ArticleMolecular biology of the cell2007
MRX-dependent DNA damage response to short telomeres.
Article in Molecular biology of the cell, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 49 citations in OpenAlex.
- A role for nucleosome remodellers during resection of deprotected telomeres in yeast.PloS one · 2026Article
- Rif2 interaction with Rad50 counteracts Tel1 functions in checkpoint signalling and DNA tethering by releasing Tel1 from MRX binding.Nucleic acids research · 2024Article
- Mechanism of MRX inhibition by Rif2 at telomeres.Nature communications · 2021Article
- The telomere-binding protein Rif2 and ATP-bound Rad50 have opposing roles in the activation of yeast Tel1The Journal of biological chemistry · 2019Article
- Tel1 Activation by the MRX Complex Is Sufficient for Telomere Length Regulation but Not for the DNA Damage Response inGenetics · 2019Article
- Single Stem Cell Imaging and Analysis Reveals Telomere Length Differences in Diseased Human and Mouse Skeletal Muscles.Stem cell reports · 2017Article
- Telomere shortening triggers a feedback loop to enhance end protection.Nucleic acids research · 2017Article
- The RNA binding protein Npl3 promotes resection of DNA double-strand breaks by regulating the levels of Exo1.Nucleic acids research · 2017Article
- Nonhomologous End-Joining with Minimal Sequence Loss Is Promoted by the Mre11-Rad50-Nbs1-Ctp1 Complex inGenetics · 2017Article
- Regulation of telomere metabolism by the RNA processing protein Xrn1.Nucleic acids research · 2017Article
- 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
- Resection is responsible for loss of transcription around a double-strand break in Saccharomyces cerevisiae.eLife · 2015Article
- Escape of Sgs1 from Rad9 inhibition reduces the requirement for Sae2 and functional MRX in DNA end resection.EMBO reports · 2015Article
- Mec1/ATR regulates the generation of single-stranded DNA that attenuates Tel1/ATM signaling at DNA ends.The EMBO journal · 2014Article
- Dna2 is involved in CA strand resection and nascent lagging strand completion at native yeast telomeres.The Journal of biological chemistry · 2013Article
- Tbf1 and Vid22 promote resection and non-homologous end joining of DNA double-strand break ends.The EMBO journal · 2013Article
- A balance between Tel1 and Rif2 activities regulates nucleolytic processing and elongation at telomeres.Molecular and cellular biology · 2012Article
- Telomeric DNA damage is irreparable and causes persistent DNA-damage-response activation.Nature cell biology · 2012Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Telomere structure allows cells to distinguish the natural chromosome ends from double-strand breaks (DSBs). However, DNA damage response proteins are intimately involved in telomere metabolism, suggesting that functional telomeres may be recognized as DNA damage during a time window. Here we show by two different systems that short telomeres are recognized as DSBs during the time of their replication, because they induce a transient MRX-dependent DNA damage checkpoint response during their prolonged elongation. The MRX complex, which is recruited at telomeres under these conditions, dissociates from telomeres concomitantly with checkpoint switch off when telomeres reach a new equilibrium length. We also show that MRX recruitment to telomeres is sufficient to activate the checkpoint independently of telomere elongation. We propose that MRX can signal checkpoint activation by binding to short telomeres only when they become competent for elongation. Because full-length telomeres are refractory to MRX binding and the shortest telomeres are elongated of only a few base pairs per generation, this limitation may prevent unscheduled checkpoint activation during an unperturbed S phase.
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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.