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Cited by 623Telomeres, Telomerase, and SenescenceDNA Repair MechanismsDNA and Nucleic Acid Chemistry

The DOI matches its Crossref record; 36 of the 36 references it cites were found in a registry or an index.

DNA processing is not required for ATM-mediated telomere damage response after TRF2 deletion

Celli, Giulia B., de Lange, Titia·2005·Nature Cell Biology
DOI 10.1038/ncb1275
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Abstract

Telomere attrition and other forms of telomere damage can activate the ATM kinase pathway. What generates the DNA damage signal at mammalian chromosome ends or at other double-strand breaks is not known. Telomere dysfunction is often accompanied by disappearance of the 3' telomeric overhang, raising the possibility that DNA degradation could generate the structure that signals. Here we address these issues by studying telomere structure after conditional deletion of mouse TRF2, the protective factor at telomeres. Upon removal of TRF2 from TRF2(F/-) p53-/- mouse embryo fibroblasts, a telomere damage response is observed at most chromosome ends. As expected, the telomeres lose the 3' overhang and are processed by the non-homologous end-joining pathway. Non-homologous end joining of telomeres was abrogated in DNA ligase IV-deficient (Lig4-/-) cells. Unexpectedly, the telomeres of TRF2-/- Lig4-/- p53-/- cells persisted in a free state without undergoing detectable DNA degradation. Notably, the telomeres retained their 3' overhangs, but they were recognized as sites of DNA damage, accumulating the DNA damage response factors 53BP1 and gamma-H2AX, and activating the ATM kinase. Thus, activation of the ATM kinase pathway at chromosome ends does not require overhang degradation or other overt DNA processing.

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Crossref · 10.1038/ncb1275

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Metadata

Authors
Celli, G. B., & de Lange, T.
Affiliations
NYU Langone Health (US)
Venue
Nature Cell Biology
Publisher
Springer Science and Business Media LLC
Published
2005-06-19
Volume
7
Issue
7
Pages
712-718
ISSN
  • 1465-7392 (ISSN-L)
  • 1476-4679
DOI
10.1038/ncb1275
OpenAlex
W2035389897
Semantic Scholar
f4e3c6cbe3167cb507269beefcc7ad01ad45332d
Cited by
623
References
36
Citations by year
2026: 9 · 2025: 14 · 2024: 28 · 2023: 19 · 2022: 16 · 2021: 27 · 2020: 26 · 2019: 20 · 2018: 22 · 2017: 37 · 2016: 24 · 2015: 37 · 2014: 41 · 2013: 37 · 2012: 41
FWCI
20.17
Type
journal article
Language
en
Open access
closed
Licence
www.springer.com/tdm (tdm)
Locations
  • Nature Cell Biology (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institute of General Medical Sciences (GM49046-12)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA and Nucleic Acid Chemistry
Keywords
ATM kinase, TRF2, telomere shortening, non-homologous end joining, DNA ligase IV, DNA damage signaling, 53BP1, γH2AX, telomere dysfunction, p53-deficient cells
MeSH terms
Tumor Suppressor p53-Binding Protein 1, DNA Ligase ATP, Animals, Cells, Cultured, Chromosomal Proteins, Non-Histone, Crosses, Genetic, DNA, DNA Damage, DNA-Binding Proteins, Embryo, Mammalian, Fibroblasts, Histones, Mice, Transgenic, Phosphoproteins, Phosphorylation, DNA Ligases, Transfection, Tumor Suppressor Protein p53, Telomere, Protein Serine-Threonine Kinases, Gene Deletion, In Situ Hybridization, Fluorescence, Mice, Knockout, Cell Cycle Proteins, rap1 GTP-Binding Proteins, Tumor Suppressor Proteins, Telomeric Repeat Binding Protein 1, Telomeric Repeat Binding Protein 2, Intracellular Signaling Peptides and Proteins, Mice, Ataxia Telangiectasia Mutated Proteins, Checkpoint Kinase 2

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