Genetic control of intrachromosomal recombination in Saccharomyces cerevisiae. I. Isolation and genetic characterization of hyper-recombination mutations.

TLDR

Eight complementation groups of recessive mutations (hpr genes) that increase mitotic intrachromosomal recombination have been identified in *Saccharomyces cerevisiae*. The study aims to determine whether these genes regulate distinct recombination pathways or different outcomes of the same pathway. Mutants were examined for sensitivity to DNA‑damaging agents and for mutator activity. The hpr mutants preferentially enhance intrachromosomal gene conversion or marker loss, with new CDC2 and CDC17 alleles identified; hpr5 displays biased gene conversion, hpr1 shows a weaker interchromosomal effect, and the data indicate that gene conversion and reciprocal exchange can be genetically separated.

Abstract

Abstract Eight complementation groups have been defined for recessive mutations conferring an increased mitotic intrachromosomal recombination phenotype (hpr genes) in Saccharomyces cerevisiae. Some of the mutations preferentially increase intrachromosomal gene conversion (hpr4, hpr5 and hpr8) between repeated sequences, some increase loss of a marker between duplicated genes (hpr1 and hpr6), and some increase both types of events (hpr2, hpr3 and hpr7). New alleles of the CDC2 and CDC17 genes were recovered among these mutants. The mutants were also characterized for sensitivity to DNA damaging agents and for mutator activity. Among the more interesting mutants are hpr5, which shows a biased gene conversion in a leu2-112::URA3::leu2-k duplication; and hpr1, which has a much weaker effect on interchromosomal mitotic recombination than on intrachromosomal mitotic recombination. These analyses suggest that gene conversion and reciprocal exchange can be separated mutationally. Further studies are required to show whether different recombination pathways or different outcomes of the same recombination pathway are controlled by the genes identified in this study.