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JBC Papers in Press. Published on March 28, 2002 as Manuscript M112132200 Stark et al. ATP-hydrolysis by mammalian RAD51 has a key role during homology-directed DNA repair Downloaded from Jeremy M. Stark, Peng Hu, Andrew J. Pierce, Mary Ellen Moynahan, Nathan Ellis, and / Maria Jasin* by guest on April 11, 2017 Cell Biology Program, Memorial Sloan-Kettering Cancer Center and Cornell University Graduate School of Medical Sciences, 1275 York Avenue, New York, NY 10021 USA *Corresponding author: Phone (212) 639-7438; FAX: (212) 717-3317; e-mail m-jasin@ Running title: RAD51 mutation and DNA repair in mammalian cells Key words: RAD51, Homologous recombination, DNA double-strand break, sister-chromatid exchange, mammalian cells, genomic stability Copyright 2002 by The American Society for Biochemistry and Molecular Biology, Inc. Stark et al. ABSTRACT Disruption of the gene encoding RAD51, the protein that catalyzes strand exchange during homologous recombination, leads to the accumulation of chromosome breaks and lethality in vertebrate cells. As RAD51 is implicated in BRCA1 and BRCA2-mediated tumor suppression as well as cellular viability, we have begun a functional analysis of a defined RAD51 mutation in mammalian cells. Using a dominant negative approach, we generated a mouse embryonic stem cell line that expresses an ATP hydrolysis-defective RAD51 protein, hRAD51-K133R, at comparable levels to the endogenous wild-type