Affiliation:
1. Laboratory of Genetics, University of Wisconsin Medical School, Madison, Wisconsin 53706
Abstract
ABSTRACT
Saccharomyces cerevisiae mre11
Δ mutants are profoundly deficient in double-strand break (DSB) repair, indicating that the Mre11-Rad50-Xrs2 protein complex plays a central role in the cellular response to DNA DSBs. In this study, we examined the role of the complex in homologous recombination, the primary mode of DSB repair in yeast. We measured survival in synchronous cultures following irradiation and scored sister chromatid and interhomologue recombination genetically.
mre11
Δ strains were profoundly sensitive to ionizing radiation (IR) throughout the cell cycle. Mutant strains exhibited decreased frequencies of IR-induced sister chromatid and interhomologue recombination, indicating a general deficiency in homologous recombination-based DSB repair. Since a nuclease-deficient
mre11
mutant was not impaired in these assays, it appears that the role of the
S. cerevisiae
Mre11-Rad50-Xrs2 protein complex in facilitating homologous recombination is independent of its nuclease activities.
Publisher
American Society for Microbiology
Subject
Cell Biology,Molecular Biology
Cited by
195 articles.
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