ArticleScientific reports2015
The asymmetry of telomere replication contributes to replicative senescence heterogeneity.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 34 citations in OpenAlex.
- Both genome instability and replicative senescence stem from the shortest telomere in telomerase-negative cells.Nature communications · 2026Article
- Mathematical model linking telomeres to senescence in Saccharomyces cerevisiae reveals cell lineage versus population dynamics.Nature communications · 2025Article
- Review
- Telomere biology: from disorders to hematological diseases.Frontiers in oncology · 2023Review
- Down-syndrome-induced senescence disrupts the nuclear architecture of neural progenitors.Cell stem cell · 2022Article
- Telomere shortening causes distinct cell division regimes during replicative senescence in Saccharomyces cerevisiae.Cell & bioscience · 2021Article
- Telomeres and telomerase in oncogenesis.Oncology letters · 2020Review
- The many types of heterogeneity in replicative senescence.Yeast (Chichester, England) · 2019Review
- Telomere-dependent and telomere-independent roles of RAP1 in regulating human stem cell homeostasis.Protein & cell · 2019Article
- Effect of therapies-mediated modulation of telomere and/or telomerase on cancer cells radiosensitivity.Oncotarget · 2018Review
- Telomere Maintenance Mechanisms in Cancer.Genes · 2018Review
- Effects of initial telomere length distribution on senescence onset and heterogeneity.Journal of theoretical biology · 2017Article
- Roles of telomeres and telomerase in cancer, and advances in telomerase-targeted therapies.Genome medicine · 2016Review
- XIAP-associating factor 1, a transcriptional target of BRD7, contributes to endothelial cell senescence.Oncotarget · 2016Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
In eukaryotes, the absence of telomerase results in telomere shortening, eventually leading to replicative senescence, an arrested state that prevents further cell divisions. While replicative senescence is mainly controlled by telomere length, the heterogeneity of its onset is not well understood. This study proposes a mathematical model based on the molecular mechanisms of telomere replication and shortening to decipher the causes of this heterogeneity. Using simulations fitted on experimental data obtained from individual lineages of senescent Saccharomyces cerevisiae cells, we decompose the sources of senescence heterogeneity into interclonal and intraclonal components, and show that the latter is based on the asymmetry of the telomere replication mechanism. We also evidence telomere rank-switching events with distinct frequencies in short-lived versus long-lived lineages, revealing that telomere shortening dynamics display important variations. Thus, the intrinsic heterogeneity of replicative senescence and its consequences find their roots in the asymmetric structure of telomeres.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.