I would like to see more info on this, especially which specific gene sequences the transposons were found in—but that will probably have to wait until whole-genome sequencing is cheaper.
I am not sure if it is prudent to speculate on such little evidence, but I would suspect that any useful effect these retransposons have on learning has to do with regulating the growth of dendritic spines.
And it is also possible that these are a deleterious element that we’ve just managed to mostly suppress the effects of, like P elements in fruit flies.
Still, the benefits and detriments of transposable elements in biology remains very much an open question, at least as far as I know.
If they are deleterious elements then instead of making cryonics harder, my bet would that it functions as another kind of “aging” that SENS would need to be able to fix in situ in order to achieve the grand vision of truly negligible senescence. My first thought in that direction is that you might need to create artificial work-alike “cells” to incrementally replace the ones whose DNA was becoming ever more infested with endogenous parasitic transposons… which sounds like a mature nanotechnological invention to me :-/
Unfortunately the second link will not load for me, but I’m assuming it’s this article. Here’s a pdf download of the full text.
I would like to see more info on this, especially which specific gene sequences the transposons were found in—but that will probably have to wait until whole-genome sequencing is cheaper.
I am not sure if it is prudent to speculate on such little evidence, but I would suspect that any useful effect these retransposons have on learning has to do with regulating the growth of dendritic spines.
And it is also possible that these are a deleterious element that we’ve just managed to mostly suppress the effects of, like P elements in fruit flies.
Still, the benefits and detriments of transposable elements in biology remains very much an open question, at least as far as I know.
If they are deleterious elements then instead of making cryonics harder, my bet would that it functions as another kind of “aging” that SENS would need to be able to fix in situ in order to achieve the grand vision of truly negligible senescence. My first thought in that direction is that you might need to create artificial work-alike “cells” to incrementally replace the ones whose DNA was becoming ever more infested with endogenous parasitic transposons… which sounds like a mature nanotechnological invention to me :-/
The thing is—they may have started out as a retrovirus infection, but now serve some important purpose. It’s hard to say. Very butterfly effect-y.