XRCC3 and Rad51 modulate replication fork progression on damaged vertebrate chromosomes

Judith Henry-Mowatt; Dean Jackson; Jean Yves Masson; Penny A. Johnson; Paula M. Clements; Fiona E. Benson; Larry H. Thompson; Shunichi Takeda; Stephen C. West; Keith W. Caldecott

doi:10.1016/S1097-2765(03)00132-1

XRCC3 and Rad51 modulate replication fork progression on damaged vertebrate chromosomes

Judith Henry-Mowatt, Dean Jackson, Jean Yves Masson, Penny A. Johnson, Paula M. Clements, Fiona E. Benson, Larry H. Thompson, Shunichi Takeda, Stephen C. West, Keith W. Caldecott

Research output: Contribution to journal › Article › peer-review

Abstract

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 Rad51 cooperatively modulate the progression of replication forks on damaged vertebrate chromosomes.

Original language	English
Pages (from-to)	1109-1117
Number of pages	8
Journal	Molecular Cell
Volume	11
Issue number	4
DOIs	https://doi.org/10.1016/S1097-2765(03)00132-1
Publication status	Published - 1 Apr 2003

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title = "XRCC3 and Rad51 modulate replication fork progression on damaged vertebrate chromosomes",

abstract = "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 Rad51 cooperatively modulate the progression of replication forks on damaged vertebrate chromosomes.",

author = "Judith Henry-Mowatt and Dean Jackson and Masson, {Jean Yves} and Johnson, {Penny A.} and Clements, {Paula M.} and Benson, {Fiona E.} and Thompson, {Larry H.} and Shunichi Takeda and West, {Stephen C.} and Caldecott, {Keith W.}",

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doi = "10.1016/S1097-2765(03)00132-1",

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T1 - XRCC3 and Rad51 modulate replication fork progression on damaged vertebrate chromosomes

AU - Henry-Mowatt, Judith

AU - Jackson, Dean

AU - Masson, Jean Yves

AU - Johnson, Penny A.

AU - Clements, Paula M.

AU - Benson, Fiona E.

AU - Thompson, Larry H.

AU - Takeda, Shunichi

AU - West, Stephen C.

AU - Caldecott, Keith W.

PY - 2003/4/1

Y1 - 2003/4/1

N2 - 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 Rad51 cooperatively modulate the progression of replication forks on damaged vertebrate chromosomes.

AB - 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 Rad51 cooperatively modulate the progression of replication forks on damaged vertebrate chromosomes.

U2 - 10.1016/S1097-2765(03)00132-1

DO - 10.1016/S1097-2765(03)00132-1

M3 - Article

SN - 1097-2765

VL - 11

SP - 1109

EP - 1117

JO - Molecular Cell

JF - Molecular Cell

IS - 4

ER -

XRCC3 and Rad51 modulate replication fork progression on damaged vertebrate chromosomes

Abstract

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