ArticleNucleic acids research2018
Structurally distinct Mre11 domains mediate MRX functions in resection, end-tethering and DNA damage resistance.
Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 28 citations in OpenAlex.
- A Tel1-Rad9 axis links DNA double-strand break end-tethering to repair pathway choice.Nucleic acids research · 2026Article
- The expanding roles of homologous recombination proteins in genome stability.The EMBO journal · 2026Review
- The Ku complex promotes DNA end-bridging and this function is antagonized by Tel1/ATM kinase.Nucleic acids research · 2023Article
- Yeast-based screening of cancer mutations in the DNA damage response protein Mre11 demonstrates importance of conserved capping domain residues.Molecular biology reports · 2021Article
- Sae2 and Rif2 regulate MRX endonuclease activity at DNA double-strand breaks in opposite manners.Cell reports · 2021Article
- A Rad51-independent pathway promotes single-strand template repair in gene editing.PLoS genetics · 2020Article
- Rad9/53BP1 promotes DNA repair via crossover recombination by limiting the Sgs1 and Mph1 helicases.Nature communications · 2020Article
- Checkpoint Responses to DNA Double-Strand Breaks.Annual review of biochemistry · 2020Review
- Modeling cancer genomic data in yeast reveals selection against ATM function during tumorigenesis.PLoS genetics · 2020Article
- Functional and structural insights into the MRX/MRN complex, a key player in recognition and repair of DNA double-strand breaks.Computational and structural biotechnology journal · 2020Review
- Nej1 Interacts with Mre11 to Regulate Tethering and Dna2 Binding at DNA Double-Strand Breaks.Cell reports · 2019Article
- The ATP-bound conformation of the Mre11-Rad50 complex is essential for Tel1/ATM activation.Nucleic acids research · 2019Article
- Structure-function relationships of the Mre11 protein in the control of DNA end bridging and processing.Current genetics · 2019Review
- Article
- Sae2 antagonizes Rad9 accumulation at DNA double-strand breaks to attenuate checkpoint signaling and facilitate end resection.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Review
- Xrs2 and Tel1 Independently Contribute to MR-Mediated DNA Tethering and Replisome Stability.Cell reports · 2018Article
- The MRX complex regulates Exo1 resection activity by altering DNA end structure.The EMBO journal · 2018Article
- Processing of DNA Ends in the Maintenance of Genome Stability.Frontiers in genetics · 2018Review
- Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Sae2 cooperates with the Mre11-Rad50-Xrs2 (MRX) complex to initiate resection of DNA double-strand breaks (DSBs) and to maintain the DSB ends in close proximity to allow their repair. How these diverse MRX-Sae2 functions contribute to DNA damage resistance is not known. Here, we describe mre11 alleles that suppress the hypersensitivity of sae2Δ cells to genotoxic agents. By assessing the impact of these mutations at the cellular and structural levels, we found that all the mre11 alleles that restore sae2Δ resistance to both camptothecin and phleomycin affect the Mre11 N-terminus and suppress the resection defect of sae2Δ cells by lowering MRX and Tel1 association to DSBs. As a consequence, the diminished Tel1 persistence potentiates Sgs1-Dna2 resection activity by decreasing Rad9 association to DSBs. By contrast, the mre11 mutations restoring sae2Δ resistance only to phleomycin are located in Mre11 C-terminus and bypass Sae2 function in end-tethering but not in DSB resection, possibly by destabilizing the Mre11-Rad50 open conformation. These findings unmask the existence of structurally distinct Mre11 domains that support resistance to genotoxic agents by mediating different processes.
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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.