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

Research output: Contribution to Journal/MagazineJournal articlepeer-review

  • J. Henry-Mowatt
  • D. Jackson
  • Y. J. Masson
  • P. A. Johnson
  • P. M. Clements
  • Fiona E. Benson
  • L. H. Thompson
  • S. Takeda
  • S. C. West
  • K. W. Caldecott
<mark>Journal publication date</mark>04/2003
<mark>Journal</mark>Molecular Cell
Issue number4
Number of pages9
Pages (from-to)1109-1117
Publication StatusPublished
<mark>Original language</mark>English


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.