Spontaneous homologous recombination is decreased in Rad51C-deficient hamster cells

The Chinese hamster cell mutant, CL-V4B that is mutated in the Rad51 paralog gene, Rad51C ( RAD51L2), has been described to exhibit increased sensitivity to DNA cross-linking agents, genomic instability, and an impaired Rad51 foci formation in response to DNA damage. To directly examine an effect of...

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Bibliographic Details
Published in:DNA repair 2004-10, Vol.3 (10), p.1335-1343
Main Authors: Drexler, Guido A., Rogge, Sandra, Beisker, Wolfgang, Eckardt-Schupp, Friederike, Zdzienicka, Malgorzata Z., Fritz, Eberhard
Format: Article
Language:English
Subjects:
Animals
Bacteriology
Biological and medical sciences
CHO Cells
Cricetinae
Cross-linking agents
DNA - genetics
DNA - metabolism
DNA damage
DNA-Binding Proteins - deficiency
Fibroblasts
Fundamental and applied biological sciences. Psychology
Growth, nutrition, cell differenciation
Homologous recombination
Ionizing radiation
Microbiology
Molecular and cellular biology
Molecular genetics
Mutagenesis. Repair
Rad51 paralogs
Rad51 Recombinase
Recombination, Genetic
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Summary:The Chinese hamster cell mutant, CL-V4B that is mutated in the Rad51 paralog gene, Rad51C ( RAD51L2), has been described to exhibit increased sensitivity to DNA cross-linking agents, genomic instability, and an impaired Rad51 foci formation in response to DNA damage. To directly examine an effect of the Rad51C protein on homologous recombination (HR) in mammalian cells, we compared the frequencies and rates of spontaneous HR in CL-V4B cells and in parental wildtype V79B cells, using a recombination reporter plasmid in host cell reactivation assays. Our results demonstrate that HR is reduced but not abolished in the CL-V4B mutant. We thus, provide direct evidence for a role of mammalian Rad51C in HR processes. The reduced HR events described here help to explain the deficient phenotypes observed in Rad51C mutants and support an accessory role of Rad51C in Rad51-mediated recombination.
ISSN:1568-7864
1568-7856
DOI:10.1016/j.dnarep.2004.05.002