Open AccessTargeted Inactivation of Mouse RAD52Reduces Homologous Recombination but Not Resistance to Ionizing Radiation
Author(s) -
Tonnie Rijkers,
Jody van den Ouweland,
Bruno Morolli,
A G Rolink,
Willy M. Baarends,
Petra P. H. Van Sloun,
P.H.M. Lohman,
Albert Pastink
Publication year - 1998
Publication title -
molecular and cellular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.14
H-Index - 327
eISSN - 1067-8824
pISSN - 0270-7306
DOI - 10.1128/mcb.18.11.6423
Subject(s) - rad52 , homologous recombination , biology , rad51 , dna repair , non homologous end joining , saccharomyces cerevisiae , genetics , microbiology and biotechnology , dna , mutant , dna damage , gene , flp frt recombination , gene targeting , genetic recombination , recombination
The RAD52 epistasis group is required for recombinational repair of double-strand breaks (DSBs) and shows strong evolutionary conservation. InSaccharomyces 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 ofRAD52 in embryonic stem (ES) cells resulted in a reduced frequency of homologous recombination. Unlike the yeastScrad52 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 inS. cerevisiae ,MmRAD52 is involved in recombination, although the repair of DNA damage is not affected upon inactivation, indicating thatMmRAD52 may be involved in certain types of DSB repair processes and not in others. The effect of inactivatingMmRAD52 suggests the presence of genes functionally related toMmRAD52 , which can partly compensate for the absence of MmRad52 protein.