ArticlePLoS genetics2009
RAD50 is required for efficient initiation of resection and recombinational repair at random, gamma-induced double-strand break ends.
Article in PLoS genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 45 citations in OpenAlex.
- Take a Break to Repair: A Dip in the World of Double-Strand Break Repair Mechanisms Pointing the Gaze on Archaea.International journal of molecular sciences · 2021Review
- Mechanisms restraining break-induced replication at two-ended DNA double-strand breaks.The EMBO journal · 2021Article
- Structural parameters of palindromic repeats determine the specificity of nuclease attack of secondary structures.Nucleic acids research · 2021Article
- The MRN complex promotes DNA repair by homologous recombination and restrains antigenic variation in African trypanosomes.Nucleic acids research · 2021Article
- Genetic and Molecular Approaches to Study Chromosomal Breakage at Secondary Structure-Forming Repeats.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Efficient DNA double-strand break formation at single or multiple defined sites in the Saccharomyces cerevisiae genome.Nucleic acids research · 2020Article
- DNA end resection and its role in DNA replication and DSB repair choice in mammalian cells.Experimental & molecular medicine · 2020Review
- Repair of multiple simultaneous double-strand breaks causes bursts of genome-wide clustered hypermutation.PLoS biology · 2019Article
- Guidelines for DNA recombination and repair studies: Cellular assays of DNA repair pathways.Microbial cell (Graz, Austria) · 2019Review
- Single-strand annealing between inverted DNA repeats: Pathway choice, participating proteins, and genome destabilizing consequences.PLoS genetics · 2018Article
- The global role for Cdc13 and Yku70 in preventing telomere resection across the genome.DNA repair · 2018Article
- Article
- The Vitamin E Analog Gamma-Tocotrienol (GT3) Suppresses Radiation-Induced Cytogenetic Damage.Pharmaceutical research · 2016Article
- Article
- Recombinational repair of radiation-induced double-strand breaks occurs in the absence of extensive resection.Nucleic acids research · 2016Article
- Tel1(ATM)-mediated interference suppresses clustered meiotic double-strand-break formation.Nature · 2015Article
- Cytokinesis breaks dicentric chromosomes preferentially at pericentromeric regions and telomere fusions.Genes & development · 2015Article
- DNA repair mechanisms and their biological roles in the malaria parasite Plasmodium falciparum.Microbiology and molecular biology reviews : MMBR · 2014Review
- Clustered and genome-wide transient mutagenesis in human cancers: Hypermutation without permanent mutators or loss of fitness.BioEssays : news and reviews in molecular, cellular and developmental biology · 2014Article
- Suppression of allelic recombination and aneuploidy by cohesin is independent of Chk1 in Saccharomyces cerevisiae.PloS one · 2014Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Resection of DNA double-strand break (DSB) ends is generally considered a critical determinant in pathways of DSB repair and genome stability. Unlike for enzymatically induced site-specific DSBs, little is known about processing of random "dirty-ended" DSBs created by DNA damaging agents such as ionizing radiation. Here we present a novel system for monitoring early events in the repair of random DSBs, based on our finding that single-strand tails generated by resection at the ends of large molecules in budding yeast decreases mobility during pulsed field gel electrophoresis (PFGE). We utilized this "PFGE-shift" to follow the fate of both ends of linear molecules generated by a single random DSB in circular chromosomes. Within 10 min after gamma-irradiation of G2/M arrested WT cells, there is a near-synchronous PFGE-shift of the linearized circular molecules, corresponding to resection of a few hundred bases. Resection at the radiation-induced DSBs continues so that by the time of significant repair of DSBs at 1 hr there is about 1-2 kb resection per DSB end. The PFGE-shift is comparable in WT and recombination-defective rad52 and rad51 strains but somewhat delayed in exo1 mutants. However, in rad50 and mre11 null mutants the initiation and generation of resected ends at radiation-induced DSB ends is greatly reduced in G2/M. Thus, the Rad50/Mre11/Xrs2 complex is responsible for rapid processing of most damaged ends into substrates that subsequently undergo recombinational repair. A similar requirement was found for RAD50 in asynchronously growing cells. Among the few molecules exhibiting shift in the rad50 mutant, the residual resection is consistent with resection at only one of the DSB ends. Surprisingly, within 1 hr after irradiation, double-length linear molecules are detected in the WT and rad50, but not in rad52, strains that are likely due to crossovers that are largely resection- and RAD50-independent.
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Registered trials
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