On 4 Jun 1993, Robert Bradbury wrote:
> In article <Pine.3.07.9305280832.H9641-c100000 at csuvax1> cummins at CSUVAX1.MURDOCH.EDU.AU (Dr Jim Cummins) writes:
> >There's currently a lot of interest in the role of mitochondrial DNA
> >deletions in ageing phenomena. mtDNA deletions occur much faster than in
> >somatic DNA (in eukaryotic organisms) and accumulate preferentially in
> >postmitotic cells such as muscle and brain. The end result is disorded
> >oxidative phosphorylation and spin-off of free radicals. It's possible
> >that individual yeast cells might age but the colony as a whole survives
> >through mitosis and the selective elimination of cells with defective
> >mitochondria? Just one idea.
> >
>> The articles I've seen on mitochondrial deletion accumulation/genetic
> defects indicate that the effect is very small (1-2% of mitochondrial
> genomes are defective). Given cells contain 200-700 mitochondria
> I have a very difficult time accepting the idea that a few defective
> genomes causing the problem. Additionally the aging "phenotype"
> does not appear to be the same as that of people with genetic diseases
> of the mitochondria which usually show up as heart/muscle disorders.
>> To think of it as part of the the aging process makes sense because
> the deletions do accumulate/accelerate with age. However to consider
> it a major player seems a bit of a stretch.
Check out an article by Doug Wallace in Science last year, May I think.
The mtDNA-somatic mutation theory is rapidly gaining acceptance.
Threshold effects are important, as cells don't express the defective
phenotype until they have passed through a specific threshold level of
defective mitochodria. Thismay be quite low.
Jim Cummins>
