ArticleMolecular cell2017
Homology Requirements and Competition between Gene Conversion and Break-Induced Replication during Double-Strand Break Repair.
Article in Molecular cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
65 citing papers in PubMed, 93 citations in OpenAlex.
- Replication Fork-Associated Checkpoint Mediator Mrc1/Claspin Acts in Arrest-Independent Double-Strand Break Survival.bioRxiv : the preprint server for biology · 2026Article
- Mechanisms That Govern Recombinase Fidelity Control During Eukaryotic Homologous Recombination.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- CST complex promotes second-strand synthesis in break-induced replication.Nature structural & molecular biology · 2026Article
- Highly mutagenic copying of telomeric circles promotes ALT establishment.Nature communications · 2026Article
- Mutations and structural variants arising during double-strand break repair.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Break-induced replication is activated to repair R-loop-associated double-strand breaks in SETX-deficient cells.Cell reports · 2025Article
- Mechanisms and genomic implications of break-induced replication.Nature structural & molecular biology · 2025Review
- Arp2/3 and type-I myosins control chromosome mobility and end-resection at double-strand breaks in S. cerevisiae.Nature communications · 2025Article
- Late steps of allelic break-induced replication suppress tandem duplication associated with BRCA1 deficiency.Nucleic acids research · 2025Article
- The Mediator Kinase Module regulates cell cycle re-entry and transcriptional responses following DNA damage.bioRxiv : the preprint server for biology · 2025Article
- The TONSL-MMS22L complex and FANCM form an interdependent complex on chromatin to counter replication stress.bioRxiv : the preprint server for biology · 2025Article
- Multifaceted roles of H2B mono-ubiquitylation in D-loop metabolism during homologous recombination repair.Nucleic acids research · 2025Article
- Evolutionary Nonindependence Between Human piRNAs and Their Potential Target Sites in Protein-Coding Genes.Journal of molecular evolution · 2025Article
- Review
- Stressed? Break-induced replication comes to the rescue!DNA repair · 2024Review
- The Fanconi anemia core complex promotes CtIP-dependent end resection to drive homologous recombination at DNA double-strand breaks.Nature communications · 2024Article
- Microsatellite break-induced replication generates highly mutagenized extrachromosomal circular DNAs.NAR cancer · 2024Article
- Rad53 regulates the lifetime of Rdh54 at homologous recombination intermediates.Nucleic acids research · 2023Article
- Article
- Timing of Chromosome DNA Integration throughout the Yeast Cell Cycle.Biomolecules · 2023Article
5 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
Saccharomyces cerevisiae mating-type switching is initiated by a double-strand break (DSB) at MATa, leaving one cut end perfectly homologous to the HMLα donor, while the second end must be processed to remove a non-homologous tail before completing repair by gene conversion (GC). When homology at the matched end is ≤150 bp, efficient repair depends on the recombination enhancer, which tethers HMLα near the DSB. Thus, homology shorter than an apparent minimum efficient processing segment can be rescued by tethering the donor near the break. When homology at the second end is ≤150 bp, second-end capture becomes inefficient and repair shifts from GC to break-induced replication (BIR). But when pol32 or pif1 mutants block BIR, GC increases 3-fold, indicating that the steps blocked by these mutations are reversible. With short second-end homology, absence of the RecQ helicase Sgs1 promotes gene conversion, whereas deletion of the FANCM-related Mph1 helicase promotes BIR.
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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.