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Nucleic Acids Res. 2001 Feb 1;29(3):662-7.

RAD51 supports spontaneous non-homologous recombination in mammalian cells, but not the corresponding process induced by topoisomerase inhibitors.

Author information

1
Department of Genetic and Cellular Toxicology, Wallenberg Laboratory, Stockholm University, Lilla Frescativ. 7, S-106 91 Stockholm, Sweden.

Abstract

The RAD51 protein has been shown to participate in homologous recombination by promoting ATP-dependent homologous pairing and strand transfer reactions. In the present study, we have investigated the possible involvement of RAD51 in non-homologous recombination. We demonstrate that overexpression of CgRAD51 enhances the frequency of spontaneous non-homologous recombination in the hprt gene of Chinese hamster cells. However, the rate of non-homologous recombination induced by the topoisomerase inhibitors campothecin and etoposide was not altered by overexpression of RAD51. These results indicate that the RAD51 protein may perform a function in connection with spontaneous non-homologous recombination that is not essential to or not rate-limiting for non-homologous recombination induced by camptothecin or etoposide. We discuss the possibility that the role played by RAD51 in non-homologous recombination observed here may not be linked to non-homologous end-joining.

PMID:
11160887
PMCID:
PMC30407
DOI:
10.1093/nar/29.3.662
[Indexed for MEDLINE]
Free PMC Article

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