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XRCC3 and Rad51 modulate replication fork progression on damaged vertebrate chromosomes

被引：135
作者：
Henry-Mowatt, J
Jackson, D
Masson, JY
Johnson, PA
Clements, PM
Benson, FE
Thompson, LH
Takeda, S
West, SC
Caldecott, KW
机构：
[1] Univ Manchester, Inst Sci & Technol, Dept Biomol Sci, Manchester M60 1QD, Lancs, England
[2] Canc Res UK, Clare Hall Labs, S Mimms EN6 3LD, Herts, England
[3] Univ Manchester, InterCytex, Manchester M13 9PT, Lancs, England
[4] Univ Lancaster, Inst Environm & Nat Sci, Dept Biol Sci, Lancaster LA1 4YQ, England
[5] Lawrence Livermore Natl Lab, Livermore, CA 94551 USA
[6] Kyoto Univ, Sch Med, Dept Radiat Biol, Sakyo Ku, Kyoto 6068501, Japan
[7] Univ Manchester, Sch Biol Sci, Manchester M13 9PT, Lancs, England
来源：
MOLECULAR CELL | 2003年 / 11卷 / 04期
基金：
英国医学研究理事会;
关键词：
D O I：
10.1016/S1097-2765(03)00132-1
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：
The mechanisms by which the progression of eukaryotic replication forks is controlled after DNA damage are unclear. We have found that fork progression is slowed by cisplatin or UV treatment in intact vertebrate cells and in replication assays in vitro. Fork slowing is reduced or absent in irs1SF CHO cells and XRCC3(-/-) chicken DT40 cells, indicating that fork slowing is an active process that requires the homologous recombination protein XRCC3. The addition of purified human Rad51C-XRCC3 complex restores fork slowing in permeabilized XRCC3(-/-) cells. Moreover, the requirement for XRCC3 for fork slowing can be circumvented by addition of human Rad51. These data demonstrate that the recombination proteins XRCC3 and Rad(51) cooperatively modulate the progression of replication forks on damaged vertebrate chromosomes.
引用
收藏
页码：1109 / 1117
页数：9
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