If the difference would be just about transposon-supressors in the soma in mole rats, we wouldn’t see them to have less transposon-derived repeats in their genome.
That’s a good point, my previous idea about NMR somatic transposon suppression is probably incorrect.
According to the article naked mole rats have “efficient DNA damage repair”. Efficient DNA repair in germline tells means that transposons will doublicate less in the germline cells and it’s therefore easier for evolution to reduce the transposon count.
Following the article’s citation for the ‘efficient DNA damage repair’ claim, we get this study, that analyzes NMR, human and mouse liver tissue (not germline), and finds that, compared to mice, humans and NMRs have higher expression of genes central to DNA repair pathways. The paper then reminds the reader that both humans and NMRs live longer than mice, so maybe DNA repair makes organisms live longer.
This is consistent with johnswentworth’s model of:
where DNA repair pathways slow the progress of the DNA damage / mitochondrial ROS feedback loop, making aging progress at a slower rate.
So it looks like:
NMRs have DNA repair pathways in the soma that are abnormally active for a rodent their size
NMRs have fewer transposon-derived repeats in their genome, indicating vigilant transposon suppression in the germline
These mechanisms counter aging, but come with some hidden cost to fitness, and that’s why humans don’t have even higher DNA repair activity, or more vigilant germline transposon suppression
But what are these hidden costs? Surely there is variation among humans w.r.t rates of somatic DNA repair, and effectiveness of germline transposon suppression. Why aren’t people with beneficial versions of these traits aging less, living longer, and having more children?
Edit: I think I might have (partially) answered my own question:
Why aren’t people with beneficial versions of these traits aging less, living longer, and having more children?
Even if people with less active transposons have slightly more children that’s only one part of the evolutionary equation.
The frame I was taught is evolution= natural selection + mutation + gene drift. Mutations are a force for increased transposon count (and if there’s more DNA repair there are less mutations). Natural selection is a force for decreased transposon count. You would expect those two forces to find an equilibrium so that the amount of transposons isn’t a problem at the age where an animal bears children. If you have very effecitve germline transposon suppression transposon also evolve to escape the transposon suppression.
When it comes to DNA repair I would expect that it’s simply a cost for a cell to put resources into DNA repair.
more vigilant germline transposon suppression
Without evolutionary pressure that prevents individuals with more active transposon to reproduce less that just gets the transposons to express themselves more and you have +/- zero.
Sure, but wouldn’t a hunter that stayed physically 25 until the age of 45 have a higher inclusive genetic fitness, all else being equal? (edit circa 2022-07-02: Wow, I was dumb. Red Queen hypothesis, baby.)
All else isn’t equal. Transposons replicate. That’s what transposons are about.
The genetic fitness of the hunter doesn’t really matter (that’s basically the insight Dawkins wrote about in the selfish gene). You have to look at the fitness of the transposon and what’s good for the transposon.
If a transposon copies itself into another chromosome it can increase the chance of being inherited to a child from 50% to 100%. That’s highly useful to the fitness of the transposon and worth slightly reduced lifespan of the child.
Both of those forces are at an equilibirum. Transposons copy themselves till the reduced lifespan/health isn’t worth it to double the chance of being inherited.
That’s a good point, my previous idea about NMR somatic transposon suppression is probably incorrect.
Following the article’s citation for the ‘efficient DNA damage repair’ claim, we get this study, that analyzes NMR, human and mouse liver tissue (not germline), and finds that, compared to mice, humans and NMRs have higher expression of genes central to DNA repair pathways. The paper then reminds the reader that both humans and NMRs live longer than mice, so maybe DNA repair makes organisms live longer.
This is consistent with johnswentworth’s model of:
Transposon activity → (DNA damage <-> mitochondrial ROS feedback loop) → age-associated cellular dysfunction
where DNA repair pathways slow the progress of the DNA damage / mitochondrial ROS feedback loop, making aging progress at a slower rate.
So it looks like:
NMRs have DNA repair pathways in the soma that are abnormally active for a rodent their size
NMRs have fewer transposon-derived repeats in their genome, indicating vigilant transposon suppression in the germline
These mechanisms counter aging, but come with some hidden cost to fitness, and that’s why humans don’t have even higher DNA repair activity, or more vigilant germline transposon suppression
But what are these hidden costs? Surely there is variation among humans w.r.t rates of somatic DNA repair, and effectiveness of germline transposon suppression. Why aren’t people with beneficial versions of these traits aging less, living longer, and having more children?
Edit: I think I might have (partially) answered my own question:
https://en.wikipedia.org/wiki/Antagonistic_pleiotropy_hypothesis#DNA_Damage_Theory_of_Aging
Even if people with less active transposons have slightly more children that’s only one part of the evolutionary equation.
The frame I was taught is evolution= natural selection + mutation + gene drift. Mutations are a force for increased transposon count (and if there’s more DNA repair there are less mutations). Natural selection is a force for decreased transposon count. You would expect those two forces to find an equilibrium so that the amount of transposons isn’t a problem at the age where an animal bears children. If you have very effecitve germline transposon suppression transposon also evolve to escape the transposon suppression.
When it comes to DNA repair I would expect that it’s simply a cost for a cell to put resources into DNA repair.
Without evolutionary pressure that prevents individuals with more active transposon to reproduce less that just gets the transposons to express themselves more and you have +/- zero.
Sure, but wouldn’t a hunter that stayed physically 25 until the age of 45 have a higher inclusive genetic fitness, all else being equal? (edit circa 2022-07-02: Wow, I was dumb. Red Queen hypothesis, baby.)
All else isn’t equal. Transposons replicate. That’s what transposons are about.
The genetic fitness of the hunter doesn’t really matter (that’s basically the insight Dawkins wrote about in the selfish gene). You have to look at the fitness of the transposon and what’s good for the transposon.
If a transposon copies itself into another chromosome it can increase the chance of being inherited to a child from 50% to 100%. That’s highly useful to the fitness of the transposon and worth slightly reduced lifespan of the child.
Both of those forces are at an equilibirum. Transposons copy themselves till the reduced lifespan/health isn’t worth it to double the chance of being inherited.