ArticlePLoS biology2016
Tel1 and Rif2 Regulate MRX Functions in End-Tethering and Repair of DNA Double-Strand Breaks.
Article in PLoS biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 69 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
- Mutual, spatially limited control of meiotic DNA break formation by Mre11-Rad50-Nbs1 DNA repair complex and Tel1 (ATM) protein kinase.Nucleic acids research · 2025Article
- The DNA replication checkpoint targets the kinetochore to reposition DNA structure-induced replication damage to the nuclear periphery.Cell reports · 2025Article
- Article
- Exo1 cooperates with Tel1/ATM in promoting recombination events at DNA replication forks.iScience · 2024Article
- Binding of the TRF2 iDDR motif to RAD50 highlights a convergent evolutionary strategy to inactivate MRN at telomeres.Nucleic acids research · 2024Article
- Rif2 interaction with Rad50 counteracts Tel1 functions in checkpoint signalling and DNA tethering by releasing Tel1 from MRX binding.Nucleic acids research · 2024Article
- Dynamic Properties of the DNA Damage Response Mre11/Rad50 Complex.International journal of molecular sciences · 2023Review
- The Ku complex promotes DNA end-bridging and this function is antagonized by Tel1/ATM kinase.Nucleic acids research · 2023Article
- To Fix or Not to Fix: Maintenance of Chromosome Ends Versus Repair of DNA Double-Strand Breaks.Cells · 2022Review
- Article
- The DNA damage checkpoint: A tale from budding yeast.Frontiers in genetics · 2022Review
- Novel insights into the mechanism of cell cycle kinases Mec1(ATR) and Tel1(ATM).Critical reviews in biochemistry and molecular biology · 2021Article
- The chromatin remodeler Chd1 supports MRX and Exo1 functions in resection of DNA double-strand breaks.PLoS genetics · 2021Article
- Dpb4 promotes resection of DNA double-strand breaks and checkpoint activation by acting in two different protein complexes.Nature communications · 2021Article
- Inhibition of MRN activity by a telomere protein motif.Nature communications · 2021Article
- Mechanism of MRX inhibition by Rif2 at telomeres.Nature communications · 2021Article
- Sae2 and Rif2 regulate MRX endonuclease activity at DNA double-strand breaks in opposite manners.Cell reports · 2021Article
- DNA binding modes influence Rap1 activity in the regulation of telomere length and MRX functions at DNA ends.Nucleic acids research · 2020Article
- Modeling cancer genomic data in yeast reveals selection against ATM function during tumorigenesis.PLoS genetics · 2020Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
The cellular response to DNA double-strand breaks (DSBs) is initiated by the MRX/MRN complex (Mre11-Rad50-Xrs2 in yeast; Mre11-Rad50-Nbs1 in mammals), which recruits the checkpoint kinase Tel1/ATM to DSBs. In Saccharomyces cerevisiae, the role of Tel1 at DSBs remains enigmatic, as tel1Δ cells do not show obvious hypersensitivity to DSB-inducing agents. By performing a synthetic phenotype screen, we isolated a rad50-V1269M allele that sensitizes tel1Δ cells to genotoxic agents. The MRV1269MX complex associates poorly to DNA ends, and its retention at DSBs is further reduced by the lack of Tel1. As a consequence, tel1Δ rad50-V1269M cells are severely defective both in keeping the DSB ends tethered to each other and in repairing a DSB by either homologous recombination (HR) or nonhomologous end joining (NHEJ). These data indicate that Tel1 promotes MRX retention to DSBs and this function is important to allow proper MRX-DNA binding that is needed for end-tethering and DSB repair. The role of Tel1 in promoting MRX accumulation to DSBs is counteracted by Rif2, which is recruited to DSBs. We also found that Rif2 enhances ATP hydrolysis by MRX and attenuates MRX function in end-tethering, suggesting that Rif2 can regulate MRX activity at DSBs by modulating ATP-dependent conformational changes of Rad50.
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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.