Magnus Lynch wrote:
>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.
Has anyone ever shown "gain of function" in which a mtDNA mutation leads to
less ROS production? It was my understanding that just about all of them
increased ROS production. Of course by screening a library of yeast mtDNA
mutants one might actually be able to find low ROS producers - has anyone
tried this?
Quite why a low ROS producing mito' has a selective advantage over a
medium-high ROS one is still puzzling to me. Is there any evidence that if
one artificially raises (antimycin A) or lowers (FCCP) mitochondrial ROS in
a cell, that the mitochondrial turnover is changed, or the cell degrades /
promotes replication of said mito's differently?
WRT to adding telemeres into mtDNA, I agree with Aubrey in that there are
plenty of better ways to stop oxidative damage, such as common antioxidants
(SOD, GPx, Lipids, GSH) and also physical barriers such as membranes, and
stopping the ROS at its source. Telomeres would seem to be a complicated
way to go about things - and something that if it worked, you'd think
nature would be doing it already. Maybe there's a damn good reason not to
have telomeres in mtDNA.
Paul
_________________________________________
Dr. Paul S. Brookes. (brookes at uab.edu)
UAB Department of Pathology, G004 Volker Hall
1670 University Blvd., Birmingham AL 35294 USA
Tel (001) 205 934 1915 Fax (001) 205 934 1775
http://peir.path.uab.edu/brookes
The quality of e-mails can go down as well as up
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