Requirement of Rrm3 helicase for repair of spontaneous DNA lesions in cells lacking srs2 or sgs1 helicase

被引:61
|
作者
Schmidt, KH
Kolodner, RD
机构
[1] Univ Calif San Diego, Sch Med, Ludwig Inst Canc Res, CMME 3058, La Jolla, CA 92093 USA
[2] Univ Calif San Diego, Sch Med, Dept Med, La Jolla, CA 92093 USA
[3] Univ Calif San Diego, Sch Med, Dept Cellular & Mol Med, La Jolla, CA 92093 USA
[4] Univ Calif San Diego, Sch Med, Ctr Canc, La Jolla, CA 92093 USA
关键词
D O I
10.1128/MCB.24.8.3213-3226.2004
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:3213 / 3226
页数:14
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