Relationships between a Hyper-Rec Mutation (rem1) and Other Recombination and Repair Genes in Yeast
Robert E Malone
Merl F Hoekstra
Received 1983 May 15; Accepted 1984 Jan 18.
Abstract
Mutations in theREM1 gene ofSaccharomyces cerevisiae confer a semidominant hyper-recombination and hypermutable phenotype upon mitotic cells (Golin andEsposito 1977). These effects have not been observed in meiosis. We have examined the interactions ofrem1 mutations withrad6-1, rad50-1, rad52-1 or spo11-1 mutations in order to understand the basis of therem1 hyper-rec phenotype. Therad mutations have pleiotropic phenotypes;spo11 is only defective in sporulation and meiosis. TheRAD6, RAD50 and SPO11 genes are not required for spontaneous mitotic recombination; mutations in theRAD52 gene cause a general spontaneous mitotic Rec- phenotype. Mutations inRAD50, RAD52 orSPO11 eliminate meiotic recombination, and mutations inRAD6 prevent spore formation. Evidence for the involvement ofRAD6 in meiotic recombination is less clear. Mutations in all threeRAD genes confer sensitivity to X rays; theRAD6 gene is also required for UV damage repair. To test whether any of these functions might be involved in the hyper-rec phenotype conferred byrem1 mutations, double mutants were constructed. Double mutants ofrem1 spo11 were viable and demonstratedrem1 levels of mitotic recombination, suggesting that the normal meiotic recombination system is not involved in producing therem1 phenotype. The rem1 rad6 double mutant was also viable and hadrem1 levels of mitotic recombination. Neitherrem1 rad50 norrem1 rad52 double mutants were viable. This suggests thatrem1 causes its hyper-rec phenotype because it creates lesions in the DNA that are repaired using a recombination-repair system involvingRAD50 andRAD52.
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Selected References
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