in the population?" If so, then for contagious pathogens this could be deemed a form of what is called herd immunity?
If you want to see evidence in this thread for the variance in function of HLA-B, in addition to the original book extracts I presented which mention the malaria example amongst other things, the Dengue fever paper that Taq linked to in Message 270 gives it. As I mentioned to Taq, I found the paper impenetrable.
In Message 271 I linked to a paper that shows the functional variance in the Class 2 HLA genes. I didn't find this paper any easier to digest. Quoting from your Message 271:
Functional classification of HLA Class 2 molecules. quote: This as a massive increase in functional information since Adam and Eve. I don't know the definitions for "repertoire" and "supertype". It isn't just the definitions but the context. I don't mean to appear helpless, but I have limited free time for figuring all this out on my own. --Percy
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Percy Member Posts: 22500 From: New Hampshire Joined: Member Rating: 4.9 |
Faith writes: I'm seeking the evidence that proves these two points. It may have been presented already, but not in a form I understand. It should be pretty clear by now that there isn't any. What's actually pretty clear is that evidence has been presented that we don't understand. Taq and Bluegenes suggested these two papers:
Once we understand the relevant portions of these papers we can judge the evidence. Or perhaps more easily understood evidence will be presented. --Percy
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Faith  Suspended Member (Idle past 1472 days) Posts: 35298 From: Nevada, USA Joined: |
The binding of something or other to something or other is the evidence. First it would have to be shown that this binding does something beneficial to the immune system. How are they going to prove that? But also it's all about one disease, Dengue fever. What would it prove about different functions of different alleles when it's all about one disease?
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Taq Member Posts: 10081 Joined: Member Rating: 5.1 |
Faith writes: First it would have to be shown that this binding does something beneficial to the immune system. The HLA-A and HLA-B proteins bind viral peptides and present them on the surface of the cell where they stimulate immune cells that fight off the infection. That is beneficial.
But also it's all about one disease, Dengue fever. What would it prove about different functions of different alleles when it's all about one disease? Why couldn't it demonstrate different functions with reference to one disease?
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Taq Member Posts: 10081 Joined: Member Rating: 5.1 |
Percy writes: Don't you mean that the peptides bound to the proteins produced by the alleles? That is what I was trying to communicate. I wanted to differentiate between viral proteins and HLA proteins just to make it clear.
The problem is that I can't understand the paper well enough to see how it supports this point. It is a bit dense, I will admit. The gist of it is that they looked at the sequence of each HLA allele and used a computer algorithm to predict which peptides it would bind. They then took the top 1% of predicted viral peptides and added them to the HLA proteins to see how well they bound in real life. From that data you can conclude that different alleles of each HLA gene bind a wide array of peptides, but not others. Also, HLA proteins from different alleles bind different viral peptides.
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Percy Member Posts: 22500 From: New Hampshire Joined: Member Rating: 4.9 |
Percy writes: It is a bit dense, I will admit. The gist of it is that they looked at the sequence of each HLA allele and used a computer algorithm to predict which peptides it would bind. They then took the top 1% of predicted viral peptides and added them to the HLA proteins to see how well they bound in real life. So computer simulation predicted which peptides would bind to which alleles (which really means binding to the proteins produced by each allele), but what does the "top 1% of predicted viral peptides" mean? Does that mean predicted with the highest confidence? And then they ran laboratory experiments to see how well the predictions turned out?
From that data you can conclude that different alleles of each HLA gene bind a wide array of peptides, but not others. Not sure how to interpret this. Do you mean that some alleles bind to a wide array of peptides, and some don't?
Also, HLA proteins from different alleles bind different viral peptides. This is probably the most important information from Faith's point of view, that different alleles for the same gene bind to different viral peptides, therefore there are more than two alleles with different function. The next thing that Faith wants to know is how the connection is made between binding to different peptides and improving the performance of the immune system. --Percy
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Taq Member Posts: 10081 Joined: Member Rating: 5.1
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Percy writes: So computer simulation predicted which peptides would bind to which alleles (which really means binding to the proteins produced by each allele), but what does the "top 1% of predicted viral peptides" mean? Does that mean predicted with the highest confidence? And then they ran laboratory experiments to see how well the predictions turned out? I believe top 1% refers to the binding avidity which is where you see reference to >500 nM. Avidity refers to the ability to grab something and not let go. Two of the main characteristics for protein binding are specificity and avidity. As you correctly state, then then made those small peptides to see how accurate their predictions were.
Percy writes: Do you mean that some alleles bind to a wide array of peptides, and some don't? It was poorly worded on my side. What I am saying is that there are many peptides the HLA proteins will bind, and a wide array that they won't bind. Each HLA allele has a different list of peptides that they will bind, also known as a difference in specificity.
The next thing that Faith wants to know is how the connection is made between binding to different peptides and improving the performance of the immune system. Although the HLA proteins were only tested against dengue virus, the same pattern carries over to other pathogens. Different alleles will bind differently to certain pathogens, changing the defenses you have against those pathogens. I believe bluegenes listed some of those examples in previous posts.
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NoNukes Inactive Member |
My understanding is that Faith accepts this argument. She believes that Adam and Eve together contributed at most two alleles for each gene, and that any gene today that has more than two alleles has experienced mutations, but she believes the alleles neutral, performing the same functions as the original two alleles. Where neutral means performing the same functions. Let's pick at that a bit.We know that the gene for blood type has three alleles and that the result is different types of blood that may form the same gross functions, described in a general way, but which are not compatible and thus cannot when looked at in detail be said to function the same. Siimilarly, the gene for producing fur color in rabbits has more than two alleles. This article says four. https://www.khanacademy.org/...ete-dominance-and-codominance. The result is multiple colors of rabbits, and I would call the difference in fur color functional. But it seems to me that the only examples that a Creationist cannot easily explain are limited. Dogs come from wolves so showing an increase in alleles for a gene is relevant. The Bible says that there were only two humans, so the possibility of more than two alleles is important. But for all other animals, there is no such limitation. For now, why isn't the blood type answer a sufficient example? Under a government which imprisons any unjustly, the true place for a just man is also in prison. Thoreau: Civil Disobedience (1846) History will have to record that the greatest tragedy of this period of social transition was not the strident clamor of the bad people, but the appalling silence of the good people. Martin Luther King I never considered a difference of opinion in politics, in religion, in philosophy, as cause for withdrawing from a friend. Thomas Jefferson Seems to me if its clear that certain things that require ancient dates couldn't possibly be true, we are on our way to throwing out all those ancient dates on the basis of the actual evidence. -- Faith Some of us are worried about just how much damage he will do in his last couple of weeks as president, to make it easier for the NY Times and Washington post to try to destroy Trump's presidency. -- marc9000
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Faith  Suspended Member (Idle past 1472 days) Posts: 35298 From: Nevada, USA Joined: |
Both the rabbit fur and the blood types came up earlier in the thread. Yes, they are sufficient. End of thread, thank you,.
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NoNukes Inactive Member |
Both the rabbit fur and the blood types came up earlier in the thread. Yes, they are sufficient. Okay. I would add that this particular line of argument required proving much more than was required. We know that there are some mutations that are 1) dominant, so that they could not have been hiding out in the gene pool, and 2) directly traceable to phenotypes so we know that they are not non functional. Under a government which imprisons any unjustly, the true place for a just man is also in prison. Thoreau: Civil Disobedience (1846) History will have to record that the greatest tragedy of this period of social transition was not the strident clamor of the bad people, but the appalling silence of the good people. Martin Luther King I never considered a difference of opinion in politics, in religion, in philosophy, as cause for withdrawing from a friend. Thomas Jefferson Seems to me if its clear that certain things that require ancient dates couldn't possibly be true, we are on our way to throwing out all those ancient dates on the basis of the actual evidence. -- Faith Some of us are worried about just how much damage he will do in his last couple of weeks as president, to make it easier for the NY Times and Washington post to try to destroy Trump's presidency. -- marc9000
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