ArticleNature communications2017
Break-induced replication promotes formation of lethal joint molecules dissolved by Srs2.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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.
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Who cites it
52 citing papers in PubMed, 71 citations in OpenAlex.
- The SOS response acts as a regulatory switch that balances helicase anti-recombination with transcription-replication conflict resolution activities in Escherichia coli.G3 (Bethesda, Md.) · 2026Article
- Mechanisms That Govern Recombinase Fidelity Control During Eukaryotic Homologous Recombination.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- Potential Rad54 separation of function mutation highlights unique roles during homologous recombination.PLoS genetics · 2026Article
- Genome-wide screen reveals dependence of break induced replication on several distinct checkpoints.Nature communications · 2025Article
- SRS2 is required for MUS81-dependent CO formation in zmm mutants.PLoS genetics · 2025Article
- A large C-terminal Rad52 segment acts as a chaperone to Form and Stabilize Rad51 Filaments.Nature communications · 2025Article
- Biochemical Mechanisms of Genetic Recombination and DNA Repair.Annual review of biochemistry · 2025Review
- Repair of replication-dependent double-strand breaks differs between the leading and lagging strands.Molecular cell · 2025Article
- Switch-like phosphorylation of WRN integrates end-resection with RAD51 metabolism at collapsed replication forks.Nucleic acids research · 2024Article
- Stressed? Break-induced replication comes to the rescue!DNA repair · 2024Review
- Concurrent D-loop cleavage by Mus81 and Yen1 yields half-crossover precursors.Nucleic acids research · 2024Article
- Review
- Separation of function mutants underline multiple roles of the Srs2 helicase/translocase in break-induced replication inmicroPublication biology · 2024Article
- Telomere-related DNA damage response pathways in cancer therapy: prospective targets.Frontiers in pharmacology · 2024Review
- The separation pin distinguishes the pro- and anti-recombinogenic functions of Saccharomyces cerevisiae Srs2.Nature communications · 2023Article
- Delineation of two multi-invasion-induced rearrangement pathways that differently affect genome stability.Genes & development · 2023Article
- A nuclear orthologue of the dNTP triphosphohydrolase SAMHD1 controls dNTP homeostasis and genomic stability inFrontiers in cellular and infection microbiology · 2023Article
- Contribution of Microhomology to Genome Instability: Connection between DNA Repair and Replication Stress.International journal of molecular sciences · 2022Review
- Repair of mismatched templates during Rad51-dependent Break-Induced Replication.PLoS genetics · 2022Article
- Break-induced replication: unraveling each step.Trends in genetics : TIG · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
Break-induced replication (BIR) is a DNA double-strand break repair pathway that leads to genomic instabilities similar to those observed in cancer. BIR proceeds by a migrating bubble where asynchrony between leading and lagging strand synthesis leads to accumulation of long single-stranded DNA (ssDNA). It remains unknown how this ssDNA is prevented from unscheduled pairing with the template, which can lead to genomic instability. Here, we propose that uncontrolled Rad51 binding to this ssDNA promotes formation of toxic joint molecules that are counteracted by Srs2. First, Srs2 dislodges Rad51 from ssDNA preventing promiscuous strand invasions. Second, it dismantles toxic intermediates that have already formed. Rare survivors in the absence of Srs2 rely on structure-specific endonucleases, Mus81 and Yen1, that resolve toxic joint-molecules. Overall, we uncover a new feature of BIR and propose that tight control of ssDNA accumulated during this process is essential to prevent its channeling into toxic structures threatening cell viability.
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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.