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The mode of interaction in haploid Saccharomyces cerevisiae of two pso mutations with each other and with rad mutations affected in their excision-resynthesis (rad3), error-prone (rad6), and deoxyribonucleic acid double-strand break (rad52) repair pathways was determined for various double mutant combinations. Survival data for 8-methoxypsoralen photoaddition, 254-nm ultraviolet light and gamma rays are presented. For 8-methoxypsoralen photoaddition, which induces both deoxyribonucleic acid interstrand cross-links and monoadditions, the pso1 mutation is epistatic to the rad6, rad52, and pso2 mutations, whereas it is synergistic to rad3. The pso2 mutation, which is specifically sensitive to photoaddition of psoralens, is epistatic to rad3 and demonstrates a nonepistatic interaction with rad6 and rad52. rad3 and rad6, as well as rad 6 and rad52, show synergistic interactions with each other, whereas rad 3 is epistatic to rad52. Consequently, it is proposed that PSO1 and RAD3 genes govern steps in the independent pathways. The PSO1 activity leading to an intermediate which is repaired via the three incidence pathways controlled by RAD6, RAD52, and PSO2 genes. Since pso1 interacts synergistically with rad3 and rad52 and epistatically with rad6 after UV radiation, the PSO1 gene appears to belong to the RAD6 group. For gamma ray sensitivity, pso1 is epistatic to rad6 and rad52, which suggests that this gene controls a step which is common to the two other independent pathways.

Interactions between mutations for sensitivity to psoralen photoaddition (pso) and to radiation (rad) in Saccharomyces cerevisiae