Post-replication repair in DT40 cells: translesion polymerises versus recombinases

被引:49
作者
Hochegger, H [1 ]
Sonoda, E [1 ]
Takeda, S [1 ]
机构
[1] Kyoto Univ, Fac Med, Dept Radiat Genet, Sakyo Ku, Kyoto 6068501, Japan
关键词
D O I
10.1002/bies.10403
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
Replication forks inevitably stall at damaged DNA in every cell cycle. The ability to overcome DNA lesions is an essential feature of the replication machinery. A variety of specialized polymerases have recently been discovered, which enable cells to replicate past various forms of damage by a process termed translesion synthesis. Alternatively, homologous recombination can be used to restart DNA replication across the lesion. Genetic and biochemical studies have shed light on the impact of those two post-replication repair pathways in bacteria and yeast. In vertebrates, however, a genetic approach to study post-replication repair has been compromised because many of the genes involved appear to be essential for embryonic development. We have taken advantage of the chicken cell line DT40 to perform a genetic analysis of translesion synthesis and homologous recombination and to characterize genetic interactions between these two pathways in vertebrates. In this article, we aim to summarize our current understanding of post-replication repair in DT40 in the perspective of bacterial, yeast and mammalian genetics. (C) 2004 Wiley Periodicals, Inc.
引用
收藏
页码:151 / 158
页数:8
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