A novel allele of RAD52 that causes severe DNA repair and recombination deficiencies only in the absence of RAD51 or RAD59

With the use of an intrachromosomal inverted repeat as a recombination repo rter, we have shown that mitotic recombination is dependent on the RAD52 ge ne, but I educed only fivefold by mutation of RAD51. RAD59 a component of t he RAD51-independent pathway, was identified previously by screening for mu tations that reduced inverted-repeat recombination in a rad51 strain. Here we describe a rad52 mutation, rad52R70K, that also reduced recombination sy nergistically in a rad51 background. The phenotype of the rad52R70K strain, which includes weak gamma-ray sensitivity, a fourfold reduction in the rat e of inverted-repeat recombination, elevated allelic recombination, sporula tion proficiency, and a reduction in the efficiency of mating-type switchin g and single-strand annealing, was similar to that observed for deletion of the RAD59 gene. However, rad52R70K rad59 double mutants showed synergistic defects in ionizing radiation resistance, sporulation, and mating-type swi tching. These results suggest that Rad52 and Rad59 have partially overlappi ng functions and that Rad59 can substitute for this function of Rad52 in a RAD51 rad52R70K strain.