Compensatory role for Rad52 during recombinational repair in Ustilago maydis.

TitleCompensatory role for Rad52 during recombinational repair in Ustilago maydis.
Publication TypeJournal Article
Year of Publication2008
AuthorsKojic M, Mao N, Zhou Q, Lisby M, Holloman WK
JournalMol Microbiol
Date Published2008 Mar
KeywordsAmino Acid Sequence, Animals, DNA Repair, Fungal Proteins, Green Fluorescent Proteins, Humans, Molecular Sequence Data, Mutagenesis, Phenotype, Rad51 Recombinase, Rad52 DNA Repair and Recombination Protein, Rec A Recombinases, Recombinant Fusion Proteins, Recombination, Genetic, Sequence Alignment, Sequence Homology, Amino Acid, Ultraviolet Rays, Ustilago

A single Rad52-related protein is evident by blast analysis of the Ustilago maydis genome database. Mutants created by disruption of the structural gene exhibited few discernible defects in resistance to UV, ionizing radiation, chemical alkylating or cross-linking agents. No deficiency was noted in spontaneous mutator activity, allelic recombination or meiosis. GFP-Rad51 foci were formed in rad52 cells following DNA damage, but were initially less intense than normal suggesting a possible role for Rad52 in formation of the Rad51 nucleoprotein filament. A search for interacting genes that confer a synthetic fitness phenotype with rad52 after DNA damage by UV irradiation identified the genes for Mph1, Ercc1 and the Rad51 paralogue Rec2. Testing known mutants in recombinational repair revealed an additional interaction with the BRCA2 orthologue Brh2. Suppression of the rec2 mutant's UV sensitivity by overexpressing Brh2 was found to be dependent on Rad52. The results suggest that Rad52 serves in an overlapping, compensatory role with both Rec2 and Brh2 to promote and maintain formation of the Rad51 nucleoprotein filament.

Alternate JournalMol. Microbiol.
PubMed ID18208529
Grant ListGM42482 / GM / NIGMS NIH HHS / United States
GM79859 / GM / NIGMS NIH HHS / United States

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