Search This Blog

ERV FAQ: ERVs are essential in reproduction (syncytin and the formation of the placenta). How can this be?


  1. See Abbie Smith's blog entry, "More syncytia sweetness". Primates, mice and sheep each use a different syncytin gene, from the env region of a different ERV, in a different chromosome, in order to build an essential syncytia in the placentas of their respective lineages. (A syncytium is a cell that contains many cellnuclei, as opposed to normal nuclear cells, which usually contain only one cell.) Why different syncytins from different ERVs? Different designs, different designers? Hardly. And why embed the syncytins in ERVS in the first place? What's all the other ERV baggage for?
  2. It turns out that syncytia formation is a native trick of retroviruses. HIV will deal with attacking T-cells by absorbing them into the cells it has already infected. How? By attaching them to itself and joining with them, using the very same env proteins it used to enter the original cell! Clever trick. It avoids all the tedious business of invading every T-cell in order to neutralize them.
  3. Note that the different syncytia belong to different lineages - further proof of evolutionWe can even trace their evolution through their respective family trees. See also, Mammals Made by Viruses. Why on earth would a designer take such pains to mimic the the sort of thing we expect from evolution - for no sensible reason? Why did it not mix things up a bit? Why did it never choose to produce any evidence contrary to what we would expect of evolution? See also, Gauger's Gaffe!
  4. Still think ERVs are not of retroviral origin? If so, you must have answers to these questions: If ERVs are not retroviral in origin, why do they have reverse transcriptase? What do they have integrase? Why do they have LTR promoters? Why did the Phoenix virus experiment work? Why do ERVs have host DNA repetition on either side of the integration site? Why do koalas have KoRV in both exogenous and endogenous form? Why do ERVs have the same codon bias as retroviruses? See also, The Koala's Tale.
  5. It always amazes me when people say, look! These endogenous promoters or genes do something. It _proves_ they are designed! Bits and bobs of some ERVs. Never a whole working ERV (which would likely kill you). If we don't accept that eyes were designed, just because they are useful, why would we conclude that ERVs are designed, just because the odd component has been scavenged from them?
  6. When we look at the human/chimp syncytin gene, and consider it's origin, there are two possibilities.
  • A designer or designers inserted it in the genome of both species, in exactly corresponding locations in the DNA (unnecessarily), the syncytin gene being embedded in an elaborately detailed structure that precisely, and pointlessly mimics a retroviral insertion. (See "Why do virologists and geneticists think that ERVs come from retroviruses?") A designer or designers also inserted a different syncytin, in a different location, in a different chromosome, precisely and pointlessly mimicking a different retroviral insertion in mice. And a completely different one again in sheep. The supposed designer(s) didn't bother with Elephants. Or Manatees. Or heteromyid rodents. They were designed to get along without a placental syncytiotrophoblast layer, relying instead on a layer consisting of discrete nuclear cells (cells with a single nucleus each).
  • A common ancestor of chimps and humans, its species happily reproducing like elephants, acquired a retroviral infection in a germ-line cell. When it came to reproduce, one of the retroviral genes woke up and affected the development of certain placental cells, having the effect of merging them into a single multi-nucleus cell (a syncytium) just as the corresponding gene in HIV does with T-cells today. This aided reproduction, giving an advantage in the reproductive stakes, such that more and more individuals inherited the trick, and it eventually became a ubiquitous (fixed) feature in the species. At the same time it was spreading through the population, older genes for placental development that were no longer needed mutated into uselessness, rendering the new retroviral gene (but not the rest of its accompanying retroviral baggage) essential. The same thing happened, but with a different retrovirus, in mice. And again, independently, with a different retrovirus in sheep. It did not happen in pigs, or in horses.
  • Which of the above two scenarios best explains the retroviral-like structure that is to be found at the site of the human/chimp syncytin gene?

(Return to the ERV FAQ)

18 comments:

  1. Because I did not believe organisms can be built from viruses, as biologists started to claim about 10-15 years ago, I checked the mol biol of the syncytin gene. The details demonstrate that the evolutionary scenario is far more unlikely than the scenario from the VIGE-first hypothesis, which postulates two independent integrations in a clean syncytin gene. The paper I wrote on the topic can be downloaded here: http://creation.com/journal-of-creation-273 (scroll down, pages 105-112).

    RNA-Viruses are more parsimonously explained from exogenization events, and the "virus-makes-man hypothesis " is most likely wrong. ERVs are not remnants of RNA viruses, it is the other way around: RNA virus originated in gag-pol elements known to sciencs as ERVs and one of many "variation-and-integrity assuring genetic elements" (VIGEs) we observe in the genomes (including LINEs, SINEs, alu's and SRs, transposons in plants, IS in bacteria). The fact that LINEs cannot be traced back to RNA viruses is further substantiating the VIGE first hypothesis: Viruses originate in genomes.

    ReplyDelete
    Replies
    1. Great intelligent *Scientific* talk, instead of speculating why /can / would / should God works in what way.

      Kuhn on human/ape common ancestry, citing Jonathan Wells's book The Myth of Junk DNA and arguing: DNA homology between ape and man has been reported to be 96% when considering only the current protein-mapping sequences, which represent only 2% of the total genome. However, the actual similarity of the DNA is approximately 70% to 75% when considering the full genome, including the previously presumed "junk DNA," which has now been demonstrated to code for supporting elements in transcription or expression. The 25% difference represents almost 35 million single nucleotide changes and 5 million insertions or deletions.

      Delete
    2. The ERV evidence is not about similarity, Marc, which can be notoriously like, "How long is a piece of string". No. The evidence is based on the fact that ERVs are clearly of viral origin, and cannot target specific DNA loci, therefore common loci must be common by virtue of DNA reproduction. Even if God had put "VIGES" in our DNA (acronyms sound so science-y, don't they?) and they produced retroviruses, then the retroviruses themselves would not be able to integrate back into common loci. As virtually all ERV elements in, say, chimps and humans are in corresponding loci, that means, under this speculative, unevidenced hypothesis, that they would virtually all be "VIGES". This raises the question, "What are their viral-like features FOR?" Not to re-integrate back into the DNA of gametes, because they would already be there. Perhaps to induce disease in somatic cells? No. The idea, when you think it through, is utter nonsense.

      Delete
    3. O well if its going to be "Facts" & "Clearly's"... guess You win! Folks big names mean bang, Endogenous Retro Viral sequence is a piece of DNA which was put in by a virus, inserted into our supposed ape ancestors. The only "plausible" explanation or CONsensus Evilutionists (or ape status advocates).
      Thing is Thee holly seat of Science has not proven ERVs were put in by retroviruses.
      ERVs are important in much of the genome. As Mister apetheist Dawson has finally found out....

      Delete
    4. Marc, read this. http://barryhisblog.blogspot.com/p/why-do-virologists-and-geneticists.html

      Delete
  2. Why different syncytins, embedded in different retroviral-like structures in different chromosomes, in different lineages? And what about HIV fusing T-cells? Was that subsequent evolution of the exogenated retrovirus? Where is your evidence for your ideas?

    ReplyDelete
    Replies
    1. "HIV fusing T cells..."

      What about fused muscle cells....fused trophoblast cells...? This is normal fysiology. So, you have cause and effect up-side-down. There are many genes in our genome that have the function to fuse cells in order to make a diffuse polynucleated tissue: muscle, trophoblast. How do such tissues arise? They express fusion-genes to produce fusion proteins. If an ERV (gag-pol element) captures (part of) such fusion genes it is on its way to become an RNA virus. This has happened several times. Viruses cannot have their origin outside cells, because they cannot reproduce outside cells. That is why my vision "VIGEs first" must be correct.

      Delete
    2. Many parasitic forms are degenerate, Peer, and have lost functions that their hosts now perform. Nobody know the origin of retroviruses. That includes you and me. The evidence (for example, KoRV and Phoenix) cannot be accounted for by your speculation.

      Delete
  3. Think about it, Peer. Why would a designer go through all the rigmarole you speculate about? Why not just design the syncytins in where it wanted them? Your ideas just don't make any sense.

    ReplyDelete
    Replies
    1. That is what He did. The syncytin genes are very different throughout the animal kingdom. In at least six cases ERVs integrated independently in these genes. Evolutionists would say: RNA visures delivered syncytin genes in at least six lineages independently to produce trophoblasts. What is the most parsimonious, do you think?

      Delete
    2. I did, but it is not as simple as that. It is like this:

      The most parsimonious evo-lutionary scenario relies on a great number of highly unlikely genetic events of which the selective value of individual arrangements remains highly doubtful. First, it requires the integration of a mammalian apparent LTR-retrotransposon (MaLR) in the PEX-ODAG intergenic region, which is then lost without a trace leaving only MaLR-like LTR units behind (57 and 106 base pairs, respectively). These LTR units are promoters that drive gene transcription. Strikingly, the 260 base pairs between these LTR sequences, which are independently acquired, make up a functional trophoblast specific enhancer (TSE; a genetic switch active only in trophoblastic tissue). The complete absence among species of flanking duplicated sequences, which should be present as vestiges of the original integration, does not support this hypothesis. In fact, this TSE must have been acquired together with the syncytin gene: without having trophoblastic tissue an enhancer specific for this tissue does not make sense at all. Next, an ERV-P element integrated between the PEX1 gene and the TSE, which was then replaced by ERV-H, leaving nothing behind except an ERV-P-like LTR unit of 633 base pairs. Again, the absence among species of flanking duplicated sequences, which are to be expected as vestiges of such integration events, as well as complete lack of ERV-P sequences in this region, do not support this hypothetical view. In the meantime, an RNA virus containing a syncytin gene invaded the germ line, transformed into the so-called ERV-W provirus, and then integrated in the DNA between the TSE and the ODAG gene. Finally, when the syncytin gene lost 12 nucleotides through a deletion, the locus had transformed into a trophoblast-specific information unit to regulate, control and sustain the establishment of the placenta.

      On the other hand, the "VIGE-fist Hypothesis" only invokes two LTR mediated integrations of ERV-W. Originally, the region between PEX1 and ODAG contained the syncytin gene plus its global and tissue specific regulatory elements (LTR and TSE, respectively). LTRs are required for global regulation of gene transcription and found throughout the genomes of eukaryote organisms. They can best be described as transcription control centers. It is of note that the genes present in gag-pol elements rely on LTR as promoters for their transcription. The original designof the syncytin locus did not contain gag-pol elements. The TSE is a trophoblast-specific enhancer, a genetic regulatory element (or: genetic switch) that ensures the syncytin gene is only expressed in the trophoblast, but not in other cells or tissues. After the fall, two gag-pol elements (known as ERV-H and ERV-W) sequentially integrated in this locus.

      Delete
    3. As you can see, the molecular details of the syncytin region are simply not making a plausible evolution-did-it-story. That is why I like my explanation, i.e. VIGEs-first, much better. Selection hardly plays a role in biology. Code and control mechanisms do.

      Delete
    4. This also addresses your "Which of the above two scenarios best explains the retroviral-like structure that is to be found at the site of the human/chimp syncytin gene?"

      As demonstrated above, my VIGEs-first hypothesis is the superior explanatory framework.

      I rest my case.

      Delete
    5. Fine case for a "blind superstitious dont understand SCIENCE believer" retorted with mostly typical demeaning shallow from Knowers of so much not seen, but know there is no God to which They know would do and behave in creating this and that. "What separates me from most so-called atheists is a feeling of utter humility toward the unattainable secrets of the harmony of the cosmos." - Albert Einstein

      Delete
    6. Bit of a ramble, Marc. Are you OK? Are you channeling Donald Trump?

      Re. "VIGEs", see my other comment, dated today.

      Delete
    7. I think I'd better repeat a comment of mine from above, lest anyone reads Peers comments here and thinks the creationist "VIGE" idea makes sense and I have no answer to it.

      Even if God had put "VIGES" in our DNA (acronyms sound so science-y, don't they?) and they produced retroviruses, then the retroviruses themselves would not be able to integrate back into common loci. As virtually all ERV elements in, say, chimps and humans are in corresponding loci, that means, under this speculative, unevidenced hypothesis, that they would virtually all be "VIGES". This raises the question, "What are their viral-like features FOR?" Not to re-integrate back into the DNA of gametes, because they would already be there. Perhaps to induce disease in somatic cells? No. The idea, when you think it through, is utter nonsense.

      Delete
  4. Your case, Peer, is an argument from personal incredulity, and your hypothesis makes no sense. As I pointed out in a comment in another page, an all powerful intelligent designer would have no need for such a wildly and dangerous hit-and-miss method as using a retrovirus as a vector for genetic engineering. The whole idea is absurd.

    ReplyDelete