ArticleGenetics1999
A core activity associated with the N terminus of the yeast RAD52 protein is revealed by RAD51 overexpression suppression of C-terminal rad52 truncation alleles.
Article in Genetics, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- Mechanism of Rad51 filament formation by Rad52 and Rad55-Rad57 in homologous recombination.Nature communications · 2025Article
- Biochemical characterization of the RNA-binding and RNA-DNA strand exchange activities of the human RAD52 protein.Journal of biochemistry · 2023Article
- Review
- Rad51 inhibits translocation formation by non-conservative homologous recombination in Saccharomyces cerevisiae.PloS one · 2010Article
- Interaction with RPA is necessary for Rad52 repair center formation and for its mediator activity.The Journal of biological chemistry · 2008Article
- The consequences of Rad51 overexpression for normal and tumor cells.DNA repair · 2008Review
- Molecular anatomy of the recombination mediator function of Saccharomyces cerevisiae Rad52.The Journal of biological chemistry · 2008Article
- Article
- Rad52 promotes postinvasion steps of meiotic double-strand-break repair.Molecular cell · 2008Article
- Rad52 multimerization is important for its nuclear localization in Saccharomyces cerevisiae.DNA repair · 2008Article
- Conservative repair of a chromosomal double-strand break by single-strand DNA through two steps of annealing.Molecular and cellular biology · 2006Article
- Different mating-type-regulated genes affect the DNA repair defects of Saccharomyces RAD51, RAD52 and RAD55 mutants.Genetics · 2006Article
- Cells expressing murine RAD52 splice variants favor sister chromatid repair.Molecular and cellular biology · 2006Article
- Multiple start codons and phosphorylation result in discrete Rad52 protein species.Nucleic acids research · 2006Article
- The N-terminal DNA-binding domain of Rad52 promotes RAD51-independent recombination in Saccharomyces cerevisiae.Genetics · 2003Article
- Investigation of the stability of yeast rad52 mutant proteins uncovers post-translational and transcriptional regulation of Rad52p.Genetics · 2003Article
- Role of RAD52 epistasis group genes in homologous recombination and double-strand break repair.Microbiology and molecular biology reviews : MMBR · 2002Review
- Structure of the single-strand annealing domain of human RAD52 protein.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Assembly of RecA-like recombinases: distinct roles for mediator proteins in mitosis and meiosis.Proceedings of the National Academy of Sciences of the United States of America · 2001Review
- Links between replication and recombination in Saccharomyces cerevisiae: a hypersensitive requirement for homologous recombination in the absence of Rad27 activity.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
C-terminal rad52 truncation and internal deletion mutants were characterized for their ability to repair MMS-induced double-strand breaks and to produce viable spores during meiosis. The rad52-Delta251 allele, encoding the N-terminal 251 amino acids of the predicted 504-amino-acid polypeptide, supports partial activity for both functions. Furthermore, RAD51 overexpression completely suppresses the MMS sensitivity of a rad52-Delta251 mutant. The absence of the C terminus in the truncated protein makes it likely that suppression occurs by bypassing the C-terminal functions of Rad52p. RAD51 overexpression does not suppress the low level of spore viability that the rad52-Delta251 allele causes and only partially suppresses the defect in rad52 alleles encoding the N-terminal 292 or 327 amino acids. The results of this study also show that intragenic complementation between rad52 alleles is governed by a complex relationship that depends heavily on the two alleles involved and their relative dosage. In heteroallelic rad52 diploids, the rad52-Delta251 allele does not complement rad52 missense mutations altering residues 61 or 64 in the N terminus. However, complementation is achieved with each of these missense alleles when the rad52-Delta251 allele is overexpressed. Complementation also occurs between rad52-Delta327 and an internal deletion allele missing residues 210 through 327. We suggest that the first 251 amino acids of Rad52p constitute a core domain that provides critical RAD52 activities.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.