🚀 go-pugleaf

I meant that a number of repeats of the telomeric sequence TTAGGG should
be incorparated into the circular mitochondrial genome.

Magnus

rjk3 wrote:
> 
> 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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