From: Joao Magalhaes (joao.magalhaes@fundp.ac.be)
Date: Sun Dec 08 2002 - 11:56:38 MST
Hi!
First of all, thanks for your opinions. I appreciate it. As for your
thoughts, I don't think our theories are that far apart. Basically, you
focus on mutations while I prefer more subtle changes in the DNA.
At 09:35 07-12-2002 -0800, you wrote:
> > I do see great differences in rate of aging amongst genetically similar
> > species, which makes me think rate of aging is a result of some small
> > alterations in the genetic program.
>
>I'd tend to agree with this as well, though it isn't clear the extent
>to which small mutations can have a large effect. The very mixed p53
>story in mice (both shortened and normal lifespans depending on the
>mutations in and expression of p53) is just one case in point.
I'm not just talking about mutations that alter the genome. When I refer to
DNA damage, I'm including telomere shortening, chromatin structure--certain
3D-formations alter transcription and allow for cancer, and perhaps, I
speculate, aging too--, methylation, etc.
> > In other words, if a
> > yeast or a bacterial culture can divide eternally despite free radicals,
> > UV-damage, DNA mutations, etc., why assume--and most gerontologists
> > do--that our cells cannot cope with these processes?
>
>It isn't that they can't cope -- its that they aren't tuned "just right".
>If protein deamidation is functioning as a "molecular clock" that is
>a signal as to when to recycle poorly functioning proteins, then
>what is the probability that 30,000 proteins have the correct
>molecular structure that signals cells to recycle a protein
>just at the time it becomes dysfunctional?
I'm not sure I understand what you're trying to say. Are you suggesting
that yeast are better tuned than human cells to deal with stress?
>You need to keep in mind however, that the yeast cell is out for
>its own survival. The cells in mammals however are out for the
>survival of the organism. They must have a program that says
>to not kill the collective to benefit themselves.
>
>The things to consider are that the Werner's syndrome protein is an
>exonuclease (i.e. it chews up DNA) and the fact that p53 modulates
>its activity.
I understand cancer is one problem absent from yeast. Yet Drosophila and C.
elegans, as far as I know, don't have cancer and still age. How do you
explain them?
Best wishes.
Joao
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