Friday, 13 January 2017

Was Human Intelligence Made Possible By A Virus?

Viruses in the genome important for our brain | Lund University.

Well no, perhaps human intelligence was not caused by a virus as such but according to new research, its evolution may well have been made possible by an ancient retrovirus which infected an early vertebrate ancestor.

In a blog just a couple of days ago, I explained the origin of the endogenous retroviruses (EVRs) which now form 5%-10% of the human genome, much of it believed to be junk. I also explained that some of it might well have been exapted for other purposes, just as you might expect of a lot of 'spare' DNA hanging around for tens, maybe hundreds, of millions of years.

That blog concerned the origin of EVRs and how recent research has shown that they very probably arose very early in the evolution of vertebrates in a marine environment. ERVs themselves might well be the result of faulty replication of retrotransposons as part of the original genome of the host or a related species, which became pathological and maybe exogenous before being reincorporated as ERVs possibly in another species.

This blog deals with recent research which raises the possibility that an exapted ERVs might have been essential for human intelligence to have evolved and now play a part on the genetic control of neural networks. It concerns a protein, TRIM28, which binds to ERVs, so regulating transcription and expression of adjacent genes. The research by a team from Lund University, Sweden, was published yesterday, open access, in the journal Cell Reports:

Highlights
  • Stage- and region-specific expression of ERVs during human brain development
  • TRIM28 binds to ERVs and induces hetereochromatin in human neural progenitor cells
  • Knockdown of TRIM28 in hNPCs results in the upregulation of ERV expression
  • Protein-coding genes located near upregulated ERVs are upregulated

Summary
Endogenous retroviruses (ERVs), which make up 8% of the human genome, have been proposed to participate in the control of gene regulatory networks. In this study, we find a region- and developmental stage-specific expression pattern of ERVs in the developing human brain, which is linked to a transcriptional network based on ERVs. We demonstrate that almost 10,000, primarily primate-specific, ERVs act as docking platforms for the co-repressor protein TRIM28 in human neural progenitor cells, which results in the establishment of local heterochromatin. Thereby, TRIM28 represses ERVs and consequently regulates the expression of neighboring genes. These results uncover a gene regulatory network based on ERVs that participates in control of gene expression of protein-coding transcripts important for brain development.

Per Ludvik Brattås, Marie E. Jönsson, Liana Fasching, Jenny Nelander Wahlestedt, Mansoureh Shahsavani, Ronny Falk, Anna Falk, Patric Jern, Malin Parmar, Johan Jakobsson
TRIM28 Controls a Gene Regulatory Network Based on Endogenous Retroviruses in Human Neural Progenitor Cells
Cell Reports
, Volume 18 , Issue 1 , 1 - 11 DOI: http://dx.doi.org/10.1016/j.celrep.2016.12.010

© 2016 The Authors. Published open access.
Reprinted under Creative Commons Attribution–NonCommercial–NoDerivatives 4.0 International licence (CC BY-NC-ND 4.0).

As the press release from Lund University explains:

[The researchers] 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.

Two years ago, Johan Jakobsson’s team showed that ERV had a regulatory role in neurons specifically. However, this study was conducted on mice, whereas the new study – published in the journal Cell Reports – was made using human cells.

The differences between mice and humans are particularly important in this context. Many of the retroviruses that have been built into the human DNA do not exist in species other than humans and our closest relatives – gorillas and chimpanzees. They seem to have incorporated themselves into the genome some 35–45 million years ago, when the evolutionary lineage of primates was divided between the Old and New World. [My emphasis]

“Much of what we know about the overall development of the brain comes from the fruit fly, zebrafish and mouse. However, if endogenous retroviruses affect brain function, and we have our own set of these ERV, the mechanisms they affect may have contributed to the development of the human brain”, says Johan Jakobsson.

Although this is still under investigation and still remains to be established beyond reasonable doubt, it's beginning to look like our intelligent brain only evolved due to infection of a remote common ancestor some 35-45 million years ago.

Now, I can readily see a creationists trying to point to this as evidence of some sort of long-term plan (ignoring of course the fact that 35-45 million years ago was much earlier than 6000 years and that any long-term plan of this sort would have been predicated on a future divergence of hominids and the other apes) but what I would like to see is some sort of explanation of why this potential for high intelligence was installed in chimpanzees and gorillas and then not used.

By contrast, I can't see any problem with this discovery for the Theory of Evolution. Perhaps a creationist could explain why it doesn't explain the known facts, other than that they don't want it to, or for some rehearsed dogmatic slogan such as 'evolution is impossible'.

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