ArticleMolecular and cellular biology2011
Activation of protein kinase Tel1 through recognition of protein-bound DNA ends.
Article in Molecular and cellular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 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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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
23 citing papers in PubMed, 29 citations in OpenAlex.
- Tel1 is recruited at chromosomal loop/axis contact sites to modulate meiotic DNA double-strand breaks interference.PLoS genetics · 2025Article
- Sae2 controls Mre11 endo- and exonuclease activities by different mechanisms.Nature communications · 2024Article
- Exo1 cooperates with Tel1/ATM in promoting recombination events at DNA replication forks.iScience · 2024Article
- γH2A/γH2AX Mediates DNA Damage-Specific Control of Checkpoint Signaling inInternational journal of molecular sciences · 2024Article
- Novel insights into the mechanism of cell cycle kinases Mec1(ATR) and Tel1(ATM).Critical reviews in biochemistry and molecular biology · 2021Article
- Checkpoint functions of RecQ helicases at perturbed DNA replication fork.Current genetics · 2021Review
- Review
- Tel1/ATM prevents degradation of replication forks that reverse after topoisomerase poisoning.EMBO reports · 2018Article
- Functions and regulation of the MRX complex at DNA double-strand breaks.Microbial cell (Graz, Austria) · 2016Review
- The MRX Complex Ensures NHEJ Fidelity through Multiple Pathways Including Xrs2-FHA-Dependent Tel1 Activation.PLoS genetics · 2016Article
- Tel1 and Rif2 Regulate MRX Functions in End-Tethering and Repair of DNA Double-Strand Breaks.PLoS biology · 2016Article
- Sae2 Function at DNA Double-Strand Breaks Is Bypassed by Dampening Tel1 or Rad53 Activity.PLoS genetics · 2015Article
- Requirement of the FATC domain of protein kinase Tel1 for localization to DNA ends and target protein recognition.Molecular biology of the cell · 2015Article
- Synthetic viability genomic screening defines Sae2 function in DNA repair.The EMBO journal · 2015Article
- Synthetic cytotoxicity: digenic interactions with TEL1/ATM mutations reveal sensitivity to low doses of camptothecin.Genetics · 2014Article
- Ddc2 mediates Mec1 activation through a Ddc1- or Dpb11-independent mechanism.PLoS genetics · 2014Article
- Multifunctional role of ATM/Tel1 kinase in genome stability: from the DNA damage response to telomere maintenance.BioMed research international · 2014Review
- DNA resection proteins Sgs1 and Exo1 are required for G1 checkpoint activation in budding yeast.DNA repair · 2013Article
- Article
- Preserving Yeast Genetic Heritage through DNA Damage Checkpoint Regulation and Telomere Maintenance.Biomolecules · 2012Article
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
4 authors at 1 institution in 3 countries.
Funding
Abstract
Double-strand breaks (DSBs) in chromosomal DNA elicit a rapid signaling response through the ATM protein kinase. ATM corresponds to Tel1 in budding yeast. Here we show that the catalytic activity of Tel1 is altered by protein binding at DNA ends via the Mre11-Rad50-Xrs2 (MRX) complex. Like ATM, Tel1 is activated through interaction with the MRX complex and DNA ends. In vivo, Tel1 activation is enhanced in sae2Δ or mre11-3 mutants after camptothecin treatment; both of these mutants are defective in the removal of topoisomerase I from DNA. In contrast, an sae2Δ mutation does not stimulate Tel1 activation after expression of the EcoRI endonuclease, which generates "clean" DNA ends. In an in vitro system, tethering of Fab fragments to DNA ends inhibits MRX-mediated DNA end processing but enhances Tel1 activation. The mre11-3 mutation abolishes DNA end-processing activity but does not affect the ability to enhance Tel1 activation. These results support a model in which MRX controls Tel1 activation by recognizing protein-bound DNA ends.
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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.