Telomere length homeostasis
Open accessAbstract
The physical ends of chromosomes, known as telomeres, protect chromosome ends from nucleolytic degradation and DNA repair activities. Conventional DNA replication enzymes lack the ability to fully replicate telomere ends. In addition, nucleolytic activities contribute to telomere erosion. Short telomeres trigger DNA damage checkpoints, which mediate cellular senescence. Telomere length homeostasis requires telomerase, a cellular reverse transcriptase, which uses an internal RNA moiety as a template for the synthesis of telomere repeats. Telomerase elongates the 3' ends of chromosomes, whereas the complementary strand is filled in by conventional DNA polymerases. In humans, telomerase is ubiquitously expressed only during the first weeks of embryogenesis, and is subsequently downregulated in most cell types. Correct telomere length setting is crucial for long-term survival. The telomere length reserve must be sufficient to avoid premature cellular senescence and the acceleration of age-related disease. On the other side, telomere shortening suppresses tumor formation through limiting the replicative potential of cells. In recent years, novel insight into the regulation of telomerase at chromosome ends has increased our understanding on how telomere length homeostasis in telomerase-positive cells is achieved. Factors that recruit telomerase to telomeres in a cell cycle-dependent manner have been identified in Saccharomyces cerevisiae. In humans, telomerase assembles with telomeres during S phase of the cell cycle. Presumably through mediating formation of alternative telomere structures, telomere-binding proteins regulate telomerase activity in cis to favor preferential elongation of the shortest telomeres. Phosphoinositide 3-kinase related kinases are also required for telomerase activation at chromosome ends, at least in budding and fission yeast. In vivo analysis of telomere elongation kinetics shows that telomerase does not act on every telomere in each cell cycle but that it exhibits an increasing preference for telomeres as their lengths decline. This suggests a model in which telomeres switch between extendible and nonextendible states in a length-dependent manner. In this review we expand this model to incorporate the finding that telomerase levels also limit telomere length and we propose a second switch between a non-telomerase-associated "extendible" and a telomerase-associated "extending" state.
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Two key regulators of telomerase activity are the actual structure of telomeres and the cell cycle-dependent creation of active telomerase; both restrict telomerase activity at chromosome ends during the S phase of each cell cycle.
“Two different key regulators of TA are the actual structure of telomeres and the cell cycle-dependent creation of active telomerase. Both of them seem to restrict TA at chromosome ends during the S phase of each cell cycle [188].”
From Current and Future Trends of Colorectal Cancer Treatment: Exploring Advances in Immunotherapy (2024) · cites this paper as [188]
Throughout the cell cycle, telomeres fluctuate between different states (stationary/nonextendible, elongetable, and elongating).
“Throughout the cell cycle, telomeres fluctuate between different states (stationary/nonextendible, elongetable, and elongating) [188].”
From Current and Future Trends of Colorectal Cancer Treatment: Exploring Advances in Immunotherapy (2024) · cites this paper as [188]
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Human Telomeres Have Different Overhang Sizes at Leading versus Lagging Strands
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3 Telomerase Biochemistry and BiogenesisPreprint
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Self-citation
Flagged first, then by citations
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Aubert, G., & Lansdorp, P. M. (2008) · Physiological Reviews · doi:10.1152/physrev.00026.2007 · Cited by 1,188 · see citing works
Telomerase and cancer therapeutics
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A RAP1/TRF2 Complex Inhibits Nonhomologous End-Joining at Human Telomeric DNA Ends
Bae, N. S., & Baumann, P. (2007) · Molecular Cell · doi:10.1016/j.molcel.2007.03.023 · Cited by 215 · see citing works
Current and Future Trends of Colorectal Cancer Treatment: Exploring Advances in Immunotherapy
Nikolouzakis, T. K., Chrysos, E., Docea, A. O., Fragkiadaki, P., Souglakos, J., Tsiaoussis, J., & Tsatsakis, A. (2024) · Cancers · doi:10.3390/cancers16111995 · Cited by 37 · see citing works
Telomeres and telomerase in the clinical management of colorectal cancer
Piñol-Felis, C., Fernández-Marcelo, T., Viñas-Salas, J., & Valls-Bautista, C. (2017) · Clinical and Translational Oncology · doi:10.1007/s12094-016-1559-0 · Cited by 13 · see citing works
- Authors
- Hug, N., & Lingner, J.
- Affiliations
- ISREC Foundation (CH)
- Corresponding author
- Lingner, Joachim
- Venue
- Chromosoma
- Published
- 2006-06-02
- Volume
- 115
- Issue
- 6
- Pages
- 413-425
- ISSN
- 0009-5915 (ISSN-L)
- 1432-0886
- OpenAlex
- W2032694449
- Cited by
- 291
- References
- 125
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 7 · 2023: 8 · 2022: 7 · 2021: 16 · 2020: 5 · 2019: 9 · 2018: 13 · 2017: 23 · 2016: 17 · 2015: 17 · 2014: 16 · 2013: 19 · 2012: 23
- FWCI
- 2.45
- Type
- journal article
- Language
- en
- Open access
- green
- infoscience.epfl.ch
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Chromosoma (publishedVersion)
- PubMed (publishedVersion)
- reroDoc Digital Library (submittedVersion)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion, cc-by-nc-nd)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA and Nucleic Acid Chemistry
- Keywords
- telomere length homeostasis, telomerase, telomere shortening, DNA damage checkpoint, cellular senescence, telomere-binding proteins, S phase, age-related diseases, tumor suppression
- MeSH terms
- Animals, Cell Cycle, Homeostasis, Humans, Models, Biological, Saccharomyces cerevisiae, Telomere, Telomerase, Telomere-Binding Proteins
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.
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