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Nucleic Acids Research 2004 32(17):5104-5112; doi:10.1093/nar/gkh848
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Published online 27 September 2004

Nucleic Acids Research, Vol. 32 No. 17 © Oxford University Press 2004; all rights reserved

DNA polymerase ß overexpression stimulates the Rad51-dependent homologous recombination in mammalian cells

Yvan Canitrot, Jean-Pascal Capp, Nadine Puget, Anne Bieth, Bernard Lopez1, Jean-Sébastien Hoffmann and Christophe Cazaux*

Genetic Instability and Cancer Group, Institut de Pharmacologie et de Biologie Structurale UMR CNRS 5089, 205 route de Narbonne, 31077 Toulouse, France and 1 Département de Radiobiologie et Radiopathologie, 60-68 avenue Gal Leclerc, UMR 217 CNRS-CEA, 92265 Fontenay aux Roses cedex, France

* To whom correspondence should be addressed at Genetic Instability and Cancer Group, Institut de Pharmacologie et de Biologie Structurale UMR CNRS 5089, 205 route de Narbonne, 31077 Toulouse cedex 4, France. Tel: 33 5 61 17 59 61; Fax: 33 5 61 17 59 94; Email: cazaux{at}ipbs.fr
Correspondence may also be addressed to Jean-Sébastien Hoffmann. Tel: +33 5 61 17 59 75; Fax: +33 5 61 17 59 94; Email: jseb{at}ipbs.fr

Received July 27, 2004; Revised and Accepted September 7, 2004

Overexpression of DNA polymerase ß (polß), an error-prone DNA repair enzyme, has been shown to result in mutagenesis, aneuploidy and tumorigenesis. To further investigate the molecular basis leading to cancer-associated genetic changes, we examined whether the DNA polß could affect homologous recombination (HR). Using mammalian cells carrying an intrachromosomal recombination marker we showed that the DNA polß overexpression increased the HR mostly by enhancing gene conversion. Concomitantly, we observed the generation of DNA strand breaks as well as a DNA polß-dependent formation of Rad51 foci. The stimulation of HR was abolished by the coexpression of a dominant negative form of Rad51, suggesting that the Rad51 was involved in the increased HR events. The expression of different DNA polß mutants lacking polymerase activity did not result in HR stimulation, indicating that the DNA synthesis activity of DNA polß was related to this phenotype. These results provide new insights into the molecular mechanisms of the genetic instability observed in DNA polß overexpressing tumour cells.


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