Cited by 797Telomeres, Telomerase, and SenescenceGenetics, Aging, and Longevity in Model OrganismsDNA and Nucleic Acid Chemistry

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Senescence Induced by Altered Telomere State, Not Telomere Loss

Karlseder, Jan, Smogorzewska, Agata, de Lange, Titia·2002·Science

DOI 10.1126/science.1069523

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Abstract

Primary human cells in culture invariably stop dividing and enter a state of growth arrest called replicative senescence. This transition is induced by programmed telomere shortening, but the underlying mechanisms are unclear. Here, we report that overexpression of TRF2, a telomeric DNA binding protein, increased the rate of telomere shortening in primary cells without accelerating senescence. TRF2 reduced the senescence setpoint, defined as telomere length at senescence, from 7 to 4 kilobases. TRF2 protected critically short telomeres from fusion and repressed chromosome-end fusions in presenescent cultures, which explains the ability of TRF2 to delay senescence. Thus, replicative senescence is induced by a change in the protected status of shortened telomeres rather than by a complete loss of telomeric DNA.

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Authors: Karlseder, J., Smogorzewska, A., & de Lange, T.
Affiliations: Rockefeller University (US)
Laboratory for Cell Biology and Genetics, The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA.
ORCID: Karlseder, Jan
Smogorzewska, Agata
Venue: Science
Publisher: American Association for the Advancement of Science (AAAS)
Published: 2002-03-29
Volume: 295
Issue: 5564
Pages: 2446-2449
ISSN: 0036-8075 (ISSN-L)
1095-9203
DOI: 10.1126/science.1069523
OpenAlex: W2088926897
Cited by: 796
References: 25
Citations by year: 2026: 10 · 2025: 11 · 2024: 22 · 2023: 11 · 2022: 14 · 2021: 22 · 2020: 18 · 2019: 19 · 2018: 26 · 2017: 22 · 2016: 20 · 2015: 29 · 2014: 24 · 2013: 22 · 2012: 35
FWCI: 47.76
Type: journal article
Language: en
Open access: closed
Locations: Science (publishedVersion)
PubMed (publishedVersion)
Funders: National Institute on Aging (AG 16643)
National Cancer Institute (R01CA076027, CA76027)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › 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: replicative senescence, telomere shortening, TRF2, telomere length, telomere fusion, primary human cells, growth arrest
MeSH terms: Antigens, Polyomavirus Transforming, Cell Division, Cell Line, Cells, Cultured, DNA, DNA-Binding Proteins, Humans, Oncogene Proteins, Viral, Repressor Proteins, Retroviridae, Transformation, Genetic, Tumor Suppressor Protein p53, Retinoblastoma Protein, Telomere, Cellular Senescence, Telomeric Repeat Binding Protein 2, Papillomavirus E7 Proteins

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Senescence Induced by Altered Telomere State, Not Telomere Loss

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