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.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Amino Acid Sequence
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Cell Cycle / physiology
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Cell Cycle Proteins / genetics
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Cell Cycle Proteins / metabolism
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Cell Death / physiology
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Cell Division / physiology
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Cell Size
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Cell Survival / physiology
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DNA Damage*
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DNA Helicases / genetics
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DNA Helicases / metabolism*
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DNA Repair*
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DNA Replication
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Gene Silencing
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Molecular Sequence Data
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Phenotype
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RecQ Helicases
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Recombination, Genetic
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Saccharomyces cerevisiae / cytology
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Saccharomyces cerevisiae / genetics*
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Saccharomyces cerevisiae / physiology
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Saccharomyces cerevisiae Proteins / genetics
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Saccharomyces cerevisiae Proteins / metabolism*
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Sequence Alignment
Substances
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Cell Cycle Proteins
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Saccharomyces cerevisiae Proteins
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SRS2 protein, S cerevisiae
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Rrm3 protein, S cerevisiae
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SGS1 protein, S cerevisiae
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DNA Helicases
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RecQ Helicases