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Published online
doi:10.1083/jcb.200811079
The Journal of Cell Biology, Vol. 185, No. 4, 587-600
The Rockefeller University Press, 0021-9525 $30.00
© Badie et al.
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Article

RAD51C facilitates checkpoint signaling by promoting CHK2 phosphorylation



Sophie Badie, Chunyan Liao, Maria Thanasoula, Paul Barber, Mark A. Hill, and Madalena Tarsounas

Cancer Research UK/Medical Research Council Gray Institute for Radiation Oncology and Biology, University of Oxford, Oxford OX3 7DQ, England, UK

Correspondence to Madalena Tarsounas: madalena.tarsounas{at}rob.ox.ac.uk

The RAD51 paralogues act in the homologous recombination (HR) pathway of DNA repair. Human RAD51C (hRAD51C) participates in branch migration and Holliday junction resolution and thus is important for processing HR intermediates late in the DNA repair process. Evidence for early involvement of RAD51 during DNA repair also exists, but its function in this context is not understood. In this study, we demonstrate that RAD51C accumulates at DNA damage sites concomitantly with the RAD51 recombinase and is retained after RAD51 disassembly, which is consistent with both an early and a late function for RAD51C. RAD51C recruitment depends on ataxia telangiectasia mutated, NBS1, and replication protein A, indicating it functions after DNA end resection but before RAD51 assembly. Furthermore, we find that RAD51C is required for activation of the checkpoint kinase CHK2 and cell cycle arrest in response to DNA damage. This suggests that hRAD51C contributes to the protection of genome integrity by transducing DNA damage signals in addition to engaging the HR machinery.

Abbreviations used in this paper: ATM, ataxia telangiectasia mutated; ATR, ATM related; CENP-F, centromeric protein F; DSB, double-stranded DNA break; HR, homologous recombination; hRAD51C, human RAD51C; HU, hydroxyurea; IR, ionizing radiation; MEF, mouse embryonic fibroblast; MRN, MRE11–RAD50–NBS1; RPA, replication protein A; shRNA, short hairpin RNA; ssDNA, single-stranded DNA.

© 2009 Badie et al.
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