A really interesting new preprint was published in August by Nicholas Stroustrup's lab in Barcelona, Spain. Declines in mRNA synthesis set the rate of organismal aging looks at the way an enzyme called RNA Polymerase II (RNAPII) changes as worms get older. This particular enzyme is used by a wide range of species to read DNA and create mRNA. That process is called transcription. The paper is worth reading. I have put a summary and analysis of this paper on Rapamycin News here
What the paper basically says is that the amount of mRNA produced reduces as worms get older and this happens because of a reduction in the availability of RNAPII. It also says that the reason RNAPII availability reduces is because it is destroyed by the cell. A protein called ubiqutin is added to RNAPII to tell the cell to destroy the protein.
RNAPII starts at the start of a gene and moves down it to read the gene and create mRNA. It is a bit like a copy typist. A cell needs an individual copy of RNAPII each time a cell needs to produce some mRNA (at times more than one copy of a protein can be produced from a single mRNA).
It has been known for some time that when RNAPII gets stuck (stalled) it can end up being marked for destruction. Degradation of DNA damage-independently stalled RNA polymerase II is independent of the E3 ligase Elc1 is a paper that showed that it did not require DNA damage to cause the degradation of RNA Pol II.
There have been lots of interesting papers looking at the limitations on protein production that occur with ageing. Where the most recent paper is helpful is that it shows how the cell manages the availability of RNAPII. Basically there is a system of homeostasis so if the system of transcription gets stuck then fewer RNAPII enzymes are made available so that transcription slows down (in the sense of the initiation of transcription slowing down).
I think the ageing component of this is caused by shortage of acetyl-CoA as that is needed to acetylate the histone as RNAPII passes down the gene.
We should be grateful to Nicholas Stroustrup and his team for their excellent work with this preprint.
What the paper basically says is that the amount of mRNA produced reduces as worms get older and this happens because of a reduction in the availability of RNAPII. It also says that the reason RNAPII availability reduces is because it is destroyed by the cell. A protein called ubiqutin is added to RNAPII to tell the cell to destroy the protein.
RNAPII starts at the start of a gene and moves down it to read the gene and create mRNA. It is a bit like a copy typist. A cell needs an individual copy of RNAPII each time a cell needs to produce some mRNA (at times more than one copy of a protein can be produced from a single mRNA).
It has been known for some time that when RNAPII gets stuck (stalled) it can end up being marked for destruction. Degradation of DNA damage-independently stalled RNA polymerase II is independent of the E3 ligase Elc1 is a paper that showed that it did not require DNA damage to cause the degradation of RNA Pol II.
There have been lots of interesting papers looking at the limitations on protein production that occur with ageing. Where the most recent paper is helpful is that it shows how the cell manages the availability of RNAPII. Basically there is a system of homeostasis so if the system of transcription gets stuck then fewer RNAPII enzymes are made available so that transcription slows down (in the sense of the initiation of transcription slowing down).
I think the ageing component of this is caused by shortage of acetyl-CoA as that is needed to acetylate the histone as RNAPII passes down the gene.
We should be grateful to Nicholas Stroustrup and his team for their excellent work with this preprint.
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