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Endogenous retroviruses made us human?

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From Carrie Arnold at Nova:

One of the few survivors of the asteroid impact 65 million years ago was a small, furry, shrew-like creature that lived in underground burrows and only ventured out at night, when predators weren’t active. The critter—already the product of some 100 million years of evolution—looked like a modern mammal, with body hair and mammary glands, except for one tiny detail: according to a recent genetic study, it didn’t have a placenta. And its kind might never have evolved one if not for a chance encounter with a retrovirus.

Unlike most viruses, which infect, replicate, and then leave their host, retroviruses elbow their way into their host’s genome where they are copied and passed on to daughter cells for the life of the host. This retrovirus, however, managed to sneak its way into one of our ancestor’s sperm or egg cells, able to be passed on to every cell in every subsequent generation. Virus and host had become one.

In that would-be mammal living 160 million years ago, a symbiotic retrovirus enabled it to evolve a placenta over many generations. In order to let a fetus mature inside a mother’s uterus, an animal needed a way to provide oxygen and nutrients while removing waste and keeping both blood supplies separate. More.

That took a lot of accidental engineering, right?

Scientists are discovering that the so-called “junk DNA”—a significant portion of which is from symbiotic viruses—is actually a potent force in the evolution of new species. Although the evolution of pregnancy via the placenta might be some of the most persuasive evidence that viruses stashed deep within the genome can help give rise to new species, it’s not the only proof. New studies revealing the role of endogenous retroviruses in the more recent evolution of humans show that these snippets of DNA are helping to blur the boundary between human and virus. Humans are, in a very real sense, part virus.

Yet viruses are not becoming human. And we actually don’t know very much about viruses.

Note the role of supposed junk DNA.

See also: Human origins: The war of trivial explanations

Another accidental use for junk DNA

and

Why is devolution counterintuitive?

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Comments
BA77 @5:
[...] we have to take what we can get from Nature. They are not exactly nonpartisan in all this as you well know.
Yes, agree.Dionisio
October 15, 2016
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ERVs and transposons: wonderful tools of Intelligent Design!gpuccio
October 15, 2016
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A better Explanation for the "placenta-virus" can be found here: http://creation.com/images/pdfs/tj/j27_3/j27_3_105-112.pdf RNA viruses have their origin in transposon-like genetic elements commonly known as ERVs, not the otherway around.Peer
October 14, 2016
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Great fairy story at the beginning there. Apart from the brute fact that we're all here, now, is there any evidence that any of this actually happened?ScuzzaMan
October 14, 2016
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Agreed Dionisio, but we have to take what we can get from Nature. They are not exactly nonpartisan in all this as you well know.bornagain77
October 13, 2016
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BA77 @2:
The key to our complexity lies in how these genes are regulated by the remaining 99% of our DNA, known as the genome’s ‘dark matter’.,,,
Very interesting! Thank you for posting it here. However, the above quoted statement is not quite accurate. The genes are regulated by the complex regulatory machinery that utilizes -among other things- the genome's dark matter. There's more to cellular biology beyond the DNA. Don't forget we're dealing with complex complexity (on steroids). :)Dionisio
October 13, 2016
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That is ASSUMING that that part of the genome is the result of a past viral infection. The actual evidence for that is lacking. More likely it was already included in the original created kinds.aarceng
October 13, 2016
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Semi Related:
The dark side of the human genome - Kelly Rae Chi - Nature 538, 275–277 (13 October 2016) Excerpt: Fifteen years ago, scientists celebrated the first draft of the sequenced human genome. At the time, they predicted that humans had between 25,000 and 40,000 genes that code for proteins. That estimate has continued to fall. Humans actually seem to have as few as 19,000 such genes1 — a mere 1–2% of the genome. The key to our complexity lies in how these genes are regulated by the remaining 99% of our DNA, known as the genome's 'dark matter'.,,, Scientists have generated a list of such elements by using biochemical assays to probe DNA sequences, RNA transcripts, regulatory proteins bound to DNA and RNA and epigenetic signatures — the chemical tags on DNA and the proteins packaging it — that also affect gene expression. So far, the data suggest that there are hundreds of thousands of functional regions in the human genome whose task is to control gene expression: it turns out that much more space in the human genome is devoted to regulating genes than to the genes themselves. Scientists are now trying to validate each predicted element experimentally to ascertain its function — a mammoth task, but one for which they now have a powerful new tool.,,, But it is still a daunting endeavour: more than 3 million regulatory DNA regions, thought to contain some 15 million binding sites for regulatory proteins called transcription factors, control gene expression in the human cell types studied thus far. About 150,000 may be active in any given cell type.,,, regulatory elements have a bewildering array of functions and forms, which makes tackling them a formidable challenge. Even the best-known types, such as spots in the genome known as promoters, which lie next to a gene where transcription begins, and enhancers — regions that when bound by specific transcription factors alter the likelihood of a gene being read — are hard to study. In addition to the sheer number of these sites, estimated at 15 million, enhancers may be positioned thousands of base pairs away from the gene that they control.,,, Thus far, ENCODE and Roadmap have offered up important clues, but the real proof that these predicted regulatory elements actually do something comes from a functional test. For genes, this mostly entails deleting them one at a time and observing the consequences in a cell assay or animal model. This is less easy to do for the non-coding genome because many of the elements are redundant, and so deleting just one might not alter gene expression or produce an obvious change. “It's a huge challenge that we have at the moment to really distinguish between functional and non-functional elements,,," http://www.nature.com/nature/journal/v538/n7624/full/538275a.html
bornagain77
October 13, 2016
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Off Topic:
Do Miracles Violate the Laws of Nature? | RE: David Hume | Stephen C. Meyer, PhD https://www.youtube.com/watch?v=mYc8kSSHxSI
bornagain77
October 13, 2016
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