ArticlePLoS genetics2010
Defective resection at DNA double-strand breaks leads to de novo telomere formation and enhances gene targeting.
Article in PLoS genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 132 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
132 citing papers in PubMed, 174 citations in OpenAlex.
- Dpb11 facilitates the colocalization of Mec1-Ddc2 with its activators on gapped DNA.Cell reports · 2026Article
- CST complex promotes second-strand synthesis in break-induced replication.Nature structural & molecular biology · 2026Article
- Genome-wide screen reveals dependence of break induced replication on several distinct checkpoints.Nature communications · 2025Article
- Molecular interplay between the DNA damage checkpoint kinase Mec1-Ddc2 and its activator Dpb11 on gapped DNA.bioRxiv : the preprint server for biology · 2025Article
- The editable landscape of the yeast genome reveals hotspots of structural variant formation.Science advances · 2025Article
- Insight into meiotic DNA end resection: Mechanisms and regulation.DNA repair · 2025Review
- Catalytically inactive Cas9 attenuates DNA end resection: A potential application for region-restricted random mutagenesis.iScience · 2025Article
- Assessment and Mitigation of CRISPR-Cas9-Induced Nontargeted Translocations.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- RPA and Rad27 limit templated and inverted insertions at DNA breaks.Nucleic acids research · 2025Article
- Interstitial telomeric sequences promote gross chromosomal rearrangement via multiple mechanisms.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Mechanism of BCDX2-mediated RAD51 nucleation on short ssDNA stretches and fork DNA.Nucleic acids research · 2024Article
- Stressed? Break-induced replication comes to the rescue!DNA repair · 2024Review
- Article
- The functional significance of the RPA- and PCNA-dependent recruitment of Pif1 to DNA.EMBO reports · 2024Article
- Gene duplication and deletion caused by over-replication at a fork barrier.Nature communications · 2023Article
- Article
- ssDNA accessibility of Rad51 is regulated by orchestrating multiple RPA dynamics.Nature communications · 2023Article
- Flexible Attachment and Detachment of Centromeres and Telomeres to and from Chromosomes.Biomolecules · 2023Review
- Cdc14 phosphatase counteracts Cdk-dependent Dna2 phosphorylation to inhibit resection during recombinational DNA repair.Nature communications · 2023Article
- Simple-to-use CRISPR-SpCas9/SaCas9/AsCas12a vector series for genome editing in Saccharomyces cerevisiae.G3 (Bethesda, Md.) · 2021Article
72 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 1 country.
Funding
Abstract
The formation of single-stranded DNA (ssDNA) at double-strand break (DSB) ends is essential in repair by homologous recombination and is mediated by DNA helicases and nucleases. Here we estimated the length of ssDNA generated during DSB repair and analyzed the consequences of elimination of processive resection pathways mediated by Sgs1 helicase and Exo1 nuclease on DSB repair fidelity. In wild-type cells during allelic gene conversion, an average of 2-4 kb of ssDNA accumulates at each side of the break. Longer ssDNA is formed during ectopic recombination or break-induced replication (BIR), reflecting much slower repair kinetics. This relatively extensive resection may help determine sequences involved in homology search and prevent recombination within short DNA repeats next to the break. In sgs1Delta exo1Delta mutants that form only very short ssDNA, allelic gene conversion decreases 5-fold and DSBs are repaired by BIR or de novo telomere formation resulting in loss of heterozygosity. The absence of the telomerase inhibitor, PIF1, increases de novo telomere pathway usage to about 50%. Accumulation of Cdc13, a protein recruiting telomerase, at the break site increases in sgs1Delta exo1Delta, and the requirement of the Ku complex for new telomere formation is partially bypassed. In contrast to this decreased and alternative DSB repair, the efficiency and accuracy of gene targeting increases dramatically in sgs1Delta exo1Delta cells, suggesting that transformed DNA is very stable in these mutants. Altogether these data establish a new role for processive resection in the fidelity of DSB repair.
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.