ArticleThe EMBO journal2010
Ku prevents Exo1 and Sgs1-dependent resection of DNA ends in the absence of a functional MRX complex or Sae2.
Article in The EMBO journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 209 papers.
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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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Who cites it
209 citing papers in PubMed.
- Mechanisms and disease relevance of DNA break repair pathway choice.Nature reviews. Molecular cell biology · 2026Review
- A Tel1-Rad9 axis links DNA double-strand break end-tethering to repair pathway choice.Nucleic acids research · 2026Article
- Ku70-SAP domain has an overlapping function with DNA-PKcs in limiting the lateral movement of the Ku ring along DNA.Nucleic acids research · 2026Article
- Insights into the functional coordination of LigD and Ku in bacterial nonhomologous end joining.Scientific reports · 2026Article
- Nonhomologous end joining-the importance of end tethering and beyond.Genes & development · 2026Review
- Visualization and quantification of rDNA instabilities in mammalian cells and mouse models.Nucleic acids research · 2026Article
- A role for nucleosome remodellers during resection of deprotected telomeres in yeast.PloS one · 2026Article
- 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
- Fmp45 promotes Rad53 dephosphorylation via Ptc2 interaction to attenuate checkpoint signaling and maintain genome stability.Journal, genetic engineering & biotechnology · 2025Article
- RAD50 missense variants differentially affect the DNA damage response and mitotic progression.FEBS letters · 2025Article
- The histone chaperone CAF-1 prevents homologous recombination-mediated instability of the budding yeast ribosomal DNA during replication-coupled DNA double-strand break repair.Nucleic acids research · 2025Article
- Article
- Pathogenic variants in MAEA disrupt DNA replication fork stability and are associated with developmental abnormalities in humans.Science advances · 2025Article
- Arp2/3 and type-I myosins control chromosome mobility and end-resection at double-strand breaks in S. cerevisiae.Nature communications · 2025Article
- DNA nicks in both leading and lagging strand templates can trigger break-induced replication.Molecular cell · 2025Article
- Article
- Proteasome-mediated degradation of long-range nucleases negatively regulates resection of DNA double-strand breaks.iScience · 2024Article
- FSP1 inhibition enhances olaparib sensitivity in BRCA-proficient ovarian cancer patients via a nonferroptosis mechanism.Cell death and differentiation · 2024Article
- Selective inhibition of DNA ligase IV provides additional efficacy to the treatment of anaplastic thyroid cancer.Frontiers in oncology · 2024Article
- Multi-step processing of replication stress-derived nascent strand DNA gaps by MRE11 and EXO1 nucleases.Nature communications · 2023Article
149 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors.
Funding
Abstract
In this study, we investigate the interplay between Ku, a central non-homologous end-joining component, and the Mre11-Rad50-Xrs2 (MRX) complex and Sae2, end-processing factors crucial for initiating 5'-3' resection of double-strand break (DSB) ends. We show that in the absence of end protection by Ku, the requirement for the MRX complex is bypassed and resection is executed by Exo1. In contrast, both the Exo1 and Sgs1 resection pathways contribute to DSB processing in the absence of Ku and Sae2 or when the MRX complex is intact, but functionally compromised by elimination of the Mre11 nuclease activity. The ionizing radiation sensitivity of a mutant defective for extensive resection (exo1Δ sgs1Δ) cannot be suppressed by the yku70Δ mutation, indicating that Ku suppression is specific to the initiation of resection. We provide evidence that replication-associated DSBs need to be processed by Sae2 for repair by homologous recombination unless Ku is absent. Finally, we show that the presence of Ku exacerbates DNA end-processing defects established in the sae2Δ sgs1Δ mutant, leading to its lethality.
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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.