ArticleMolecular and cellular biology1994
Mutations in XRS2 and RAD50 delay but do not prevent mating-type switching in Saccharomyces cerevisiae.
Article in Molecular and cellular biology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers.
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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.
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Who cites it
117 citing papers in PubMed, 230 citations in OpenAlex.
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- Checkpoint and recombination pathways independently suppress rates of spontaneous homology-directed chromosomal translocations in budding yeast.Frontiers in genetics · 2025Article
- Checkpoint Responses to DNA Double-Strand Breaks.Annual review of biochemistry · 2020Review
- Help or hindrance: how do microtubule-based forces contribute to genome damage and repair?Current genetics · 2020Review
- Modeling cancer genomic data in yeast reveals selection against ATM function during tumorigenesis.PLoS genetics · 2020Article
- Systematic analysis of linker histone PTM hotspots reveals phosphorylation sites that modulate homologous recombination and DSB repair.DNA repair · 2020Article
- Astral microtubule forces alter nuclear organization and inhibit DNA repair in budding yeast.Molecular biology of the cell · 2019Article
- The ATP-bound conformation of the Mre11-Rad50 complex is essential for Tel1/ATM activation.Nucleic acids research · 2019Article
- Review
- The MRX complex regulates Exo1 resection activity by altering DNA end structure.The EMBO journal · 2018Article
- Repair of a Site-Specific DNA Cleavage: Old-School Lessons for Cas9-Mediated Gene Editing.ACS chemical biology · 2018Review
- Dna2 initiates resection at clean DNA double-strand breaks.Nucleic acids research · 2017Article
- Genetic and biochemical evidences reveal novel insights into the mechanism underlyingJournal of biosciences · 2016Article
- Functions and regulation of the MRX complex at DNA double-strand breaks.Microbial cell (Graz, Austria) · 2016Review
- RPA homologs and ssDNA processing during meiotic recombination.Chromosoma · 2016Review
- MTE1 Functions with MPH1 in Double-Strand Break Repair.Genetics · 2016Article
- Role of Double-Strand Break End-Tethering during Gene Conversion in Saccharomyces cerevisiae.PLoS genetics · 2016Article
- Synthetic viability genomic screening defines Sae2 function in DNA repair.The EMBO journal · 2015Article
- Interdependence of the rad50 hook and globular domain functions.Molecular cell · 2015Article
57 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
5 authors at 2 institutions in 2 countries.
Funding
Abstract
In Saccharomyces cerevisiae, a large number of genes in the RAD52 epistasis group has been implicated in the repair of chromosomal double-strand breaks and in both mitotic and meiotic homologous recombination. While most of these genes are essential for yeast mating-type (MAT) gene switching, neither RAD50 nor XRS2 is required to complete this specialized mitotic gene conversion process. Using a galactose-inducible HO endonuclease gene to initiate MAT switching, we have examined the effect of null mutations of RAD50 and of XRS2 on intermediate steps of this recombination event. Both rad50 and xrs2 mutants exhibit a marked delay in the completion of switching. Both mutations reduce the extent of 5'-to-3' degradation from the end of the HO-created double-strand break. The steps of initial strand invasion and new DNA synthesis are delayed by approximately 30 min in mutant cells. However, later events are still further delayed, suggesting that XRS2 and RAD50 affect more than one step in the process. In the rad50 xrs2 double mutant, the completion of MAT switching is delayed more than in either single mutant, without reducing the overall efficiency of the process. The XRS2 gene encodes an 854-amino-acid protein with no obvious similarity to the Rad50 protein or to any other protein in the database. Overexpression of RAD50 does not complement the defects in xrs2 or vice versa.
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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.