Commentary
Timing is everything: cell cycle control of Rad52
-
* Corresponding author: Rodney Rothstein rothstein@cancercenter.columbia.edu
1 Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Building 10, Room 4B04, 10 Center Drive, Bethesda, MD 20892, USA
2 Department of Genetics & Development, Columbia University Medical Center, 701 West 168th Street, HHSC 1608, New York, NY 10032-2704, USA
Cell Division 2010, 5:7 doi:10.1186/1747-1028-5-7
Published: 23 February 2010Abstract
Regulation of the repair of DNA double-strand breaks by homologous recombination is extremely important for both cell viability and the maintenance of genomic integrity. Modulation of double-strand break repair in the yeast Saccharomyces cerevisiae involves controlling the recruitment of one of the central recombination proteins, Rad52, to sites of DNA lesions. The Rad52 protein, which plays a role in strand exchange and the annealing of single strand DNA, is positively regulated upon entry into S phase, repressed during the intra-S phase checkpoint, and undergoes posttranslational modification events such as phosphorylation and sumoylation. These processes all contribute to the timing of Rad52 recruitment, its stability and function. Here, we summarize the regulatory events affecting the Rad52 protein and discuss how this regulation impacts DNA repair and cell survival.