|
Register | Sign In |
|
QuickSearch
Thread ▼ Details |
|
Thread Info
|
|
|
Author | Topic: Y.E.C. Model: Was there rapid evolution and speciation post flood? | ||||||||||||||||||||||||||||||||||||||||
bluegenes Member (Idle past 2508 days) Posts: 3119 From: U.K. Joined:
|
Faith writes: bluegenes writes: Perhaps it would be easier to explain directly how the new alleles are advantageous, and how they are necessarily different in how they function. The main problem for me, I think, is that you are assuming there is such a thing as "new alleles" that perform necessary functions for the immune system. This is really the same problem I've been having all along on this subject. Not "assuming". Observing.
Faith writes: I don't have a problem with these genes being polymorphous or with the idea that the alleles differ very slightly and that "they are necessarily different in how they function" as long as I assume that they are built in and not mutations. They have to be mutations, except for an original maximum of 4 alleles per gene.
Faith writes: (quoting paper)
quote: Understanding this by my YEC model the idea would be that the necessary alleles were already present and then selected. 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.
Faith writes: This article actually sounds like it assumes that beneficial mutations practically appear as needed, such as here:
quote: I would expect that somehow the solution to the problem has to be already present in the system and then it's selected. That is, it was created to function as it does, it didn't evolve for that purpose. Mutations don't just occur as needed but that's how this sounds. 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.
Faith writes: bluegenes writes: Bear in mind that there are several of these very polymorphous genes, and that if the Adam & Eve maximum of 4 alleles was all that was available to us, then homozygosity would be common (1/4 of the population on each gene, and most people on at least one). Homozygosity occurs after many generations of selection as I thinki of it, or by founder effect. But if a gene's function can be illustrated by a Mendel square there's no need for homozygosity to develop rapidly. This shouldn't occur with the skin color or eye color genes that function according to the Mendel square. If these genes you are talking about can be expressed in a Mendel square I'd like to see it. They can't be shown in a two allele square. They have multiple codominant alleles. There are a massive amount of phenotypes.
Faith writes: But it's probably that you've chosen a case that is too difficult for me to think through, and since it involves only a few genes I don't think it's very useful for a debate about the YEC model, which seems to me to be able to account for the vast majority of genes, and probably these too but if I'm unable to think it through it isn't a good example for this debate. 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.
Faith writes: And again, I'm going with two, not four, alleles, per Adam and Eve's genes. 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
|
||||||||||||||||||||||||||||||||||||||||
bluegenes Member (Idle past 2508 days) Posts: 3119 From: U.K. Joined:
|
Faith writes: bluegenes writes: Faith writes: The main problem for me, I think, is that you are assuming there is such a thing as "new alleles" that perform necessary functions for the immune system. This is really the same problem I've been having all along on this subject. Not "assuming". Observing. Well nothing yet has shown anything actually observed, that I have seen. Didn't you read the paper? The major histocompatibility complex (MHC) and its functions. NCBI Faith writes: It's all assumed. Ah! Either you didn't read it all, or didn't understand all of it.
Faith writes: These are assumed to be "alleles" for starters, and since alleles are alternative forms of a gene it is assumed that they do something to alter the gene's product in a beneficial way. 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.
Faith writes: There isn't even a discussion of the fact that they are mutations, which are known to be predominantly neutral, they're just called "alleles." I've had to keep bringing that up. It's a major problem for this whole idea. Variation in the MHC is definitely advantageous, not neutral.
Faith writes: bluegenes writes: Faith writes: I don't have a problem with these genes being polymorphous or with the idea that the alleles differ very slightly and that "they are necessarily different in how they function" as long as I assume that they are built in and not mutations. They have to be mutations, except for an original maximum of 4 alleles per gene. Yes they do have to be mutations, meaning they are not alleles according to my YEC model, and it still has to be shown that they ARE alleles as claimed. And please start noting that I'm using the idea of two alleles per gene for Adam and Eve, considering them to have had identical genomes -- not the presumed maximum of 4. They're alleles by definition, and there are far more than "slight" differences on them.
Faith writes: I keep suggesting that the "high frequency" is an illusion if the alleles are neutral mutations that don't change the function of the original allele. In that case they would be passed on to the next generations, and if you are counting them separately from other forms of the same allele they may look like they have high frequency when it's nothing but their continued existence in the population because there's no reason for them to be selected out. 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%..
Faith writes: You assume selection because they persist at all, and count any degree of persistence as increase in frequency when they are not increasing at any greater rate than all the other forms of the same allele, because they are essentially the same allele. This argument I keep making needs to be addressed. 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.
Faith writes: bluegenes writes: 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. No, let's get this much sorted out please.1) There are TWO alleles and two only, per gene, in my YEC model. 2) YOU are calling these mutations "alleles," and I am denying that they are alleles, at least saying that you have not shown that they do anything different than the original allele did. As I hope you now understand from the paper, they are are there because of their difference in function.
Faith writes: 3) YOU are saying that they are positively selected, and I am saying that is an illusion as explained above. Then your YEC model must be false. It (the YEC model) requires rapid strong positive selection to explain what we see in the MHC.
Faith writes: 4) Therefore the YEC model I'm using does not have to accept any of this. They aren't alleles, they aren't positively selected. Your model has no obligation to be true, certainly.
Faith writes: bluegenes writes: Bear in mind that there are several of these very polymorphous genes, and that if the Adam & Eve maximum of 4 alleles was all that was available to us, then homozygosity would be common (1/4 of the population on each gene, and most people on at least one). Homozygosity in individuals at particular loci occurs at that rate, but not in the whole population unless those individuals get reproductively isolated among themselves. I'm a bb, my father was a bb, my mother and siblings are all Bb. This is a pretty common situation. The original Scandinavians may have been so predominantly bb that even a Bb was rare, but that's the result of migration and reproductive isolation. In any case I'm not sure I'm getting your point about the immune system. If the genes are codominant you aren't going to get homozygosity anyway, are you? 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.
|
||||||||||||||||||||||||||||||||||||||||
bluegenes Member (Idle past 2508 days) Posts: 3119 From: U.K. Joined: |
Percy writes: 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. 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.
quote: 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!
|
||||||||||||||||||||||||||||||||||||||||
bluegenes Member (Idle past 2508 days) Posts: 3119 From: U.K. Joined: |
Percy writes: Putting my ignorance on full display, I found this paragraph particularly difficult:
quote: 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.
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. There are several genes (polygeny) that produce the proteins that detect and present "poisonous" foreign bodies (antigens) to anti-bodies. (Forget classes for now).
Percy writes: 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? Yes. It does actually state that indirectly in the second sentence of the bit you quoted above.
quote: I quoted another extract from the same paper (actually, a book) in Message 189quote: 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.
Percy writes: 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. No. It means more than 200 on some individual genes.
Percy writes: 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. 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?
|
||||||||||||||||||||||||||||||||||||||||
bluegenes Member (Idle past 2508 days) Posts: 3119 From: U.K. Joined:
|
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?
|
||||||||||||||||||||||||||||||||||||||||
bluegenes Member (Idle past 2508 days) Posts: 3119 From: U.K. Joined: |
Faith on another thread reffering to this one writes: If that paper is above Percy's pay grade as he put it, it's certainly above mine. I read what I was able to read, and nothing you said gave evidence that new alleles actually exist. As I keep saying the "evidence" of supposed positive selection shown by increased frequency is an illusion if the allele in question is really a neutral mutation, which would be passed on and easily look like increased frequency based on your assumption. You seem to think that paper actually shows that new alleles give immunity to different parasites, but it doesn't. It assumes it. 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?
|
||||||||||||||||||||||||||||||||||||||||
bluegenes Member (Idle past 2508 days) Posts: 3119 From: U.K. Joined:
|
Taq writes: 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. 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. quote: This as a massive increase in functional information since Adam and Eve.
|
||||||||||||||||||||||||||||||||||||||||
bluegenes Member (Idle past 2508 days) Posts: 3119 From: U.K. Joined: |
Percy writes: 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. 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.
|
||||||||||||||||||||||||||||||||||||||||
bluegenes Member (Idle past 2508 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
|
||||||||||||||||||||||||||||||||||||||||
bluegenes Member (Idle past 2508 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."
|
||||||||||||||||||||||||||||||||||||||||
bluegenes Member (Idle past 2508 days) Posts: 3119 From: U.K. Joined: |
Percy writes: 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? 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.
Percy writes: I found the paper impenetrable. 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
|
||||||||||||||||||||||||||||||||||||||||
bluegenes Member (Idle past 2508 days) Posts: 3119 From: U.K. Joined: |
Percy writes: Faith doesn't have a problem with more than 2 alleles. What she has a problem with is more than 2 alleles where the additional alleles do anything different than the original alleles. She claims that the new alleles must do the same things the old alleles did, i.e., have the same functions as the old alleles. She claims that the new alleles cannot have new functions. 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. quote:
|
||||||||||||||||||||||||||||||||||||||||
bluegenes Member (Idle past 2508 days) Posts: 3119 From: U.K. Joined: |
Percy writes: What this table tells us is that we know very little about which HLA-B alleles protect against which pathogens. For most of them all that is known is that they're associated with the immune system, or that they're associated with disease, which is consistent with Faith's assertion that mutations are only harmful. 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).
|
||||||||||||||||||||||||||||||||||||||||
bluegenes Member (Idle past 2508 days) Posts: 3119 From: U.K. Joined: |
Percy writes: This is already more than four alleles with positive effects. 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.
|
||||||||||||||||||||||||||||||||||||||||
bluegenes Member (Idle past 2508 days) Posts: 3119 From: U.K. Joined: |
mike the wiz writes: A number of factors are involved, beneficial mutations potentially, but not the type that creates new information in the genome,. 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.
mike writes: ..but there is allopatric speciation to consider which may have been very rapid for the first few hundred years post-flood before it settled down, almost an explosion of variety I imagine. Post-flood, there would be no more antediluvian world. Logically this represents a major change for all organisms. Pre-flood they would have lived in more gentle, more uniform climates, the bible says there was increased longevity. So the speciation post-flood, the pressure would have been superb immediately after the flood, different populations spreading out with new selection pressures on those animals. Certainly. Their former niches no longer exist, the environment has changed dramatically, and that definitely means new and strong selection pressures.
mike writes: As for the misconception that there was, "rapid evolution" after the flood, that is usually a sign people are indolent about the mathematics. If you do the basic mathematics you will see that natural selection, or even call it, "evolution" if you want, does not depend upon a passage of time, it depends upon the amount of generations you can get within a passage of time. 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.
mike writes: edit; I have written more about this issue here in message one of this thread;Bot Verification... (the numbers I give are only guesses of course, about the generation spans, just approximations, I have no great knowledge of how long it is for each generation of the various species, but basically it's just to show you that we would expect more speciation and diversity for organisms with fast generation spans.) 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.
|
|
|
Do Nothing Button
Copyright 2001-2023 by EvC Forum, All Rights Reserved
Version 4.2
Innovative software from Qwixotic © 2024