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Xrcc3 is recruited to DNA double strand breaks early and independent of Rad51 by Anthony L. Forget; Brian T. Bennett; Kendall L. Knight is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

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## Abstract Rad51‐mediated homologous recombination (HR) is essential for maintenance of genome integrity. The Xrcc3 protein functions in HR DNA repair, and studies suggest it has multiple roles at different stages in this pathway. Defects in vertebrate __XRCC3__ result in elevated levels of spontaneous and DNA damage‐induced chromosomal abnormalities, as well as increased sensitivity to DNA damaging agents. Formation of DNA damaged‐induced nuclear Rad51 foci requires Xrcc3 and the other Rad51 paralog proteins (Rad51B, Rad51C, Rad51D, Xrcc2), thus supporting a model in which an early function of Xrcc3 involves promoting assembly of active Rad51 repair complexes. However, it is not known whether Xrcc3 or other Rad51 paralog proteins accumulate at DNA breaks, and if they do whether their stable association with breaks requires Rad51. Here we report for the first time that Xrcc3 forms distinct foci in human cells and that nuclear Xrcc3 begins to localize at sites of DNA damage within 10 min after radiation treatment. RNAi‐mediated knock down of Rad51 has no effect on the DNA damage‐induced localization of Xrcc3 to DNA breaks. Our data are consistent with a model in which Xrcc3 associa

Who reads Xrcc3 is recruited to DNA double strand breaks early and independent of Rad51?

Author

Anthony L. Forget; Brian T. Bennett; Kendall L. Knight

Publisher

John Wiley and Sons; Wiley (John Wiley & Sons); John Wiley & Sons Inc.; Wiley (ISSN 0730-2312)

Published

2004

Language

EN

Field

Biochemistry, Genetics and Molecular Biology (Life Sciences)