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ERV FAQ: Don't retroviruses target particular locations in the DNA? Doesn't this explain corresponding ERVs?

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  1. It would be great if we could use retroviral-like vehicles to precisely target positions in DNA. Think of the possibilities that would open up. It would be a wonderful tool for gene therapy, including cancer treatment, treatment for genetically inherited diseases, anti-viral therapy, genetic engineering, and pure research. That is why retroviral integration has been studied so carefully. Unfortunately, integrase, the enzyme that actually does the integration of a new DNA sequence into the DNA of the host organism, does not target specific loci. Update: Since the writing of the preceding, CRISPR interference has begun to become a powerful "gene editing" tool which has enormous possibilities because it can manipulate DNA in a very precise manner. Of course, CRISPR gene editing does not use retroviral-native integrases.
  2. Actual studies of integration sites include HIV integration site selection: Analysis by massively parallel pyrosequencing reveals association with epigenetic modifications and Retroviral DNA Integration: ASLV, HIV, and MLV Show Distinct Target Site Preferences and many others. While the title of the second paper sounds interesting from the creationist point of view, it doesn't help. What these sorts of studies do is to survey real retroviral integration sites, using the same types of cell from the same individuals (identical DNA) in order to find any statistical 'preference' for certain types of area (in an existing gene, not in a gene, near a promoter etc.) Typically, they find some overall patterns, but no repetition of integration sites within 500 samples of the same cell type with the same retrovirus. This is not the locus specificity required to account for 200,000 integrations in precisely corresponding loci. Only common inheritance can account for them.

7 comments:

  1. Of the approximately 90'000 ERVs per haploid genome, only a handful is activated in somatic cells. They are a sessile part of the genome silenced by the piwi-RNAs pathways and direct methylation. Their activity is mainly observed during meiosis, which shows they are the variation-inducing mechanism of the gametes. Each original baranome (the pluripotent, uncommitted genomes of primordial creatures) must have had a number of VIGEs, some of which we still find on the same location in distinct species. In specified baranomes, VIGEs may have been located on the exact same positions (the T-zero location), which then explains why some VIGEs such as ERVs, can be found in the same location in, for instance, primates and humans. Further, sequence-dependent integration of VIGEs in the germ line may be meiosis specific (nobody studied integration mechanisms during meiosis, but merely in diploid cell models during mitosis). Accumulation of VIGEs speeds up over time (due to loss of control of the piwi pathway) and is a major cause of aging.

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    1. Peer, I see that you blog at "Creation Ministries International". Have you signed up to their statement of faith which says,

      "Facts are always subject to interpretation by fallible people who do not possess all information. By definition, therefore, no interpretation of facts in any field, including history and chronology, can be valid if it contradicts the scriptural record."

      Are you an infallible person in possession of all information, such that you can justify this statement? And how can anyone trust you to take an honest, objective view?

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    2. If you like a challenge, you might like to attempt to answer my questions @ http://barryhisblog.blogspot.com/p/in-science-we-apply-principle-of.html

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    3. Barry, I am not an infallible person; I merely checked the syncytine claims because from a selcetionsits point of view ERVs and LINEs should not be around and active. And then I made some rather interesting observations. All I ask from you is to read the paper with an open mind. Imo, my hypothesis is better than the one proposed by the evolutionary community because it requires less assumptions and less improbable genetic events.

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    4. "...from a selcetionsits point of view ERVs and LINEs should not be around and active." What makes you say that?

      I've just commented on your paper, BTW. Think about it, Peer. Why would a designer go through all the rigmarole you speculate about? Why not just design features in where it wanted them? Your ideas just don't make any sense.

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  2. ERVs and LINEs are redundant elements which cannot be kept stable in the genome by selection, so it requires a mechanism to keep them in. That mechanism is autonomous replication independent from the genome. ERVs are mobile genetic regulators to make sure there is variation in the offspring. And LINEs have important function in genome contraction during cell devisions and gene silencing. How it works will soon be published. Further, why-would-the-designer-do-this-or-that-questions are theology, I-m only doing science-questions and leave theology to the theologists. If you-ve read my paper you know that the VIGEs first is the better, more parsimonous explanation. What the evolutionists want, Darwinian atheists in particular, is a almost entirely useless genome, which is such a load of bogus that serious geneticists and evolutionary biologists do not even want to consider this any longer. Most likely, the whole thing was frontloaded, designed to vary, to adapt and to evolve. That-s the best explanation of what we observe. Darwinian arguments all stem from ignorance about biology. Read my papers on the design of life and you will start to understand how it works. Think free, be sceptic.

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    1. I can't read your papers if you don't tell me where they are, "Anonymous". (And I'd rather be skeptic than sceptic, thank you. P) )

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