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Background  In  Saccharomyces cerevisiae , Rad59 is required for multiple homologous recombination mechanisms and viability in DNA replication-defective  rad27  mutant cells. Recently, four  rad59  missense alleles were found to have distinct effects on homologous recombination that are consistent with separation-of-function mutations. The  rad59-K166A  allele alters an amino acid in a conserved α-helical domain, and, like the  rad59  null allele diminishes association of Rad52 with double-strand breaks. The  rad59-K174A  and  rad59-F180A  alleles alter amino acids in the same domain and have genetically similar effects on homologous recombination. The  rad59-Y92A  allele alters a conserved amino acid in a separate domain, has genetically distinct effects on homologous recombination, and does not diminish association of Rad52 with double-strand breaks.    Results  In this study,  rad59  mutant strains were crossed with a  rad27  null mutant to examine the effects of the  rad59  alleles on the link between viability, growth and the stimulation of homologous recombination in replication-defective cells. Like the  rad59  null allele,  rad59-K166A  was synthetically lethal in combination with  rad27 . The  rad59-K174A  and  rad59-F180A  alleles were not synthetically lethal in combination with  rad27,  had effects on growth that coincided with decreased ectopic gene conversion, but did not affect mutation, unequal sister-chromatid recombination, or loss of heterozygosity. The  rad59-Y92A  allele was not synthetically lethal when combined with  rad27 , stimulated ectopic gene conversion and heteroallelic recombination independently from  rad27 , and was mutually epistatic with  srs2 . Unlike  rad27 , the stimulatory effect of  rad59-Y92A  on homologous recombination was not accompanied by effects on growth rate, cell cycle distribution, mutation, unequal sister-chromatid recombination, or loss of heterozygosity.    Conclusions  The synthetic lethality conferred by  rad59  null and  rad59-K166A  alleles correlates with their inhibitory effect on association of Rad52 with double-strand breaks, suggesting that this may be essential for rescuing replication lesions in  rad27  mutant cells. The  rad59-K174A  and  rad59-F180A  alleles may fractionally reduce this same function, which proportionally reduced repair of replication lesions by homologous recombination and growth rate. In contrast,  rad59-Y92A  stimulates homologous recombination, perhaps by affecting association of replication lesions with the Rad51 recombinase. This suggests that Rad59 influences the rescue of replication lesions by multiple recombination factors.

Alleles of the homologous recombination gene, RAD59, identify multiple responses to disrupted DNA replication in Saccharomyces cerevisiae