Induction of the cytoplasmic 'petite' mutation in pso mutants of Saccharomyces cerevisiae by photoaddition of furocoumarins or by ultraviolet radiation.

The induction of the cytoplasmic 'petite' mutation (or rho-) after photoaddition of either 8-methoxypsoralen (8-MOP) or 3-carbethoxypsoralen (3-CPs), after 254 nm u.v. and after 6-N-hydroxyaminopurine treatment was examined in three pso mutants in comparison to wild-type Saccharomyces cerevisiae. In three pso mutants which are defective in the induction of nuclear reverse and forward mutations, the photoaddition of 8-MOP enhanced the induction of rho-. This was true for cells in both exponential and stationary phases of growth. After photoaddition of 3-CPs in both growth phases the frequency of rho- was enhanced in pso3-1 whereas pso1-1 showed the same response as the wild-type. In pso2-1 the frequency of rho- was reduced. After treatment with 254 nm u.v. in the stationary phase of growth, rho- induction was increased in pso1-1 and pso3-1 cells as compared to wild-type cells. However, when treated in the exponential phase of growth all three pso mutants showed reduced rho- frequency. The data indicate that the defect in the repair of furocoumarins plus light-induced lesions controlled by nuclear genes (pso) interferes to various extents with the fate of mitochondrial lesions. The frequency of rho- mutants induced in the pso mutants by an analogue of adenine, 6-N-hydroxyaminopurine, was similar to that observed in the wild-type strain, suggesting that this drug may also act at the mitochondrial level as a direct mutagen in yeast.