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.
