Control of sister chromatid recombination by histone H2AX

被引:180
作者
Xie, AY
Puget, N
Shim, I
Odate, S
Jarzyna, I
Bassing, CH
Alt, FW
Scully, R
机构
[1] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Dept Med, Boston, MA 02115 USA
[2] Childrens Hosp, Howard Hughes Med Inst, Boston, MA 02115 USA
[3] Ctr Blood Res, Boston, MA 02115 USA
[4] Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA
关键词
D O I
10.1016/j.molcel.2004.12.007
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Histone H2AX has a role in suppressing genomic instability and cancer. However, the mechanisms by which it performs these functions are poorly understood. After DNA breakage, H2AX is phosphorylated on serine 139 in chromatin near the break. We show here that H2AX serine 139 enforces efficient homologous recombinational repair of a chromosomal double-strand break (DSB) by using the sister chromatid as a template. BRCA1, Rad51, and CHK2 contribute to recombinational repair, in part independently of H2AX H2AX(-/-) cells show increased use of single-strand annealing, an error-prone deletional mechanism of DSB repair. Therefore, the chromatin response around a chromosomal DSB, in which H2AX serine 139 phosphorylation plays a central role, "shapes" the repair process in favor of potentially error-free interchromatid homologous recombination at the expense of error-prone repair. H2AX phosphorylation may help set up a favorable disposition between sister chromatids.
引用
收藏
页码:1017 / 1025
页数:9
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