DNA double-strand break repair-pathway choice in somatic mammalian cells

被引：980
作者：
Scully, Ralph [1 ]
Panday, Arvind [1 ,2 ,3 ]
Elango, Rajula [1 ,2 ,3 ]
Willis, Nicholas A. [1 ]
机构：
[1] Beth Israel Deaconess Med Ctr, Div Hematol Oncol, Dept Med, Boston, MA 02215 USA
[2] Beth Israel Deaconess Med Ctr, Canc Res Inst, Boston, MA 02215 USA
[3] Harvard Med Sch, Boston, MA 02115 USA
来源：
NATURE REVIEWS MOLECULAR CELL BIOLOGY | 2019年 / 20卷 / 11期
关键词：
REPLICATION FORK REVERSAL; CROSS-LINK REPAIR; END-JOINING PATHWAYS; RECOMBINATION EXECUTION CHECKPOINT; INTERPHASE CHROMOSOME BREAKS; TRACT GENE CONVERSION; HOMOLOGOUS-RECOMBINATION; DAMAGE-RESPONSE; MMS22L-TONSL COMPLEX; GENOMIC STABILITY;
D O I：
10.1038/s41580-019-0152-0
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
The major pathways of DNA double-strand break (DSB) repair are crucial for maintaining genomic stability. However, if deployed in an inappropriate cellular context, these same repair functions can mediate chromosome rearrangements that underlie various human diseases, ranging from developmental disorders to cancer. The two major mechanisms of DSB repair in mammalian cells are non-homologous end joining (NHEJ) and homologous recombination. In this Review, we consider DSB repair-pathway choice in somatic mammalian cells as a series of 'decision trees', and explore how defective pathway choice can lead to genomic instability. Stalled, collapsed or broken DNA replication forks present a distinctive challenge to the DSB repair system. Emerging evidence suggests that the 'rules' governing repair-pathway choice at stalled replication forks differ from those at replication-independent DSBs.
引用
收藏
页码：698 / 714
页数：17
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