|
Register | Sign In |
|
QuickSearch
Thread ▼ Details |
|
Thread Info
|
|
|
Author | Topic: Y.E.C. Model: Was there rapid evolution and speciation post flood? | |||||||||||||||||||||||||||||||||||||||||||||||
Percy Member Posts: 22502 From: New Hampshire Joined: Member Rating: 4.9
|
Faith writes: Because the claim is that these "alleles" code for a different protein and different function of the gene than the allele whose sequence they changed, but there is no evidence that they code for anything other than the original allele did (the one at that particular locus whose sequence they changed). A change in sequence that does not change the protein or function is just a neutral mutation. Calling it an allele confuses things. NosyNed is trying to accommodate your objection to the definition to "allele", but I believe it will just cause confusion. "Allele" has a definition and you can't change it. An allele is any unique nucleotide sequence for a gene. Some alleles produce different proteins and functions, some don't, but they're all alleles.
Please define what a 'bona fide' allele is so we can tell it apart from others. Its sequence codes for a different protein and different trait than other sequences for the same locus. Just to emphasize the point, this is an incorrect definition of allele. An allele is any unique nucleotide sequence at a gene locus. It does not need to code for a different protein to be a different allele. When a mutation causes a new and unique nucleotide sequence then it is a new allele, whether it codes for a new protein or not. The nucleotide sequence of an allele is divided into nucleotide triplets called codons. Each 3-nucleotide codon codes for an amino acid that will be added in sequence to the protein as it is constructed. This table from Wikipedia shows which codons create which amino acids (it's big and very legible if you expand it):
It's false to call it an allele if it only does what all the others do at that locus despite its different sequence. Since you've said it one more time I want to emphasize one more time that this is incorrect. A different nucleotide sequence is a different allele, whether it produces a different protein or not.
mutations are KNOWN to be predominantly neutral. Because most of the genome is non-coding, most mutations occur in non-coding regions and are therefore neutral. But mutations that occur in coding regions are *not* "predominantly neutral." As you can see in the chart above, most single nucleotide mutations will result in different amino acids and therefore different proteins. --Percy
|
|||||||||||||||||||||||||||||||||||||||||||||||
Percy Member Posts: 22502 From: New Hampshire Joined: Member Rating: 4.9 |
bluegenes writes: Didn't you read the paper? The major histocompatibility complex (MHC) and its functions. NCBI I tried to read this paper but found it outside my pay grade. It might help if you could boil the paper down into something less technically dense.
As I hope you now understand from the paper, they are are there because of their difference in function.
I don't think this diagram will be understood without some provided background about what "peptide antigen binding" is and so forth. I kind of get it because I slogged through the first quarter or so of that paper, but I could do with some clarification, too. --Percy
|
|||||||||||||||||||||||||||||||||||||||||||||||
Percy Member Posts: 22502 From: New Hampshire Joined: Member Rating: 4.9
|
Putting my ignorance on full display, I found this paragraph particularly difficult:
quote: 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: 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
|
|||||||||||||||||||||||||||||||||||||||||||||||
Percy Member Posts: 22502 From: New Hampshire Joined: Member Rating: 4.9 |
PaulK writes: quote: 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
|
|||||||||||||||||||||||||||||||||||||||||||||||
Percy Member Posts: 22502 From: New Hampshire Joined: Member Rating: 4.9 |
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
|
|||||||||||||||||||||||||||||||||||||||||||||||
Percy Member Posts: 22502 From: New Hampshire Joined: Member Rating: 4.9 |
I'll reply to your Message 248 and Message 249 in this single message.
Taq: Here's the image for reference:
About this from the comment beneath the figure:
quote: What is a haplotype? The Wikipedia article on Haplotype offers several definitions. What does the little symbol between curly braces mean?
quote: 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: UniProt 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: There are 118 (good "quick count" by you). Faith is asking how we know which alleles produce unique proteins that do something different. --Percy
|
|||||||||||||||||||||||||||||||||||||||||||||||
Percy Member Posts: 22502 From: New Hampshire Joined: Member Rating: 4.9 |
I'm still trying to decode this paragraph from the book:
quote: Just for reference, here's the diagram listing all the genes of the MHC complex:
Let's break that paragraph down. First it says, "every person will express at least three different antigen-presenting MHC class I molecules." If there are over a hundred class I MHC genes, why do people express only "three different antigen-presenting MHC class I molecules"? Shouldn't most people be expressing many, many different molecules, sometimes as many as 200, depending upon the degree of heterozygosity. Then it says, "three (or sometimes four) MHC class II molecules." If there are around 60 class II MYC genes, why do people express only "three (or sometimes four)" MHC class II molecules. Shouldn't most people be expressing many, many different molecules, sometimes as many as 120, depending the degree of heterozygosity. Then after giving these very precise numbers of "three (or sometimes four)" it continues on to contradict itself and say "the number of different MHC molecules expressed on the cells of most people is greater." So who knows what to think? Now before you reply let me quote some of what you say about this paragraph:
bluegenes writes: 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). So you agree that it's more than "three (or sometimes four)", and the paragraph concludes by stating that it's more, but then why did they ever give figures like "three (or sometimes four)". And am I right in stating that it should be much, much more than this paragraph states or implies? This quote from the book is an important piece of the information Faith is looking for:
quote: So it is a fact that the MHC complex has over a couple hundred genes that taken together have thousands of different alleles that produce very different proteins. The question Faith has to address is how this happened in just six thousand years starting with a maximum of four alleles per gene in the population (I know Faith is claiming there were only two alleles per gene, but she's never supported this statement).
So, are you beginning to understand why I'm saying that the YECs need to include mutation and positive selection into their model? Yes, I understand, but I'm looking for the data that proves this view. Faith now has to accept that the MHC complex has hundreds even thousands of unique alleles that produce unique proteins, but she still doesn't have the frequency data, and she doesn't understand why that data indicate that it would have taken much more than six thousand years. --Percy
|
|||||||||||||||||||||||||||||||||||||||||||||||
Percy Member Posts: 22502 From: New Hampshire Joined: Member Rating: 4.9 |
jar writes: If the Bible story was true and Eve really was cloned from Adam's rib bone would "Adam and Eve: maximum possible 4" be correct or "Adam and Eve: maximum possible 2"? God would have had to change the X chromosome to a Y, so we know he made at least some genetic changes when he made Eve. It doesn't seem possible to know from just the Bible what specific genetic changes God made, so that seems to argue that the possibility of a maximum of 4 alleles per gene has to be considered, not ruled off the table. --Percy
|
|||||||||||||||||||||||||||||||||||||||||||||||
Percy Member Posts: 22502 From: New Hampshire Joined: Member Rating: 4.9 |
Faith writes: they don't look identical to me:
The two strands are mirror images of each other. A always pairs with T, and C always pairs with G. When DNA replicates by splitting the two strands, that's how identical copies form. AbE: I see this question has already been answered in better detail - apologies. One question I've sometimes wondered about, and maybe someone here has an answer, is how geneticists decide which half of the paired DNA strands to list. For example, if they provide this short DNA sequence:
AGTTCCAGT... They could just as easily have provided the sequence of the other strand:
TCAAGGTCA... Which to choose? --Percy Edited by Percy, : AbE.
|
|||||||||||||||||||||||||||||||||||||||||||||||
Percy Member Posts: 22502 From: New Hampshire Joined: Member Rating: 4.9 |
bluegenes writes: No. I guess I must have misunderstood what an "antigen presenting molecule" is. I was assuming from context that it was a synonym for a protein coded for by one of the MHC genes. Now that I know that is wrong, let me try again. Looking this up at Wikipedia I found "antigen presenting cell," but not "antigen presenting molecule." Wikipedia says that an "antigen presenting cell" is one that...well, never mind, this is getting complicated, and I'm not even sure I'm on the right track. Can you boil this down for me?
Only three of the class 1 genes are "antigen presenting" genes, and 3 (sometimes 4) in class 2, hence the 6 or 7 antigen presenting molecules. If only 3 class I genes are involved, and only 3 (sometimes 4) class II genes, then now I'm confused why Taq gave me a diagram and an Excel list of all the MHC genes. But anyway, if we're only talking about 6 or 7 genes then it would be helpful to know the names of the genes, the number of alleles for each one in the population, and how we know that the alleles produce unique proteins.
These are the famously polymorphic genes with multiple codominant alleles, hence the likelihood of most people expressing a lot more, up to double, the number of molecules. Okay, that gives us as many as 14 "antigen presenting molecules" for a single individual. --Percy
|
|||||||||||||||||||||||||||||||||||||||||||||||
Percy Member Posts: 22502 From: New Hampshire Joined: Member Rating: 4.9 |
Before replying I want to first thank everyone trying to explain this to me, even if I didn't reply to each message.
Taq writes: The MHC complex includes antigen presenting proteins and other proteins. It isn't exclusive to antigen presenting proteins. We're arguing to Faith that there are more alleles that produce functionally different proteins with significant frequencies in the population than could have arisen since Adam and Eve, and I've been inquiring about the data that proves this point, but if I've gone off track in one area maybe I've gone off track in others, too. Am I right about the point we're trying to make to Faith? If so, has the data I'm looking for been presented? If so, could someone point me to it? --Percy
|
|||||||||||||||||||||||||||||||||||||||||||||||
Percy Member Posts: 22502 From: New Hampshire Joined: Member Rating: 4.9
|
NoNukes writes: I think the answer is more simple that that. The argument is that more alleles exist than either the pair of Adam and Eve, or the collection of folks on the ark actually could have possessed. 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. Efforts have been to persuade Faith of two things:
I'm seeking the evidence that proves these two points. It may have been presented already, but not in a form I understand. This might have been mentioned already, but this was new to me: the MHC complex and the HLA complex are the same thing. --Percy
|
|||||||||||||||||||||||||||||||||||||||||||||||
Percy Member Posts: 22502 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
|
|||||||||||||||||||||||||||||||||||||||||||||||
Percy Member Posts: 22502 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
|
|||||||||||||||||||||||||||||||||||||||||||||||
Percy Member Posts: 22502 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
|
|
|
Do Nothing Button
Copyright 2001-2023 by EvC Forum, All Rights Reserved
Version 4.2
Innovative software from Qwixotic © 2024