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PMID: 9774658 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

Targeted inactivation of mouse RAD52 reduces homologous recombination but not resistance to ionizing radiation.

Molecular and cellular biology ·Vol. 18 ·No. 11 ·1998-11-00 ·Pages 6423-9

Rijkers T, Van Den Ouweland J, Morolli B, Rolink AG, Baarends WM, Van Sloun PP, Lohman PH, Pastink A

Abstract

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.

MeSH Terms
Animals B-Lymphocytes/metabolism Cell Survival/radiation effects DNA Damage/genetics DNA Repair/genetics DNA-Binding Proteins/physiology Flow Cytometry Immunoglobulin Switch Region/genetics Mice Mice, Knockout Phenotype Rad52 DNA Repair and Recombination Protein Radiation, Ionizing Recombination, Genetic/genetics Saccharomyces cerevisiae/physiology Stem Cells/metabolism T-Lymphocytes/metabolism X-Rays
Chemicals
DNA-Binding Proteins Rad52 DNA Repair and Recombination Protein Rad52 protein, mouse
Authors & Affiliations
8 authors, click to expand affiliations / ORCID
Rijkers T
MGC-Department of Radiation Genetics and Chemical Mutagenesis, Leiden University Medical Center, Leiden, The Netherlands.
Van Den Ouweland J
Morolli B
Rolink A G
Baarends W M
Van Sloun P P
Lohman P H
Pastink A
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Article Info
Journal
Molecular and cellular biology
Abbr.
Mol Cell Biol
ISSN
0270-7306
Published
1998-11-00
Pages
6423-9
Language
English
Region
United States
NLM ID
8109087
PMCID
PMC109228
Subset
IM
Analysis Services
Analysis Services

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