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Molecular and Cellular Biology, November 1998, p. 6423-6429, Vol. 18, No. 11
0270-7306/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Targeted Inactivation of Mouse RAD52 Reduces Homologous Recombination but Not Resistance to Ionizing Radiation

Tonnie Rijkers,1 Jody Van Den Ouweland,1,dagger Bruno Morolli,1 Anton G. Rolink,2 Willy M. Baarends,3 Petra P. H. Van Sloun,1 Paul H. M. Lohman,1 and Albert Pastink1,*

MGC-Department of Radiation Genetics and Chemical Mutagenesis, Leiden University Medical Center, Leiden,1 and Department of Endocrinology and Reproduction, Faculty of Medicine and Health Sciences, Erasmus University, Rotterdam,3 The Netherlands, and Basel Institute for Immunology, Basel, Switzerland2

Received 16 April 1998/Returned for modification 1 June 1998/Accepted 27 July 1998

The RAD52 epistasis group is required for recombinational repair of double-strand breaks (DSBs) and shows strong evolutionary conservation. In Saccharomyces cerevisiae, RAD52 is one of the key members in this pathway. Strains with mutations in this gene show strong hypersensitivity to DNA-damaging agents and defects in recombination. Inactivation of the mouse homologue of RAD52 in embryonic stem (ES) cells resulted in a reduced frequency of homologous recombination. Unlike the yeast Scrad52 mutant, MmRAD52-/- ES cells were not hypersensitive to agents that induce DSBs. MmRAD52 null mutant mice showed no abnormalities in viability, fertility, and the immune system. These results show that, as in S. cerevisiae, MmRAD52 is involved in recombination, although the repair of DNA damage is not affected upon inactivation, indicating that MmRAD52 may be involved in certain types of DSB repair processes and not in others. The effect of inactivating MmRAD52 suggests the presence of genes functionally related to MmRAD52, which can partly compensate for the absence of MmRad52 protein.

* Corresponding author. Mailing address: MGC-Department of Radiation Genetics and Chemical Mutagenesis, Leiden University Medical Center, Sylvius Laboratory, Wassenaarseweg 72, 2333 AL Leiden, The Netherlands. Phone: 31-71-5271603. Fax: 31-71-5221615. E-mail: Pastink{at}rullf2.medfac.leidenuniv.nl.

dagger Present address: MGC-Department of Medical Biochemistry and Chemical Mutagenesis, Leiden University Medical Center, Leiden, The Netherlands.

Molecular and Cellular Biology, November 1998, p. 6423-6429, Vol. 18, No. 11
0270-7306/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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