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Three main features regarding the loss of mitochondrial genetic markers among rho- mutants induced by ultraviolet irradiation are reported: (a) the frequency of loss of six loci examined increases with UV dose; (b) preferential loss of one region of the mitochondrial genome observed in spontaneous rho- mutants is enhanced by UV; and (c) the loss of each marker results from large deletions. Marker loss in rho- mutants was also investigated under conditions that modulate rho- induction. Liquid holding of irradiated exponential or stationary phase cells, as well as a split-dose regime applied to stationary phase cells, results in rho- mutants in which the loss of markers is correlated with rho- induction: the more sensitive the cells are to rho- induction, the more frequent are the marker losses among rho- clones derived from these cells. This correlation is not found in exponential-phase cells submitted to a split-dose treatment, suggesting that a different mechanism is involved in the latter case. It is known that UV-induced pyrimidine dimers are not excised in a controlled manner in mitochondrial DNA. However, our studies indicate that an accurate repair mechanism (of the recombinational type ?) can lead to the restoration of mitochondrial genetic information in growing cells.
M Heude, and
E Moustacchi
October 1974,
Biochimica et biophysica acta,
M Heude, and
E Moustacchi
December 1976,
Proceedings of the National Academy of Sciences of the United States of America,
M Heude, and
E Moustacchi
July 1975,
Mutation research,
M Heude, and
E Moustacchi
October 1976,
FEBS letters,
M Heude, and
E Moustacchi
April 1981,
Current genetics,
M Heude, and
E Moustacchi
December 1975,
Mutation research,
M Heude, and
E Moustacchi
July 1974,
Biochimica et biophysica acta,
M Heude, and
E Moustacchi
July 1986,
Biochemical and biophysical research communications,
M Heude, and
E Moustacchi
April 1979,
Mutation research,
M Heude, and
E Moustacchi
January 1969,
Mutation research,
