Rad52 protein stimulates DNA strand exchange by Rad51 and replication protein A

James H. New, Tomohiko Sugiyama, Elena Zaitseva, Stephen C. Kowalczykowski

Research output: Contribution to journalArticle

469 Citations (Scopus)

Abstract

The generation of a double-strand break in the Saccharomyces cerevisiae genome is a potentially catastrophic event that can induce cell-cycle arrest or ultimately result in loss of cell viability. The repair of such lesions is strongly dependent on proteins encoded by the RAD52 epistasis group of genes (RAD50-55, RAD57, MRE11, XRS2), as well as the RFA1 and RAD59 genes. rad52 mutants exhibit the most severe phenotypic defects in double-strand break repair, but almost nothing is known about the biochemical role of Rad52 protein. Rad51 protein promotes DNA strand exchange and acts similarly to RecA protein. Yeast Rad52 protein interacts with Rad51 protein, binds single- stranded DNA and stimulates annealing of complementary single-stranded DNA. We find that Rad52 protein stimulates DNA strand exchange by targeting Rad51 protein to a complex of replication protein A (RPA) with single-stranded DNA. Rad52 protein affects an early step in the reaction, presynaptic filament formation, by overcoming the inhibitory effects of the competitor, RPA. Furthermore, stimulation is dependent on the concerted action of both Rad51 protein and RPA, implying that specific protein-protein interactions between Rad52 protein, Rad51 protein and RPA are required.

Original languageEnglish (US)
Pages (from-to)407-410
Number of pages4
JournalNature
Volume391
Issue number6665
DOIs
StatePublished - Jan 22 1998

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Rad52 DNA Repair and Recombination Protein
Replication Protein A
DNA
Single-Stranded DNA
Proteins
Rec A Recombinases
Fungal Proteins
Protein Transport
Cell Cycle Checkpoints
Genes
Saccharomyces cerevisiae
Cell Survival
Complementary DNA
Genome

ASJC Scopus subject areas

  • General

Cite this

New, J. H., Sugiyama, T., Zaitseva, E., & Kowalczykowski, S. C. (1998). Rad52 protein stimulates DNA strand exchange by Rad51 and replication protein A. Nature, 391(6665), 407-410. https://doi.org/10.1038/34950

Rad52 protein stimulates DNA strand exchange by Rad51 and replication protein A. / New, James H.; Sugiyama, Tomohiko; Zaitseva, Elena; Kowalczykowski, Stephen C.

In: Nature, Vol. 391, No. 6665, 22.01.1998, p. 407-410.

Research output: Contribution to journalArticle

New, JH, Sugiyama, T, Zaitseva, E & Kowalczykowski, SC 1998, 'Rad52 protein stimulates DNA strand exchange by Rad51 and replication protein A', Nature, vol. 391, no. 6665, pp. 407-410. https://doi.org/10.1038/34950
New JH, Sugiyama T, Zaitseva E, Kowalczykowski SC. Rad52 protein stimulates DNA strand exchange by Rad51 and replication protein A. Nature. 1998 Jan 22;391(6665):407-410. https://doi.org/10.1038/34950
New, James H. ; Sugiyama, Tomohiko ; Zaitseva, Elena ; Kowalczykowski, Stephen C. / Rad52 protein stimulates DNA strand exchange by Rad51 and replication protein A. In: Nature. 1998 ; Vol. 391, No. 6665. pp. 407-410.
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AB - The generation of a double-strand break in the Saccharomyces cerevisiae genome is a potentially catastrophic event that can induce cell-cycle arrest or ultimately result in loss of cell viability. The repair of such lesions is strongly dependent on proteins encoded by the RAD52 epistasis group of genes (RAD50-55, RAD57, MRE11, XRS2), as well as the RFA1 and RAD59 genes. rad52 mutants exhibit the most severe phenotypic defects in double-strand break repair, but almost nothing is known about the biochemical role of Rad52 protein. Rad51 protein promotes DNA strand exchange and acts similarly to RecA protein. Yeast Rad52 protein interacts with Rad51 protein, binds single- stranded DNA and stimulates annealing of complementary single-stranded DNA. We find that Rad52 protein stimulates DNA strand exchange by targeting Rad51 protein to a complex of replication protein A (RPA) with single-stranded DNA. Rad52 protein affects an early step in the reaction, presynaptic filament formation, by overcoming the inhibitory effects of the competitor, RPA. Furthermore, stimulation is dependent on the concerted action of both Rad51 protein and RPA, implying that specific protein-protein interactions between Rad52 protein, Rad51 protein and RPA are required.

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