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The Case for Common Descent from ERVs: A tutorial for MarkE

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  • #31
    Originally posted by marke View Post
    Would you say then, that the evidence shows that all of God's creatures have similar ERVs just as all of God's creatures have similarities of DNA or else they would die?
    No. Why do you ask?

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    • #32
      Originally posted by marke View Post
      You honestly don't know? Let me simplify. Which came first, the chicken or the egg?
      The egg. The ancestors of chickens laid eggs.
      Sorry. Here is the clean version of the question. Do you think science irrefutably demonstrates that ERVs are only inherited from humans, or do you think humans might also have inherited ERVs from animals, like mice, for instance?


      The evidence is that ERVs invade ancestral cells and these are inherited by descendant species. Look through my posts again.

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      • #33
        Originally posted by User55 View Post
        No. Why do you ask?
        Simply to point out the fact that, apart from ERV similarities with mice, no other similarities between human ERVs and animal ERVs have been even studied outside of primates. Why? Because that is all secularists have ever tried to prove in their speculations about speciation. Changes in animals do not disprove the Bible, but if they can overthrow Adam as the federal head of the human race then they think they will have disproven God, the ultimate goal of their endless hopeless research.
        I am not a NPB-Onlyist (No Perfect Bible Onlyist), nor a NA/UBS-Onlyist. Marke

        If this book be not infallible, where shall we find infallibility? We have given up the Pope, for he has blundered often and terribly; but we shall not set up instead of him a horde of little popelings fresh from college. C. H. Spurgeon

        For that Revised Version I have but little care as a general rule, holding it to be by no means an improvement upon our common Authorized Version. C.H. Spurgeon

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        • #34
          Originally posted by User55 View Post
          The egg. The ancestors of chickens laid eggs.
          Really? I've never read a peer-reviewed article clearly demonstrating that. What "ancestors" are we talking about and when did egg-laying first take place? Just outside the secularist 'Garden of Goo?'

          The evidence is that ERVs invade ancestral cells and these are inherited by descendant species. Look through my posts again.
          I think I have the gist of it. You think assumptions about ERV inheritance based upon assumptions of evolution coupled with evolutionist assumptions about how ERVs contribute to cells somehow prove evolutionist assumptions of speciation to be fact. I see a problem with your reasoning even if you don't.
          I am not a NPB-Onlyist (No Perfect Bible Onlyist), nor a NA/UBS-Onlyist. Marke

          If this book be not infallible, where shall we find infallibility? We have given up the Pope, for he has blundered often and terribly; but we shall not set up instead of him a horde of little popelings fresh from college. C. H. Spurgeon

          For that Revised Version I have but little care as a general rule, holding it to be by no means an improvement upon our common Authorized Version. C.H. Spurgeon

          Comment


          • #35
            Originally posted by marke View Post
            Simply to point out the fact that, apart from ERV similarities with mice, no other similarities between human ERVs and animal ERVs have been even studied outside of primates. Why? Because that is all secularists have ever tried to prove in their speculations about speciation. Changes in animals do not disprove the Bible, but if they can overthrow Adam as the federal head of the human race then they think they will have disproven God, the ultimate goal of their endless hopeless research.
            Shared ERVs have been found among many groups of animals. They provide proof of their evolutionary relationships too. Primates had their genomes sequenced first, because they were expected to have the genomes most similar to humans (a prediction of evolutionary theory that was of course borne out) and were expected to shed the most light on the human genome itself, telling us what our most recent evolutionary changes were.

            That chimps and humans shared common ancestors is sufficient on its own to disprove special creation and the story of Adam and Eve, but no serous, unbiased scientist or scholar has believed them for a very long time anyway. And disproving them does not disprove God. Attempts to either prove or disprove God are a futile waste of time, and have nothing to do with the work of virologists, geneticists and evolutionary scientists. To suggest that that is what they are trying to do is, forgive me but its true, a conspiracy theory for wingnuts.

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            • #36
              Originally posted by marke View Post
              Really? I've never read a peer-reviewed article clearly demonstrating that. What "ancestors" are we talking about and when did egg-laying first take place? Just outside the secularist 'Garden of Goo?'
              The chicken's direct ancestors were probably red junglefowl.

              I think I have the gist of it. You think assumptions about ERV inheritance based upon assumptions of evolution coupled with evolutionist assumptions about how ERVs contribute to cells somehow prove evolutionist assumptions of speciation to be fact. I see a problem with your reasoning even if you don't.
              I would really like for you to point out, anywhere in this thread, where I have made an assumption, as opposed to a conclusion based on the evidence. Have at it. I'm fed up with his meaningless and false accusation of "assumptions". Put your money where your mouth is, Mark, and show me. Saying I make assumptions and have problems with my reasoning is meaningless noise otherwise.

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              • #37
                Originally posted by User55 View Post
                Syncytins.

                Various animal lineages have genes for syncytins, which are located in ERVs. A syncytin is involved in the formation of an interface layer between the placenta and the womb which is called the syncytium layer. If this gene is disabled in mice, the placenta does not form properly and the mouse embryo dies. Therefore, there is at least one ERV gene that is essential to the species that possesses it.

                Does this make syncytins evidence of design for any, or all ERVs? Well, we are often told that common features mean a common designer using common designs. But syncytins are not common designs at all, ("common", in the sense of being shared across the board). There are different syncytins in different taxonomic groups of animals, in different locations in different ERVs. Within each taxonomic group, we have the same ERV in the same location, but go to other groups, (say, from primates to rodents to two-toed ungulates) and you have different syncytins in different ERVs in different locations. But in every case, the synctin involved appears in the place where, in a provirus, an env gene appears. An env gene (short for environment) is responsible for attaching a retrovirus to the outer coat of the host cell, and allowing material to pass between it and the cell interior. What does a syncytin do? It allows placental cells to attach to the cells of the uterus, and allow material to pass between them! The facts are consistent with a different retrovirus becoming endogenized in the ancestors of each group, and its env gene being coopted by evolution. IOW, the endogenization/evolutionary hypothesis fits the data in fine detail. The ID hypothesis just says designerdidit, but cannot explain the details.

                It gets worse. Evolution would predict a nested hierarchy of sycnctins that matches the evolutionary one in each and every syncytin case. It does. The ID hypothesis, once again, fails to account for this - especially where the syncytins are inactive in one branch of the group, and not in another.

                It gets worse still. The ERVs that contain these syncytins also include the genes for reverse transcriptase and integrase. Genes that, as we have seen, only make sense in the context of viral replication. What are they doing here?

                Even worse: Syncytin containing ERVs are a tiny minority of ERVs. What are the rest for, if they were designed?

                And just when you don't think it can possibly get any worse, the syncytin-bearing ERVs, just like all ERVs, bear the hallmark of the action of integrase - the repetition of native DNA either side of an insertion site, an insertion that is not targetted. ERVs at the same sites in different species mean that they are inherited from the single cell that received the insertion from an exogenous retrovirus.

                Differential Evolutionary Fate of an Ancestral Primate Endogenous Retrovirus Envelope Gene, the EnvV Syncytin, Captured for a Function in Placentation

                Next - other objections from the ID camp, unless you have any questions or objections yourself.
                A HERV-K provirus in chimpanzees, bonobos and gorillas, but not humans.

                This is a finding that is trotted out by creationists in an attempt to claim that it is contradictory to all the other evidence. Not so. It is well known that variants of genes have their own evolutionary trajectories, and that species represent a "majority vote" of genes. There is no reason why the same would not be true of ERVs. Go to the link, where there is a diagram that makes the pont clearer.

                The implication of the viral explanation for endogenous retroviruses (ERVs) is that different kinds of creatures, sharing ERVs in corresponding locations, must have inherited those ERVs from common ancestors.

                One way in which evolution-deniers try to confuse the issue is by pointing to a study that identified one ERV, HERV-K-GC1, that is present in chimpanzees, bonobos and gorillas, but not in humans. doi:10.1016/S0960-9822(01)00227-5 How this could be is explained in the paper. This page presents that explanation in a simplified manner.

                The scientific consensus is that gorillas split from the common ancestor of all four species, followed by humans, followed by the chimpanzee-bonobo spit.

                How, then, could HERV-K-GC1 be inherited from the common ancestor of all four species by gorillas, chimpanzees and bonobos, but not by humans? Surely there is something wrong here? Doesn't this result contradict the science?

                Well, in order to be a contradiction, the result would have to be an impossible one, according to the science. So is the result impossible?

                Consider what the viral hypothesis says. An ERV is introduced into a population of organisms by the integration of a retrovirus into a single germ-line cell. Offspring descended from that germ-line cell may or may not inherit that ERV. If any offspring do inherit it, and their offspring too, and so on, that ERV will spread among the population. If it eventually spreads to every individual, we say it is fixed in the population, and every subsequent offspring will inherit it. But all the while it is not fixed, there will exist in the population, individuals with the ERV, and individuals without. Of course, the ERV may eventually die out, as opposed to becoming fixed. In this case, it is the pre-intergration allele that becomes fixed once more. Bear in mind that at the time of writing, there is good evidence that chimps and humans share some 200,000 ERVs and ERV remnants. It is hardly out of the question that such exceptional cases can arise.

                This all means that individuals, populations or species that descend from a population that has an ERV that is not fixed need not inherit that ERV.

                In other words, common ERVs testify to common ancestors, while the absence of a common ERV does not falsify common ancestry.
                We know of cases where ERVs are present in one sub-populations of humans and not in others. So much for them being part of our basic design.

                And in the case of koalas, there is an active virus, infecting koalas and causing disease, which has also endoginized in one DNA location in one group, in another DNA location in another group, and not endogenized at all in a third group. An active, disease-causing virus! How much more evidence do you need to prove that ERVs derive from retroviruses?

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                • #38
                  And Marke runs away.

                  http://forums.carm.org/vbb/showthrea...31#post4400731

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