Carl Zimmer is, hands down, one of the best science writers out there. Its no surprise, then, that he is almost as obsessed with viruses as I am. Viruses are our past and our future, and Zimmer *gets* it.
So while I am busy in the lab this week, I will happily point you to a piece he recently wrote about ERVs and embryos.
Regarding the paper he is writing about-- I dont think the active ERVs are 'doing' anything in embryos. I dont think we have evidence that the active 'silent' viruses are genuinely domesticated. I think the ERV activity is probably a side-effect of alterations in epigenetics, rather than a 'cause' of totipotent cells. Regardless, ERV might show us directly or indirectly how to induce totipotency.... sweeeeeeeet!!
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Thanks! I hope I didn't imply that the ERV themselves were doing anything--just that their promoters have been tacked onto a bunch of host genes active at the two-cell stage. This is actually even cooler from an evolutionary perspective: viruses supply components for re-wiring whole networks of host genes. (Gunther Wagner at Yale first turned me onto this fact.)
On the other hand, the paper notes that at the two-cell stage, there is a whole lot of crazy activity among mobile elements, LINES and such. I wonder if this somehow adaptive for the elements themselves--taking advantage of a good moment to proliferate?
The title of the paper is 'Embryonic stem cell potency fluctuates with endogenous retrovirus activity', so if someone doesnt have access to the paper they might think that the ERVs are the ones fluctuating potency-- I just wanted to make it clear that it might not be the viruses themselves creating the effect :)
And yes, I think it is the viruses (and other mobile elements) just taking advantage of the altered epigenetic state (its like recess for transposable elements), rather than being active players in the process.
But maybe not!
First (except for those who beat me!)
Dude, Carl Zimmer just commented on your blog.
You win at the internet.
Forever.
It seems implausible to me that a burst of activity of transposable elements does not have functional consequences and is not controlled. Especially if the state it all occurs in is triggered and then anti-triggered.
Maybe not every transposable element that shows activity is functional (after all, if some random retrovirus infected the cell at that state it would get incorporated), but it is extremely implausible that eukaryotes would have such a vulnerable period if it were not necessary.
I suspect this is a feature of eukaryotes and not of mammals.
what about this article?:
http://www.sciencedaily.com/releases/2002/08/020802075138.htm
way would ervs cant be functional?
the history prove us that we can be wrong, like the so called junk dna.
thinks about the human like a complex self repliact organic robot that made of 100000 parts(proteins). we are still no know much about it.
Carl is not just 'one of the best science writers,' he is the best.
Wouldn't it be funny if the primate pre-frontal lobe was the result of a flu bug?
Make that 8,000 miles -southwest- of London.
It is quite a thrill to see others debating the importance of ERVS in development. I agree that we have not yet demonstrated that viruses are "causing totipotency" although they certainly appear to be "marking totipotency" with ES cultures. I do think we definitively demonstrate that viruses provide useful regulatory modules which can coordinate gene expression for key developmental genes. Other transposons have also been shown to re-wire gene regulatory networks so this idea is not new. I am currently working on strategies to block the activity of these virus promoters to see how this may impact early embryo development. This may help us to fuel the debate as to whether ERVs are passive or active players in mammals.