Arrested replication fork processing: Interplay between checkpoints and recombination

被引:86
作者
Lambert, Sarah
Froget, Benoit
Carr, Antony M. [1 ]
机构
[1] Univ Sussex, Genome Damage & Stabil Ctr, Brighton BN1 6EQ, E Sussex, England
[2] Ctr Univ Orsay, Inst Curie, CNRS, UMR 2027, F-91405 Orsay, France
基金
英国医学研究理事会;
关键词
RFB; replication fork arrest; replication restart; RTS1; S-PHASE CHECKPOINT; DOUBLE-STRAND BREAKS; RNA-POLYMERASE-I; SPONTANEOUS MITOTIC RECOMBINATION; GROSS CHROMOSOMAL REARRANGEMENTS; HOLLIDAY JUNCTION RESOLVASE; IRRADIATED ESCHERICHIA-COLI; RIBOSOMAL DNA-REPLICATION; FISSION YEAST GENE; SCHIZOSACCHAROMYCES-POMBE;
D O I
10.1016/j.dnarep.2007.02.024
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
The arrest of DNA replication by DNA damage, nucleotide depletion, DNA-protein complexes or following clashes between transcription and replication factors all have the capacity to promote genome instability. In this review, we discuss how DNA replication is regulated by the checkpoint pathways that stabilise arrested replication forks and the recombination factors that process specific DNA structures resulting from fork arrest. We examine what is known about the interplay between the checkpoints and the recombination apparatus and review the evidence for a recombination-based fork restart pathway in eukaryotes. (C) 2007 Elsevier B.V. All rights reserved.
引用
收藏
页码:1042 / 1061
页数:20
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