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Author | Topic: Y.E.C. Model: Was there rapid evolution and speciation post flood? | |||||||||||||||||||||||||||||||||||||||
Taq Member Posts: 10045 Joined: Member Rating: 5.3 |
14174dm writes: My understanding of genes and alleles is that when we say this gene controls such, we mean that we found a statistical link between the gene and the effect. We haven't traced the protein and its impacts through every cell and biochemical process. For the specific paper on eye color, this is an accurate description. For some alleles the biochemical and physical interactions are understood at the molecular level.
When we see this allele at the gene causing blue eyes, are we also seeing what else it does? For example, adrenaline increases heart rate, opens airways and increases the emotional aspect of memories. It is entirely possible that the alleles affeting eye color also have functions elsewhere that are being selected for.
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Taq Member Posts: 10045 Joined: Member Rating: 5.3 |
Faith writes: And as the Mendel squares easily demonstrate, more than two alleles per gene are not needed for all the diversity we see in living things. How so? You seem to just assert this without any backing.
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Taq Member Posts: 10045 Joined: Member Rating: 5.3 |
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). Where is the evidence that they have the same function?
They aren't alleles according to what I say above, they are merely mutations, changes in the DNA sequence that do not code for a new protein or a new trait, and in my model there are lots of mutations occurring all the time, most of them neutral which is why I'm assuming that's what these are, or deleterious. Mutations ARE increasing. In my model they are not true alleles and they are not a good thing for the organism. Do all chimp genes function exactly the same as human genes, in your model?
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Taq Member Posts: 10045 Joined: Member Rating: 5.3 |
Faith writes: There is no evidence one way or the other, but it needs to be proved and can't be assumed that the function is not the same. You can't assume they have the same function, either.
Faith writes: Since most mutations are known to be neutral, others deleterious and very very few very iffily beneficial, it ought to be common sense to provide evidence that any mutation is beneficial, but no, all these on this thread are ASSUMED to be beneficial. We don't need to assume that the genetic differences between humans and chimps are beneficial. We can directly observe that they are beneficial in both humans and chimps. Therefore, we know that changes in DNA can and are beneficial. No assumption needed.
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Taq Member Posts: 10045 Joined: Member Rating: 5.3 |
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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Taq Member Posts: 10045 Joined: Member Rating: 5.3
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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.
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Taq Member Posts: 10045 Joined: Member Rating: 5.3 |
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: Complete sequence and gene map of a human major histocompatibility complex | Nature 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: UniProt If you scroll down to polymorphisms, it lists about 120 known alleles for the gene, at least by my quick count.
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Taq Member Posts: 10045 Joined: Member Rating: 5.3 |
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.
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Taq Member Posts: 10045 Joined: Member Rating: 5.3 |
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: HLA Nomenclature @ hla.alleles.org For HLA-DRB1 they have 2,058 alleles listed.
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Taq Member Posts: 10045 Joined: Member Rating: 5.3 |
Percy writes: What is a haplotype? The Wikipedia article on Haplotype offers several definitions. Genes close to one another tend to stay together because fewer cross over events happen between them during meiosis. Therefore, some alleles on neighboring genes will stay together. For example, you may tend to see allele1 from gene A and allele 2 from gene B at a higher ratio than would be predicted by chance (i.e. a random shuffle). As to a "composite of different haplotypes", I'm not sure exactly what they are talking about. They could be talking about a composite of DNA from different people, different strands of DNA (remember that human DNA is diploid so it has two strands), or a combination of both.
What does the little symbol between curly braces mean? The Greek letter Psi is meant to denote pseudogenes (Psi ---> pseudo).
Does this mean that for some loci different people can have different genes instead of different alleles? That is what it means. This usually indicates that some people will have a gene at a specific location while others just have a gap. It can also indicate a difference in copy number, such as one person having 1 geneA and other people have duplication of 2 geneA at the same position.
There are 118 (good "quick count" by you). I counted the number across and the number of rows, so don't be too impressed.
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Taq Member Posts: 10045 Joined: Member Rating: 5.3 |
Faith writes: they don't look identical to me: They look identical to a molecular biologist. Let's use this piece of DNA as our example:
5'--GTGGACCAGT--3' 3'--CACCTGGTCA--5' Across from each base is it's mirror image. G is the mirror image of C, C is the mirror image of G, A is the mirror image of T, and T is the mirror image of A. Think of it like your hand being held up to a mirror. If you hold your right hand up to a mirror it isn't an identical copy of your hand, but is instead a mirror image that more resembles your left hand. Your left and right hands are mirror images of each other. The 5' and 3' denote the ends of each DNA strand, as you will see the two DNA strands go in opposite directions. The 5' and 3' come from the number of carbon atoms on the sugar that forms the backbone of DNA:
When proteins copy DNA they start at the 5' end and stop at the 3' end. So when we copy DNA we go from the double stranded form to the single stranded forms
5'--GTGGACCAGT--3' 3'--CACCTGGTCA--5' DNA polymerases then copy each single strand from the 5' to 3' strand, placing the mirror image of each base on the new strand. This results in two double stranded pieces of DNA:
5'--GTGGACCAGT--3' 3'--CACCTGGTCA--5' ---copy--> <---copy-- 5'--GTGGACCAGT--3' 3'--CACCTGGTCA--5' What you end up with is two identical double strands of DNA. Edited by Taq, : No reason given. Edited by Taq, : No reason given. Edited by Taq, : No reason given.
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Taq Member Posts: 10045 Joined: Member Rating: 5.3 |
New Cat's Eye writes: Chirality! In the case of DNA bases it isn't chirality. However, mirror image serves as a good analogy even if it can be confusing if we discuss chirality. I didn't think "complementary bases" would be as easy to understand.
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Taq Member Posts: 10045 Joined: Member Rating: 5.3 |
Faith writes: That's beautiful. And you guys don't believe in intelligent design! Not when we can watch this all happen right in front of us without any intelligent designer involved.
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Taq Member Posts: 10045 Joined: Member Rating: 5.3
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Faith writes: Ooooooobviously I understood some of it. Sheesh. Let's see if you are able to understand this paper: http://www.jimmunol.org/...3/11/03/jimmunol.1302101.full.pdf It is rather straightforward. They looked at several alleles for the HLA-A and HLA-B genes. They then tested them against multiple peptides (i.e. short proteins) from the Dengue fever virus. What they found is that different alleles bound different peptides, proof that they have different functions (table 1 from the paper). Since they were able to show that more than two alleles for each gene bound different peptides, this demonstrates that are more than two alleles for these genes as defined by function.
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Taq Member Posts: 10045 Joined: Member Rating: 5.3 |
Percy writes: 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?
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.
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