ArticleThe EMBO journal2008
Break dosage, cell cycle stage and DNA replication influence DNA double strand break response.
Article in The EMBO journal, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 155 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.
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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
155 citing papers in PubMed, 232 citations in OpenAlex.
- The Role of Arp2/3 in End-Resection During DNA Double-Strand Break Repair.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- CTCF primes repressive chromatin for rapid BRCA1/BARD1 recruitment to drive homologous recombination repair of DNA double-strand breaks.Nucleic acids research · 2026Article
- CST complex promotes second-strand synthesis in break-induced replication.Nature structural & molecular biology · 2026Article
- Insights into Ovarian Cancer: Unraveling the Role of DNA Double-strand Break-related Genes in Pathogenesis and Therapeutic Avenues.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- Asymmetrical recognition and processing of double-strand breaks formed during DNA replication.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Cohesin reconstitution and homologous recombination repair of DNA double-strand breaks in late mitosis.eLife · 2025Article
- The CST complex mediates a post-resection non-homologous end joining repair pathway and promotes local deletions in Saccharomyces cerevisiae.Cell genomics · 2025Article
- Insight into meiotic DNA end resection: Mechanisms and regulation.DNA repair · 2025Review
- Arp2/3 and type-I myosins control chromosome mobility and end-resection at double-strand breaks in S. cerevisiae.Nature communications · 2025Article
- DNA Damage and Replication Stress Checkpoints.Annual review of biochemistry · 2025Review
- Multifaceted roles of H2B mono-ubiquitylation in D-loop metabolism during homologous recombination repair.Nucleic acids research · 2025Article
- Repair of replication-dependent double-strand breaks differs between the leading and lagging strands.Molecular cell · 2025Article
- Article
- CRISPR/Cas9-induced double-strand breaks in the huntingtin locus lead to CAG repeat contraction through DNA end resection and homology-mediated repair.BMC biology · 2024Article
- Yeast Nat4 regulates DNA damage checkpoint signaling through its N-terminal acetyltransferase activity on histone H4.PLoS genetics · 2024Article
- Yeast EndoG prevents genome instability by degrading extranuclear DNA species.Nature communications · 2024Article
- Cyclin F-EXO1 axis controls cell cycle-dependent execution of double-strand break repair.Science advances · 2024Article
- Proteasome-mediated degradation of long-range nucleases negatively regulates resection of DNA double-strand breaks.iScience · 2024Article
- Dbf4-dependent kinase promotes cell cycle controlled resection of DNA double-strand breaks and repair by homologous recombination.Nature communications · 2024Article
- Yeast EndoG prevents genome instability by degrading cytoplasmic DNA.Research square · 2024Article
95 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
2 authors at 1 institution in 1 country.
Funding
Abstract
DNA double strand breaks (DSBs) can be repaired by non-homologous end joining (NHEJ) or homology-directed repair (HR). HR requires nucleolytic degradation of 5' DNA ends to generate tracts of single-stranded DNA (ssDNA), which are also important for the activation of DNA damage checkpoints. Here we describe a quantitative analysis of DSB processing in the budding yeast Saccharomyces cerevisiae. We show that resection of an HO endonuclease-induced DSB is less extensive than previously estimated and provide evidence for significant instability of the 3' ssDNA tails. We show that both DSB resection and checkpoint activation are dose-dependent, especially during the G1 phase of the cell cycle. During G1, processing near the break is inhibited by competition with NHEJ, but extensive resection is regulated by an NHEJ-independent mechanism. DSB processing and checkpoint activation are more efficient in G2/M than in G1 phase, but are most efficient at breaks encountered by DNA replication forks during S phase. Our findings identify unexpected complexity of DSB processing and its regulation, and provide a framework for further mechanistic insights.
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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.