How Telomeres Solve the End-Protection Problem
Open accessAbstract
The ends of eukaryotic chromosomes have the potential to be mistaken for damaged or broken DNA and must therefore be protected from cellular DNA damage response pathways. Otherwise, cells might permanently arrest in the cell cycle, and attempts to “repair” the chromosome ends would have devastating consequences for genome integrity. This end-protection problem is solved by protein-DNA complexes called telomeres. Studies of mammalian cells have recently uncovered the mechanism by which telomeres disguise the chromosome ends. Comparison to unicellular eukaryotes reveals key differences in the DNA damage response systems that inadvertently threaten chromosome ends. Telomeres appear to be tailored to these variations, explaining their variable structure and composition.
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When telomeres reach a critical length, they cannot bind enough capping proteins and are sensed as exposed DNA ends, activating DDR pathways that arrest proliferation through p21 and p16.
“As telomeres reach a critical length, they become unable to bind enough telomere-capping proteins and are sensed as exposed DNA ends2, which activates the DDR pathways that, through the induction of the cell cycle inhibitors p21 and p16, arrest proliferation3,4.”
From Telomere dysfunction in ageing and age-related diseases (2022) · cites this paper as [2]
In “How Shelterin Solves the End-Protection Problem in Mammals” (page unavailable), the paper says telomeric repeats provide shelterin-binding sites and that shelterin prevents a DNA damage response at chromosome ends. It also reports that loss of TRF2 activates ATM at those ends. It does not establish the claimed critical-length threshold at which shortening leaves too few capping proteins; the p21/p16 portion is cited to other sources in the printed sentence. (LLM, conf=0.84)
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- Authors
- de Lange, T.
- Affiliations
- Laboratory of Cell Biology and Genetics, Rockefeller University, New York, NY 10021, USA.
- Venue
- Science
- Published
- 2009-11-13
- Volume
- 326
- Issue
- 5955
- Pages
- 948-952
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC2819049
- OpenAlex
- W2124242199
- Cited by
- 826
- References
- 69
- Citations by year
- 2026: 14 · 2025: 38 · 2024: 31 · 2023: 38 · 2022: 38 · 2021: 56 · 2020: 47 · 2019: 58 · 2018: 74 · 2017: 50 · 2016: 45 · 2015: 60 · 2014: 64 · 2013: 77 · 2012: 54
- FWCI
- 29.82
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (DP1OD000379)
- National Institute on Aging (R56AG016642, AG016642, R01AG016642)
- National Cancer Institute (CA076027, R01CA076027)
- National Institute of General Medical Sciences (R37GM049046, R01GM049046, GM049046)
- Topics
- Health Sciences › Medicine › Physiology › 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
- telomeres, chromosome end protection, DNA damage response, genome stability, telomere structure, telomere evolution, unicellular eukaryotes, mammalian cells
- MeSH terms
- Shelterin Complex, Animals, Chromosomes, DNA, DNA Damage, DNA Repair, DNA-Binding Proteins, Humans, Repetitive Sequences, Nucleic Acid, Yeasts, Signal Transduction, Telomere, Ciliophora, Telomerase, Chromosomes, Mammalian, Telomere-Binding Proteins, Telomeric Repeat Binding Protein 2
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