Minimal cell experiments (making cells with as small a genome as possible) have already been done successfully. This presumably removes transposons, and I have not heard that such cells had abnormally long lifespans.
One possibility is that there are at least two aging pathways-the effect of transposons, which evolution wasn’t able to eliminate, and an evolved aging pathway intended to eliminate older organisms so they don’t compete with their progeny (doing so while suffering ill health from transposon build-up would be less fit than dying and delegating reproduction to one’s less transposon-heavy offspring).
There is significant evidence that most organisms have evolved to eventually deliberately die, independent of problems like transposons that aren’t intentional on the level of the organism. Yamanaka factors can reverse some symptoms of aging, and appear to do so by activating a rejuvenation pathway. This makes perfect sense if the body deliberately ordinarily reserves that pathway for gamete production, while letting itself deteriorate. It is extremely confusing if aging is purely damage, however. Yamanaka factors don’t provide new information (other than the order to rejuvenate) or resources; a body that is doing its best to avoid aging wouldn’t seem to benefit from them, and could presumably evolve to produce them if evolution found this desirable. Other examples include the beneficial effects of removing old blood plasma (this appears to trick the body into thinking it is younger, which should work on a deliberately aging organism but not one that aged purely through damage), the fact that rat brain cells deteriorate as the perceive the brain to gradually stiffen with age, but rejuvenate if their ability to detect stiffness is removed, and the fact that some species of octopuses commit suicide after reproducing, and refrain from doing so if a particular gland is removed.
If both transposons and a deliberate aging pathway contribute to aging, it would be very interesting to see what happens in an organism with both transposon inactivation and Yamanaka factor treatment. Neither appears to create massive life extension on its own, but together they might do so, or at least point out worthwhile directions for further inquiry.
I have a HIV-positive friend whose epigenetic age is 6 years younger than his real age of ~32. I wonder if his antivirals helped… (they reduce genomic instability from transposons, though I expect this effect to be stronger in older)
Minimal cell experiments (making cells with as small a genome as possible) have already been done successfully. This presumably removes transposons, and I have not heard that such cells had abnormally long lifespans.
The minimal cell experiments were done with mycoplasma, which (as far as I know) does not age. More generally, as I understand it, most bacteria don’t age, at least not in any sense similar to animals.
Also, I expect wild-type mycoplasma already had no transposons in its genome, since the organism evolved under very heavy evolutionary pressure for a small genome. (That’s why it was chosen for the minimal cell experiments.)
An initial search doesn’t confirm whether or not mycoplasma age. Bacteria do age though; even seemingly-symmetrical divisions yield one “parent” bacterium that ages and dies.
If mycoplasma genuinely don’t, that would be fascinating and potentially yield valuable clues on the aging mechanism.
Oh wow, that’s really neat. I doubt that it has any relevance to the aging mechanisms of multicellular organisms, but very cool in its own right. And definitely not transposon-mediated.
Minimal cell experiments (making cells with as small a genome as possible) have already been done successfully. This presumably removes transposons, and I have not heard that such cells had abnormally long lifespans.
One possibility is that there are at least two aging pathways-the effect of transposons, which evolution wasn’t able to eliminate, and an evolved aging pathway intended to eliminate older organisms so they don’t compete with their progeny (doing so while suffering ill health from transposon build-up would be less fit than dying and delegating reproduction to one’s less transposon-heavy offspring).
There is significant evidence that most organisms have evolved to eventually deliberately die, independent of problems like transposons that aren’t intentional on the level of the organism. Yamanaka factors can reverse some symptoms of aging, and appear to do so by activating a rejuvenation pathway. This makes perfect sense if the body deliberately ordinarily reserves that pathway for gamete production, while letting itself deteriorate. It is extremely confusing if aging is purely damage, however. Yamanaka factors don’t provide new information (other than the order to rejuvenate) or resources; a body that is doing its best to avoid aging wouldn’t seem to benefit from them, and could presumably evolve to produce them if evolution found this desirable. Other examples include the beneficial effects of removing old blood plasma (this appears to trick the body into thinking it is younger, which should work on a deliberately aging organism but not one that aged purely through damage), the fact that rat brain cells deteriorate as the perceive the brain to gradually stiffen with age, but rejuvenate if their ability to detect stiffness is removed, and the fact that some species of octopuses commit suicide after reproducing, and refrain from doing so if a particular gland is removed.
If both transposons and a deliberate aging pathway contribute to aging, it would be very interesting to see what happens in an organism with both transposon inactivation and Yamanaka factor treatment. Neither appears to create massive life extension on its own, but together they might do so, or at least point out worthwhile directions for further inquiry.
https://www.brown.edu/news/2019-02-06/aging
I have a HIV-positive friend whose epigenetic age is 6 years younger than his real age of ~32. I wonder if his antivirals helped… (they reduce genomic instability from transposons, though I expect this effect to be stronger in older)
Fascinating!
This is golden, thank you! I wonder if healthy adults should take ARVs...
The minimal cell experiments were done with mycoplasma, which (as far as I know) does not age. More generally, as I understand it, most bacteria don’t age, at least not in any sense similar to animals.
Also, I expect wild-type mycoplasma already had no transposons in its genome, since the organism evolved under very heavy evolutionary pressure for a small genome. (That’s why it was chosen for the minimal cell experiments.)
An initial search doesn’t confirm whether or not mycoplasma age. Bacteria do age though; even seemingly-symmetrical divisions yield one “parent” bacterium that ages and dies.
If mycoplasma genuinely don’t, that would be fascinating and potentially yield valuable clues on the aging mechanism.
Do you have a reference on that? I’m familiar with how it works with budding yeast, but I’ve never heard of anything like that in a prokaryote.
https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.0030058
This is the source I found. It’s fairly old, so if you’ve found something that supersedes it I’d be interested.
Oh wow, that’s really neat. I doubt that it has any relevance to the aging mechanisms of multicellular organisms, but very cool in its own right. And definitely not transposon-mediated.