SENSITIVITIES TO MONOCHROMATIC 254‐nm AND 365‐nm RADIATION OF CLOSELY RELATED STRAINS OF Saccharomyces cerevisiae WITH DIFFERING REPAIR CAPABILITIES

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Abstract
Abstract— Sensitivity to monochromatic 254‐ and 365‐nm radiation was compared in closely related yeast strains with defects in one or more of the excision‐repair (rad1), error‐prone repair (rad18), or recombinational‐repair (rad51) pathways. At 254 nm, mutants defective in a single repair pathway exhibited slight to moderate UV sensitivity; those defective in two separate pathways were somewhat more UV sensitive, while triple mutants defective in all three pathways exhibited extreme UV sensitivity with a lethal event corresponding to 0.05 J m−2. Repair defects also rendered mutants sensitive to 365‐nm radiation; strains with single defects exhibited slight sensitivity, mutants with two defective pathways were more sensitive, and triple mutants exhibited maximal sensitivity with a lethal event corresponding to 2.4 times 104 J m−2. In the triple mutant (rad1, rad18, rad51) at both 254 and 365 nm, the dose per lethal event was almost identical with comparable values in a repair‐deficient double mutant (uvrA, recA) of Escherichia coli. In the E. coli mutant pyrimidine dimers are believed to be the primary cause of lethality at both wavelengths. Evidence for dimer involvement in the yeast mutant was obtained by demonstrating that lethality at both 254 and 365 nm was photoreactivated by light at 405 nm.