https://www.nature.com/articles/s41586-023-05922-y
There has been a bit of a buzz about this paper.
I personally think this is downstream of the long genes not working hypothesis for more see the link below.
I think the reason for RNAPII running faster is a greater availability of substrate where not stalled. The causes of these are hypothesised variously to be
a) Shortage of splicing factors
b) DNA Damage
c) Shortage of Acetyl-CoA. (that’s my hypothesis)
Still I thought I would post this as I have not seen it in the forum.
I have been spending further time reading up on autophagy and in particular the question as to why mitophagy being increased is clearly good for health (as it is). I was surprised to learn that the average half life of mitochondria in some mammalian tissues is only around the 10 days to a fortnight range. I wonder, therefore, as to the mechanism which makes mitophagy a good thing.
It strikes me that it could be clearing out damaged mitochondria that are not being cleared out in the normal 10 day process. I have no idea how to test for this, however.