🚀 go-pugleaf

Aubrey de Grey is far better qualified than I to answer this, but I have
one observation:  mitochondrial genes are circular.  This implies they
do not have ends, hence no telomeres to play with.  Or did I miss
something?

Any further work with the P66 gene knockout mice that reduced apoptosis
and extend life in rodents?


In article <38B40E08.A8B475D4@cam.ac.uk>,
  Magnus Lynch <mdl24@cam.ac.uk> wrote:
> It is thought that mitochondrial mutations caused by oxidative damage
to
> the mitochondrial genome are an important mechanism of aging. It is
> proposed that certain of these mutations reduce the rate of free
radical
> production giving that mitochondrium a survival advantage within the
> cell. Selection subsequently causes the mutant mitochondrial genome to
> become the predominant species within that cell. [de Grey, A.D.N.J.
> BioEssays 19,161]. An intervention which has been proposed to test
this
> theory is to encode the mitochondrial genes in the nuclear genome and
> transport them into the mitochonrium. This will be extremely
informative
> but still requires significant work.
>
> It has been demonstrated that telomeric sequences preferentially
> accumulate oxidative damage [Exp Cell Res, 1998 Feb, 239:1, 152-60]. I
> propose that telomeric sequences be incorporated in a mitochondrial
> genome and that this might slow the accumulation of mutations in
coding
> regions of the genome. Although this intervention would not be as
useful
> as the one discussed above, it has the advantage of being simple to
> implement in the immediate future.
>
> Does anybody think that this intervention would have any effect? Am I
> correct in thinking that it would be simple to implement?
>
> Magnus
>


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