ArticleGenetics2005
A genetic screen for top3 suppressors in Saccharomyces cerevisiae identifies SHU1, SHU2, PSY3 and CSM2: four genes involved in error-free DNA repair.
Article in Genetics, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
68 citing papers in PubMed, 106 citations in OpenAlex.
- Mapping the genetic landscape of the DNA damage response with Cas12a-based combinatorial knockout screens.bioRxiv : the preprint server for biology · 2026Article
- A Rfa1-MN-based system reveals new factors involved in the rescue of broken replication forks.PLoS genetics · 2025Article
- Repair of DNA double-strand breaks in plant meiosis: role of eukaryotic RecA recombinases and their modulators.Plant reproduction · 2023Review
- RAD51 paralog function in replicative DNA damage and tolerance.Current opinion in genetics & development · 2021Review
- The Shu complex prevents mutagenesis and cytotoxicity of single-strand specific alkylation lesions.eLife · 2021Article
- Review
- Distinct pathways of homologous recombination controlled by the SWS1-SWSAP1-SPIDR complex.Nature communications · 2021Article
- Regulation of RAD51 at the Transcriptional and Functional Levels: What Prospects for Cancer Therapy?Cancers · 2021Review
- Review
- Genome Profiling for Aflatoxin BG3 (Bethesda, Md.) · 2020Article
- Cooperative interactions facilitate stimulation of Rad51 by the Swi5-Sfr1 auxiliary factor complex.eLife · 2020Article
- The human Shu complex functions with PDS5B and SPIDR to promote homologous recombination.Nucleic acids research · 2019Article
- Unresolved Recombination Intermediates Cause aGenetics · 2019Article
- The Rad51 paralogs facilitate a novel DNA strand specific damage tolerance pathway.Nature communications · 2019Article
- The BRCA Tumor Suppressor Network in Chromosome Damage Repair by Homologous Recombination.Annual review of biochemistry · 2019Review
- Article
- Homologous Recombination: To Fork and Beyond.Genes · 2018Review
- Shu complex SWS1-SWSAP1 promotes early steps in mouse meiotic recombination.Nature communications · 2018Article
- Sgs1 helicase is required for efficient PCNA monoubiquitination and translesion DNA synthesis in Saccharomyces cerevisiae.Current genetics · 2018Article
- Putting together and taking apart: assembly and disassembly of the Rad51 nucleoprotein filament in DNA repair and genome stability.Cell stress · 2018Review
8 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Helicases of the RecQ family and topoisomerase III are evolutionarily conserved proteins important for maintenance of genome stability. In Saccharomyces cerevisiae, loss of the TOP3 gene, encoding topoisomerase III, results in a phenotype of slow growth, DNA damage sensitivity, meiotic defects, and hyperrecombination. The sole RecQ helicase in budding yeast, Sgs1, interacts with Top3 both physically and genetically, and the two proteins are thought to act in concert in vivo. Much recent genetic and biochemical evidence points to the role of RecQ helicases and topoisomerase III in regulating homologous recombination (HR) during DNA replication. Previously, we found that mutations in HR genes partially suppress top3 slow growth. Here, we describe the analysis of four additional mutational suppressors of top3 defects: shu1, shu2, psy3, and csm2. These genes belong to one epistasis group and their protein products interact with each other, strongly suggesting that they function as a complex in vivo. Their mutant phenotype indicates that they are important for error-free repair of spontaneous and induced DNA lesions, protecting the genome from mutation. These mutants exhibit an epistatic relationship with rad52 and show altered dynamics of Rad52-YFP foci, suggesting a role for these proteins in recombinational repair.
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Registered trials
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.