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Molecular and Cellular Biology, April 2004, p. 3213-3226, Vol. 24, No. 8
0270-7306/04/$08.00+0     DOI: 10.1128/MCB.24.8.3213-3226.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Requirement of Rrm3 Helicase for Repair of Spontaneous DNA Lesions in Cells Lacking Srs2 or Sgs1 Helicase

Kristina H. Schmidt1 and Richard D. Kolodner1,2,3*

Ludwig Institute for Cancer Research, Departments of Medicine and Cellular and Molecular Medicine,1 Cancer Center, University of California—San Diego School of Medicine, La Jolla, California 920932

Received 21 July 2003/ Returned for modification 29 August 2003/ Accepted 21 January 2004

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 G2/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.

* Corresponding author. Mailing address: Ludwig Institute for Cancer Research, UCSD School of Medicine-CMME 3058, 9500 Gilman Dr., La Jolla, CA 92093-0669. Phone: (858) 534-7802, ext. 7804. Fax: (858) 534-7750. E-mail: rkolodner{at}ucsd.edu.

Molecular and Cellular Biology, April 2004, p. 3213-3226, Vol. 24, No. 8
0022-538X/04/$08.00+0     DOI: 10.1128/MCB.24.8.3213-3226.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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