ArticleGenetics2002
Mutations in homologous recombination genes rescue top3 slow growth in Saccharomyces cerevisiae.
Article in Genetics, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
64 citing papers in PubMed, 97 citations in OpenAlex.
- TOP1 and TOP2 complementarily maintain DNA replication fork progression in vertebrates.The Journal of biological chemistry · 2026Article
- The human Shu complex promotes RAD51 activity by modulating RPA dynamics on ssDNA.Nature communications · 2024Article
- Review
- Unresolved Recombination Intermediates Cause aGenetics · 2019Article
- Homologous recombination and the repair of DNA double-strand breaks.The Journal of biological chemistry · 2018Review
- Separable roles for Mec1/ATR in genome maintenance, DNA replication, and checkpoint signaling.Genes & development · 2018Article
- Sgs1 helicase is required for efficient PCNA monoubiquitination and translesion DNA synthesis in Saccharomyces cerevisiae.Current genetics · 2018Article
- Article
- Genome-wide mapping of sister chromatid exchange events in single yeast cells using Strand-seq.eLife · 2017Article
- The Shu complex is a conserved regulator of homologous recombination.FEMS yeast research · 2016Article
- Article
- Top2 and Sgs1-Top3 Act Redundantly to Ensure rDNA Replication Termination.PLoS genetics · 2015Article
- Top3-Rmi1 DNA single-strand decatenase is integral to the formation and resolution of meiotic recombination intermediates.Molecular cell · 2015Article
- Pervasive and essential roles of the Top3-Rmi1 decatenase orchestrate recombination and facilitate chromosome segregation in meiosis.Molecular cell · 2015Article
- Top3-Rmi1 dissolve Rad51-mediated D loops by a topoisomerase-based mechanism.Molecular cell · 2015Article
- Review
- Roles of type 1A topoisomerases in genome maintenance in Escherichia coli.PLoS genetics · 2014Article
- The dissolution of double Holliday junctions.Cold Spring Harbor perspectives in biology · 2014Review
- A saccharomyces cerevisiae RNase H2 interaction network functions to suppress genome instability.Molecular and cellular biology · 2014Article
- Article
4 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
6 authors at 1 institution in 1 country.
Funding
Abstract
In budding yeast, loss of topoisomerase III, encoded by the TOP3 gene, leads to a genomic instability phenotype that includes slow growth, hyper-sensitivity to genotoxic agents, mitotic hyper-recombination, increased chromosome missegregation, and meiotic failure. Slow growth and other defects of top3 mutants are suppressed by mutation of SGS1, which encodes the only RecQ helicase in S. cerevisiae. sgs1 is epistatic to top3, suggesting that the two proteins act in the same pathway. To identify other factors that function in the Sgs1-Top3 pathway, we undertook a genetic screen for non-sgs1 suppressors of top3 defects. We found that slow growth and DNA damage sensitivity of top3 mutants are suppressed by mutations in RAD51, RAD54, RAD55, and RAD57. In contrast, top3 mutants show extreme synergistic growth defects with mutations in RAD50, MRE11, XRS2, RDH54, and RAD1. We also analyzed recombination at the SUP4-o region, showing that in a rad51, rad54, rad55, or rad57 background top3Delta does not increase recombination to the same degree as in a wild-type strain. These results suggest that the presence of the Rad51 homologous recombination complex in a top3 background facilitates creation of detrimental intermediates by Sgs1. We present a model wherein Rad51 helps recruit Sgs1-Top3 to sites of replicative damage.
Indexed as
Identifiers
What OpenQuestion holds
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.