Mechanisms of replication fork protection: a safeguard for genome stability

被引:109
|
作者
Errico, Alessia [1 ]
Costanzo, Vincenzo [1 ]
机构
[1] Imperial Canc Res Fund, Clare Hall Labs, London Res Inst, DNA Damage & Genome Stabil Unit, S Mimms EN6 3LD, Herts, England
基金
欧洲研究理事会;
关键词
DNA replication; DNA repair; DNA damage; Checkpoint; ATR; SISTER-CHROMATID COHESION; DNA-POLYMERASE-ALPHA; S-PHASE CHECKPOINT; XENOPUS EGG EXTRACTS; STRAND BREAK REPAIR; MINICHROMOSOME-MAINTENANCE PROTEINS; HOMOLOGOUS RECOMBINATION REPAIR; SACCHAROMYCES-CEREVISIAE; HUMAN-CELLS; DAMAGE CHECKPOINT;
D O I
10.3109/10409238.2012.655374
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
During S-phase, the genome is extremely vulnerable and the progression of replication forks is often threatened by exogenous and endogenous challenges. When replication fork progression is halted, the intra S-phase checkpoint is activated to promote structural stability of stalled forks, preventing the dissociation of replisome components. This ensures the rapid resumption of replication following DNA repair. Failure in protecting and/or restarting the stalled forks contributes to alterations of the genome. Several human genetic diseases coupled to an increased cancer predisposition are caused by mutations in genes involved in safeguarding genome integrity during DNA replication. Both the ATR (ataxia telangiectasia and Rad3-related protein) kinase and the Replication pausing complex (RPC) components Tipin, Tim1 and Claspin play key roles in activating the intra S-phase checkpoint and in stabilizing the stalled replication forks. Here, we discuss the specific contribution of these factors in preserving fork structure and ensuring accurate completion of DNA replication.
引用
收藏
页码:222 / 235
页数:14
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