Y.E.C. Model: Was there rapid evolution and speciation post flood?

Even better. In this paper, they're classifying HLA class 2 molecules by function into 7 "supertypes", so they're looking for similarities. Even those in the same supertype only average ~46% shared peptide binding function. It looks like the products of the variant HLA alleles are virtually all significantly different in function. Functional classification of HLA Class 2 molecules.

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We found that the repertoire overlaps between molecules within the same supertype averaged about 46%, ranging from a high of 60% for the DP2 supertype to a low of 23% for the main DQ supertype (Table 3 and Fig. 2a). Average repertoire overlaps for molecules in the main DR, DR4, DRB3, main DP, and DQ7 supertypes were 46%, 55%, 31, 56, and 54%, respectively.

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This as a massive increase in functional information since Adam and Eve.

I'm still trying to decode this paragraph from the book:

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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.

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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: 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:

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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.

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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). 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

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

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: They could just as easily have provided the sequence of the other strand: Which to choose?--PercyEdited by Percy, : AbE.

No. 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. 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.Forget the rest of the genes! They do other things, known and unknown, and are not particularly polymorphic, and if not, can all be present in Adam and Eve.

The standard nomenclature is to label them the (+) and (-) strands. In prokaryotes with their circular chromosome, the + strand is determined by the strand containing the origin of replication which is the place at which replication of the genome begins. I'm not sure what the convention for choosing the positive strands in eukaryotes is, but I would guess that it is somewhat more arbitrary than that found in prokaryotes.The other standard nomenclature is to always list DNA sequences in the 5' to 3' direction. Let's say we have this double strand of DNA:

5'--ATTAGGCCA--3'
3'--TAATCCGGT--5'

For the lower strand you would list the sequence as TGGCCTAAT, which is the reverse of the double strand.As you would probably guess, some genes are found on the + strand and some on the - strand. If you are dealing with a gene then the convention is to give the sequence of the open reading frame in the 5' to 3' direction no matter what strand it is found on. Most databases will list which strand the gene is found on.Edited by Taq, : No reason given.

Just from what we know about tissue transplantation we already knew that there was a wide range of function in these alleles. The reason that finding donors is difficult is because the binding specificities of the HLA proteins has to match or be very close, and there are hundreds of alleles out there with different binding specificities.If, as Faith hypothesizes, there are only two alleles per HLA protein then it should be quite easy to find perfect matches, but that just doesn't happen with any regularity.

For Sanger sequencing, the region of interest is amplified using PCR. A forward and reverse primer is used that bind opposite strands at the extents of the target region as in the image below. After amplification, the PCR products are cleaned and all small nucleotides and primers are removed. Then half of the purified product is put in a well with forward primer and the other half is put into a well with reverse primer. These are processed so that the resulting sequence reads are complimentary which are then aligned using software. The software automatically detects that the strands are complimentary and converts one of them. A consensus sequence is generated from the aligned sequences and this is what is reported.I'm not sure if this is convention per se, but typically the strand that is amplified by the forward primer is the strand that gets reported. When designing primer pairs, typically you try to located the forward primer at the front of the gene so that the resulting sequence will end up in the same orientation as the direction the gene is transcribed. NexGen sequencing does not use primers to initiate sequencing and relies much more on software to assemble the individual sequences (100 - 150 bp) but the convention would be the same: to report a gene sequence so that the reported sequence is in the same orientation as the gene is transcribed.Occasionally you will find a sequence reported in the opposite direction, but software will usually identify it and it can be converted to match the rest of the sequences you are working with.HBD

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? 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. Okay, that gives us as many as 14 "antigen presenting molecules" for a single individual.--Percy

The MHC complex includes antigen presenting proteins and other proteins. It isn't exclusive to antigen presenting proteins.It's a bit like getting an inventory of everything in the Louvre. There are going to be paintings and statues on the list, but there are also going to be mops and buckets on the list.

Before replying I want to first thank everyone trying to explain this to me, even if I didn't reply to each message. 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

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:

• That the frequency of the alleles indicates strong selection and therefore different function. Faith rejects this argument, arguing that if the alleles did the same thing as existing alleles then they would also have strong selection.
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• That there has not been enough time since Adam and Eve to create the distribution of alleles we observe in the human population.

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

My answer to this, for the record, has been that if they are neutral mutations/alleles there is no limit on how many there would be in a given time frame. I'd also add at this point that the fact that there are so many is evidence in itself that they are neutral mutations according to the YEC framework. It should be pretty clear by now that there isn't any.

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 [edit: bluegenes] and I also discuss the paper in posts 271 and 277.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. What they found is that different peptides bound to different alleles. No two alleles bound the same peptides.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.Edited by Taq, : No reason given.