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Molecular and Cellular Biology, November 1999, p. 7681-7687, Vol. 19, No. 11
Laboratory of Genetics, University of
Wisconsin Medical School, Madison, Wisconsin 53706
Received 16 June 1999/Returned for modification 30 July
1999/Accepted 19 August 1999
Saccharomyces cerevisiae mre11
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
The Mre11-Rad50-Xrs2 Protein Complex Facilitates Homologous
Recombination-Based Double-Strand Break Repair in
Saccharomyces cerevisiae
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
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.
*
Corresponding author. Mailing address: Laboratory of
Genetics, University of Wisconsin Medical School, 445 Henry Mall,
Madison, WI 53706. Phone: (608) 265-6043. Fax: (608) 262-2976. E-mail: jpetrini{at}facstaff.wisc.edu.
Manuscript 3538 from the University of Wisconsin
Madison
Laboratory of Genetics.
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