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

Not "assuming". Observing. They have to be mutations, except for an original maximum of 4 alleles per gene. By your model, Adam and Eve would have had all the genes (the "different loci" referred to in the article) but can only have two alleles each on them, which, if they are all different, gives us only four alleles per.gene, whereas now there are many alleles at high frequency in the population (easily found in a small sample). That can only be explained by mutation and positive selection. No they don't. But relatively rare advantageous mutations can occur, then their frequency (the percentage of the population which has them) can increase via positive selection. Your model requires this, as only four alleles per. gene can be there 300 generations ago. They can't be shown in a two allele square. They have multiple codominant alleles. There are a massive amount of phenotypes. The YEC model has to account for it. The thing about the MHC is that your model can only attempt to explain it if you accept that mutation and positive selection can happen. When you hear other creationists claim that one or the other doesn't happen, or that both don't happen, you are now in a position to explain to them that they are inadvertantly describing the YEC model as false through their ignorance. That's fine, but it makes it even harder for the model to explain what's actually there, and, so far as the following generations and their MHC genes are concerned, it would make many immune systems weaker than now, because 50% would be homozygous on any given locus. The population would need a lot of mutation and positive selection to give it the defences we see now.You also need strong, rapid selection for your niche filling after the Ark. You could view all polar bear characteristics as coming from Ark bears with a kind of super genome, but only environmental selection on that genome would explain how their characteristics match the niche.Natural selection should be very popular with YECs, and they need to learn to stop inadvertently destroying their model by attacking the concept.Edited by bluegenes, : mutation

Didn't you read the paper? The major histocompatibility complex (MHC) and its functions. NCBIAh! Either you didn't read it all, or didn't understand all of it. They are alleles by definition, and it is not assumed that all those present are beneficial, it is concluded that many are because of an understanding of how variety in the MHC works, and how the variant proteins function physically. Variation in the MHC is definitely advantageous, not neutral. They're alleles by definition, and there are far more than "slight" differences on them. A 6,500yr young earther shouldn't be saying that. You won't get many new neutral alleles present in a sample of 120 people (see my Cuban example) on any genes on that time scale, and you certainly can't get the pattern of variance we see on the HLA genes, with so many of them at >2%.. We can observe a level of frequency impossible in a 300 generation neutral evolution model, and we can observe why having lots of different protein products in the MHC is advantageous.I'm suggesting that it is you YECs who require particularly strong selection in order to explain what can be observed. As I hope you now understand from the paper, they are are there because of their difference in function. Then your YEC model must be false. It (the YEC model) requires rapid strong positive selection to explain what we see in the MHC. Your model has no obligation to be true, certainly. If you have the same allele for one gene, yes. Codominant means that, if you have two alleles at the locus, you always get two immune products for the price of one, a better bargain, certainly. The more alleles available, the less chance of individuals ending up with the same ones anywhere, and the better equipped the group or species is to survive a threatening attack.

What did you make of the first extract I posted way back in the thread? It explains how we can express a great variety of antigen (toxic foreign substances) presenters (they identify and "present" the antigens to xenophobic killer cells) because of the many-gened, many-alleled nature of the system. If it sounded like Greek to you, that's partly because some of it is, but I'm sure you can get what's important.

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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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The term polymorphism comes from the Greek poly, meaning many, and morphe, meaning shape or structure. As used here, it means within-species variation at a gene locus, and thus in its protein product; the variant genes that can occupy the locus are termed alleles. 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. So there is only a small chance that the corresponding MHC locus on both the homologous chromosomes of an individual will have the same allele; most individuals will be heterozygous at MHC loci. The particular combination of MHC alleles found on a single chromosome is known as an MHC haplotype. Expression of MHC alleles is codominant, with the protein products of both the alleles at a locus being expressed in the cell, and both gene products being able to present antigens to T cells. The extensive polymorphism at each locus thus has the potential to double the number of different MHC molecules expressed in an individual and thereby increases the diversity already available through polygeny

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Then we can go from there. Important to this thread is that, although Adam and Eve could have the many gened part, they are limited in how many alleles they could have (4 maximum per loci) and now there are loads of functioning alleles in the system, certainly an advantage in dealing with the range of constantly mutating pathogens, and a massive mutational increase in positive functional information since creation, I might add!

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. There are several genes (polygeny) that produce the proteins that detect and present "poisonous" foreign bodies (antigens) to anti-bodies. (Forget classes for now). Yes. It does actually state that indirectly in the second sentence of the bit you quoted above.

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

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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. 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.

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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.

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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.

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

I think I did answer your earlier post.Faith's going for two alleles, but God might not have used standard cloning procedures, and presumably could have used genetic modification.We could, considering the sub thread, wonder why he gave them an immune system pre-fall, couldn't we?

If the paper is above your head, why are you telling us what it does and doesn't show?What did you think of the West African malaria example?

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.

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.

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

I'm many things, but I'm not "a wide-mouthed cylindrical container made of glass or pottery."

Casual language, like saying General Custer's orders killed the Indians, rather than his soldiers, or their weapons. "Guns kill" says the anti-gun lobby. "Guns don't kill, people do" say the NRA. It's lucky people like you are around to remind us all that it's actually the bullets. What the papers show is that the proteins produced by the differing alleles are different, and that they function differently in relation to pathogens. As I pointed out in the post you're replying to, the HLA-B (one gene) alleles are well known to have very different effects in relation to different diseases. If you want, I can dig up specific numbered alleles (like, from memory, HLA-B27 and HlA-B57 being good against HIV (Aids), HLA B-53 against a lethal form of West African Malaria, HLA-B7 and B51 working well against measles and so on and on and on.....Edited by bluegenes, : typo

Then research on the HLA-B gene alone proves her wrong. The variant alleles produce different proteins and definite differences in immune reactions.Here's a paper that shows differences in producing immune reactions to a measles vaccine. Three HLA-B alleles are identified that perform particularly badly, and two that perform particularly well, with others in between. Variance in HLA-B performance against measles.

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Despite the success of the current measles vaccine in controlling disease in industrialized countries, the importance of vaccine failure has become increasingly apparent. Our objective was to determine if associations exist between seronegativity after measles vaccination and class I human leukocyte antigen (HLA) alleles. We undertook a cross-sectional observational study in Rochester, Minnesota, with 242 school-age children previously recruited from a communitywide seroprevalence study. We studied two groups of subjects: 72 were seronegative (EIA =<0.8 after a single dose of measles vaccine) and 170 were seropositive (enzyme immunoassy [EIA] =<1.0 after one dose). We used the resources of Mayo Clinic's tissue typing laboratory for serotyping class I HLA-A and HLA-B alleles via microlymphocytotoxicity assays. We found no statistically significant associations with class I HLA-A but did find associations with class I HLA-B, which includes alleles associated with seronegativity (B8, B13, and B44) and those associated with seropositivity (B7 and B51).

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With enough research involving enough strains of enough pathogens, all could eventually be associated with disease, because none can cover all the ground of our many and ever varying parasites.You can add B63, B57, and B58 as having a positive effect against HIV; B44, B52,B62,B76, andB77 as having a positive effect against Dengue fever; B53 having a positive effect against Malaria; and B35, which you've got down as being bad news for those infected by HIV, is good news against infection with Prurigo Hebra (a skin disease).Ultimately, with enough knowledge, we should find good and bad news for them all.Variety is selected for, and individual alleles face positive selection every time something they're particularly effective against sweeps a local population (B53 is at high levels of frequency in malarial areas of West Africa, for example).

We could find plenty more, and your own pair of HLA-B alleles could have saved your life many times without us knowing. We tend to identify alleles that perform poorly against certain diseases because we're looking at the genes of the sick, not the healthy. But failing on one disease doesn't mean a negative mutant. The alleles failing at measles could have saved those kids' ancestors from smallpox for all we know.When an allele is very successful, like B53 against West African malaria, the success can actually cause problems. More and more people could become homozygous on the B gene, therefore decreasing their range of immunity against other things. Also, if a mutant strain of malaria arrived that could avoid recognition by B53, there could be big problems, and that new strain would become dominant.But variety means there could always be rarer alleles present that could cope with the new strain, so variety makes the species strong.

How would something new in the phenotype be formed without "new information"? (That might be best answered on an information thread I started recently Message 1).I certainly think you would be wise to put beneficial mutations in your model for all of the niche filling that is required. Certainly. Their former niches no longer exist, the environment has changed dramatically, and that definitely means new and strong selection pressures. Of course it's generations. That's always taken into account when estimating the divergence time of two populations by looking at their genomes. The reason estimates are usually very approximate is because the exact mutation rate is rarely known, but the generation gap usually is.If YECs want to put "kind" at the level of family, they will need to argue for much higher mutation rates in the past; frequently more than 100 times those currently estimated by biologists and sometimes 1000 times or more, in order to account for the neutral mutational differences of groups in the same family. Of course shorter generation times give more potential for change in a given time span, but, unfortunately, the bigger the animal, the more space and food taken up on the ark; and the longer the generation gap tends to be. Elephant generations are like ours.I'd advise at least 6 already diverged and distinct pairs on the Ark for the Elephant family, otherwise the observed difference on genomes would require lethal mutation rates.