Replication and protection of telomeres
Abstract
During the evolution of linear genomes, it became essential to protect the natural chromosome ends to prevent triggering of the DNA-damage repair machinery and enzymatic attack. Telomeres - tightly regulated complexes consisting of repetitive G-rich DNA and specialized proteins - accomplish this task. Telomeres not only conceal linear chromosome ends from detection and inappropriate repair but also provide a buffer to counteract replication-associated shortening. Lessons from many model organisms have taught us about the complications of maintaining these specialized structures. Here, we discuss how telomeres interact and cooperate with the DNA replication and DNA-damage repair machineries.
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Telomeres that can no longer exert end-protective functions are dysfunctional, and these can arise from progressive telomere attrition or perturbation of shelterin components, resulting in inappropriate chromosomal end-to-end fusions through NHEJ or HR.
“Telomeres that can no longer exert end-protective functions are said to be dysfunctional, and these telomeres could arise either from progressive telomere attrition, or when components of the shelterin complex are perturbed, resulting in inappropriate chromosomal end-to-end fusions through the non-homologous end joining (NHEJ) or homologous recombination (HR) DNA repair pathways 17.”
From Telomere dysfunction and tumour suppression: the senescence connection (2008) · cites this paper as [17]
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- Authors
- Verdun, R. E., & Karlseder, J.
- Affiliations
- Salk Institute for Biological Studies (US)
- ORCID
- Karlseder, Jan
- Venue
- Nature
- Published
- 2007-06-20
- Volume
- 447
- Issue
- 7147
- Pages
- 924-931
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W2086095857
- Cited by
- 463
- References
- 102
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 16 · 2023: 9 · 2022: 17 · 2021: 15 · 2020: 14 · 2019: 14 · 2018: 19 · 2017: 29 · 2016: 28 · 2015: 30 · 2014: 28 · 2013: 31 · 2012: 32
- FWCI
- 4.84
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- Leukemia and Lymphoma Society
- National Institutes of Health
- 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, telomere replication, telomere protection, DNA repair, chromosome ends, DNA replication, telomere shortening, telomere proteins
- MeSH terms
- Animals, DNA Damage, DNA Repair, DNA Replication, Humans, Neoplasms, Telomere, Cellular Senescence
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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