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XRCC3 and Rad51 modulate replication fork progression on damaged vertebrate chromosomes
journal contributionposted on 2023-06-07, 19:08 authored by 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 CaldecottKeith Caldecott
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.
Department affiliated with
- Sussex Centre for Genome Damage Stability Publications
NotesMost (~80%) of the work was conducted in my lab, with ~20% provided by the DJ lab. I was senior and corresponding author, and the other authors provided materials.Shoed that recombination proteinns modulate replication for progression.
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