Timing is everything: cell cycle control of Rad52

被引:26
作者
Barlow, Jacqueline H. [2 ]
Rothstein, Rodney [1 ]
机构
[1] Columbia Univ, Med Ctr, Dept Genet & Dev, New York, NY 10032 USA
[2] NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA
来源
CELL DIVISION | 2010年 / 5卷
关键词
DOUBLE-STRAND BREAK; REPLICATION PROTEIN-A; DNA-DAMAGE CHECKPOINT; HOMOLOGOUS RECOMBINATION; SACCHAROMYCES-CEREVISIAE; FORK PROGRESSION; END RESECTION; IN-VIVO; DIFFERENTIAL REGULATION; SUMO MODIFICATION;
D O I
10.1186/1747-1028-5-7
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
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页数:8
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