Affiliation:
1. Ludwig Institute for Cancer Research, Departments of Medicine and Cellular and Molecular Medicine
2. Cancer Center, University of California—San Diego School of Medicine, La Jolla, California 92093
Abstract
ABSTRACT
The Rrm3 DNA helicase of
Saccharomyces cerevisiae
interacts with proliferating cell nuclear antigen and is required for replication fork progression through ribosomal DNA repeats and subtelomeric and telomeric DNA. Here, we show that
rrm3 srs2
and
rrm3 sgs1
mutants, in which two different DNA helicases have been inactivated, exhibit a severe growth defect and undergo frequent cell death. Cells lacking Rrm3 and Srs2 arrest in the G
2
/M phase of the cell cycle with 2N DNA content and frequently contain only a single nucleus. The phenotypes of
rrm3 srs2
and
rrm3 sgs1
mutants were suppressed by disrupting early steps of homologous recombination. These observations identify Rrm3 as a new member of a network of pathways, involving Sgs1 and Srs2 helicases and Mus81 endonuclease, suggested to act during repair of stalled replication forks.
Publisher
American Society for Microbiology
Subject
Cell Biology,Molecular Biology
Cited by
79 articles.
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