Abstract
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.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Cell Line
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Cricetinae
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DNA Damage*
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DNA Repair / physiology*
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DNA-Binding Proteins / deficiency
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DNA-Binding Proteins / genetics
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DNA-Binding Proteins / metabolism*
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Gene Conversion
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Gene Expression
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Genetic Complementation Test
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Green Fluorescent Proteins
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Humans
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Luminescent Proteins / genetics
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Luminescent Proteins / metabolism
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Rad51 Recombinase
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Recombinant Proteins / genetics
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Recombinant Proteins / metabolism
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Recombination, Genetic
Substances
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DNA-Binding Proteins
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Luminescent Proteins
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Recombinant Proteins
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X-ray repair cross complementing protein 3
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Green Fluorescent Proteins
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RAD51 protein, human
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Rad51 Recombinase