Environmental and Molecular Mutagenesis (EMM) Editor's Choice - March 2012
The Editor's Choice for March is "“Uncoupling of RAD51 Focus Formation and Cell Survival After Replication Fork Stalling in RAD51D Null CHO Cells” by Salustra S. Urbin, Ingegerd Elvers, John M. Hinz, Thomas Helleday, and Larry H. Thompson.
The RAD51 family of related proteins makes up part of the cellular machinery that repairs double-strand breaks in DNA by homologous recombination repair. Ionizing radiation and chemicals that arrest DNA replication (like camptothecin, aphidicolin, or hydroxyurea) cause double-strand breaks. Following treatment of cells with these agents, RAD51 proteins localize within nuclear foci, which are considered sites of homologous recombination repair. Generally, cells carrying mutations in RAD51-related genes are more easily killed by agents that cause arrest of DNA replication. Also, such cells are typically defective in nuclear focus formation. Urbin and colleagues chose to investigate the functional properties of the relatively uncharacterized RAD51D gene product, a protein in the RAD51 family known to complex with XRCC2. The authors were able to demonstrate that cell lacking RAD51D protein were defective in focus formation, but did not show an increased sensitivity to cell killing by hydroxyurea-induced double-strand breaks. Thus, Urbin and colleagues demonstrated, for the first time, that cell survival and RAD51 focus formation can be separated as distinct cellular properties impacted by the RAD51 gene family of proteins. Environ. Mol. Mutagen. 53:114-124, March 2012. © 2012 Wiley Periodicals, Inc.