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Nucleic Acids Research, 2001, Vol. 29, No. 3 662-667
© 2001 Oxford University Press

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

Catherine Arnaudeau1, Lorène Rozier1, Christophe Cazaux2, Martine Defais2, Dag Jenssen1 and Thomas Helleday1,3,*

1Department of Genetic and Cellular Toxicology, Wallenberg Laboratory, Stockholm University, Lilla Frescativ. 7, S-106 91 Stockholm, Sweden, 2Institut de Pharmacologie et de Biologie Structurale, Centre National de la Recherche Scientifique, UMP 5089, 205 route de Narbonne, F-31077 Toulouse cedex 4, France and 3The Institute for Cancer Studies, University of Sheffield, Medical School, Beech Hill Road, Sheffield S10 2RX, UK

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.

* To whom correspondence should be addressed at: Department of Genetic and Cellular Toxicology, Wallenberg Laboratory, Stockholm University, Lilla Frescativ. 7, S-106 91 Stockholm, Sweden. Tel: +46 8 163107; Fax: +46 8 6124004; Email: helleday{at}genetics.su.se


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