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XRCC3 and RAD51 modulate replication fork progression on damaged vertebrate chromosomes.

Henry-Mowatt, J. and Jackson, D. and Masson, Y. J. and Johnson, P. A. and Clements, P. M. and Benson, Fiona E. and Thompson, L. H. and Takeda, S. and West, S. C. and Caldecott, K. W. (2003) XRCC3 and RAD51 modulate replication fork progression on damaged vertebrate chromosomes. Molecular Cell, 11 (4). pp. 1109-1117. ISSN 1097-2765

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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.

Item Type: Article
Journal or Publication Title: Molecular Cell
Subjects: Q Science > QH Natural history > QH301 Biology
Departments: Faculty of Health and Medicine > Biomedical & Life Sciences
ID Code: 9043
Deposited By: Dr Fiona E Benson
Deposited On: 21 May 2008 15:26
Refereed?: Yes
Published?: Published
Last Modified: 09 Apr 2014 22:15
Identification Number:
URI: http://eprints.lancs.ac.uk/id/eprint/9043

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