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Vol. 13, No. 20, pp. 2633-2638, October 15, 1999
1 Cell Biology Program, Memorial Sloan-Kettering Cancer
Center and Cornell University Graduate School of Medical Sciences, New
York, New York 10021 USA; 2 Biology and Biotechnology Research
Program, Lawrence Livermore National Laboratory,
Livermore, California 94551 USA
Homology-directed repair of DNA damage has recently emerged as a
major mechanism for the maintenance of genomic integrity in mammalian
cells. The highly conserved strand transferase, Rad51, is expected to
be critical for this process. XRCC3 possesses a limited sequence
similarity to Rad51 and interacts with it. Using a novel
fluorescence-based assay, we demonstrate here that error-free homology-directed repair of DNA double-strand breaks is decreased 25-fold in an XRCC3-deficient hamster cell line and can be restored to
wild-type levels through XRCC3 expression. These results establish that
XRCC3-mediated homologous recombination can reverse DNA damage that
would otherwise be mutagenic or lethal.
[Key Words: Homologous recombination; double-strand break repair; gene conversion; mammalian cells; XRCC3; Rad51-related proteins]
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