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Junk DNA returns: Retroviruses play a role in development of human brain?

brain genetics/WavebreakMediaMicro, Fotolia

From ScienceDaily:

They have determined that several thousands of the retroviruses that have established themselves in our genome may serve as “docking platforms” for a protein called TRIM28. This protein has the ability to “switch off” not only viruses but also the standard genes adjacent to them in the DNA helix, allowing the presence of ERV to affect gene expression.

This switching-off mechanism may behave differently in different people, since retroviruses are a type of genetic material that may end up in different places in the genome. This makes it a possible tool for evolution, and even a possible underlying cause of neurological diseases. In fact, there are studies that indicate a deviating regulation of ERV in several neurological diseases such as ALS, schizophrenia and bipolar disorder.

They can be found in a part of DNA that was previously considered unimportant, so called junk-DNA — a notion that researchers have now started to reconsider. Paper. (public access) – Per Ludvik Brattås et al., TRIM28 Controls a Gene Regulatory Network Based on Endogenous Retroviruses in Human Neural Progenitor Cells. Cell Reports, 2017; 18 (1): 1 DOI: 10.1016/j.celrep.2016.12.010More.

<em>Coffee</em> Tins Wasn’t there an obscene blog, a few troll waves back, that attacked design in nature on the basis of ERVs? Anyone remember?

See also: Viruses observed sending chemical messages

Large human brain size easily explained?

Human origins: The war of trivial explanations

“Junk” RNA helps regulate metabolism

Junk DNA defender just isn’t doing politeness any more.

Anyone remember ENCODE? Not much junk DNA? Still not much. (Paper is open access.)

Yes, Darwin’s followers did use junk DNA as an argument for their position.

Another response to Darwin’s followers’ attack on the “not-much-junk-DNA” ENCODE findings

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ERV was battled here nine years ago. You can google them. It was argued at the time that the ERVs were "infections" that attacked the ovum, and that was subsequently introduced to lineages, such infections increasing over time. The argument was typical population genetics. I kept pointing out that there was a 'non-random' character to the ERVs, and that really didn't fit into normal population genetics. It was argued back that the mechanism being invoked really side-stepped those used in normal models. I kept insisting that the 'non-random' character argued against the ERVs being seen as proof-positive of "common ancestry." I was told in some ways, and so many times, that I didn't understand these things. Well, it looks like the intuition I kept invoking, one based on the notion of the genome being designed, has been prove correct. These are not just some random insertions that showed up via infection of ova, and a demonstration of the truth of common ancestry. How far we've come from those initial, carved-out positions. Revisiting the discussion might be entertaining. On one of the posts, gpuccio noted a paper that seem to link ERVs to the p53 DNA, and his discussion there, given the article in the OP, seems prescient. Here's the link. PaV

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