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RESEARCH COMMUNICATION
1 Department of Microbiology and Immunology and Morse Institute for Molecular Genetics, State University of New York Downstate Medical Center, Brooklyn, New York 11203, USA; 2 Howard Hughes Medical Institute and Department of Oncological Sciences, Huntsman Cancer Institute, University of Utah School of Medicine, Salt Lake City, Utah 84112, USA; 3 Department of Oncological Sciences, Mount Sinai School of Medicine, New York, NY 10029, USA
The failure of cells to repair damaged DNA can result in genomic instability and cancer. To efficiently repair chromosomal DNA lesions, the repair machinery must gain access to the damaged DNA in the context of chromatin. Here we report that both the RSC and Swi/Snf ATP-dependent chromatin-remodeling complexes play key roles in double-strand break (DSB) repair, specifically by homologous recombination (HR). RSC and Swi/Snf are each recruited to an in vivo DSB site but with distinct kinetics. We show that Swi/Snf is required earlier, at or preceding the strand invasion step of HR, while RSC is required following synapsis for completion of the recombinational repair event.
[Keywords: Chromatin remodeling; DSB repair; HR; RSC; SWI/SNF]
Received October 18, 2004; revised version accepted June 2, 2005.
Article and publication are at http://www.genesdev.org/cgi/doi/10.1101/gad.1273105.
4 These authors contributed equally to this work.
E-MAIL brehon.laurent{at}mssm.edu; FAX (212) 987-2240.
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