ArticleFrontiers in oncology2013
Saccharomyces cerevisiae as a Model to Study Replicative Senescence Triggered by Telomere Shortening.
Article in Frontiers in oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 48 citations in OpenAlex.
- Highly mutagenic copying of telomeric circles promotes ALT establishment.Nature communications · 2026Article
- Both genome instability and replicative senescence stem from the shortest telomere in telomerase-negative cells.Nature communications · 2026Article
- Natural diversity of telomere length distributions across 100Genome research · 2026Article
- The DNA damage tolerance factor Rad5 and telomere replication.Current genetics · 2025Review
- Mathematical model linking telomeres to senescence in Saccharomyces cerevisiae reveals cell lineage versus population dynamics.Nature communications · 2025Article
- TERRA and the alternative lengthening of telomeres: a dangerous affair.FEBS letters · 2025Review
- Hog1 acts in a Mec1-independent manner to counteract oxidative stress following telomerase inactivation in Saccharomyces cerevisiae.Communications biology · 2024Article
- Review
- TERRA increases at short telomeres in yeast survivors and regulates survivor associated senescence (SAS).Nucleic acids research · 2022Article
- G-quadruplex structure of the C. elegans telomeric repeat: a two tetrads basket type conformation stabilized by a non-canonical C-T base-pair.Nucleic acids research · 2022Article
- Suppression of telomere capping defects of Saccharomyces cerevisiae yku70 and yku80 mutants by telomerase.G3 (Bethesda, Md.) · 2021Article
- Targeting cellular senescence based on interorganelle communication, multilevel proteostasis, and metabolic control.The FEBS journal · 2021Review
- Chromatin modifiers and recombination factors promote a telomere fold-back structure, that is lost during replicative senescence.PLoS genetics · 2020Article
- Exceptionally Long-Lived Individuals (ELLI) Demonstrate Slower Aging Rate Calculated by DNA Methylation Clocks as Possible Modulators for Healthy Longevity.International journal of molecular sciences · 2020Article
- The many types of heterogeneity in replicative senescence.Yeast (Chichester, England) · 2019Review
- Tel1/ATM Signaling to the Checkpoint Contributes to Replicative Senescence in the Absence of Telomerase.Genetics · 2019Article
- Quantitative assessment of changes in cell growth, size and morphology during telomere-initiated cellular senescence in Saccharomyces cerevisiae.Experimental cell research · 2019Article
- Adaptation in replicative senescence: a risky business.Current genetics · 2019Review
- A subtelomeric region affects telomerase-negative replicative senescence in Saccharomyces cerevisiae.Scientific reports · 2019Article
- Adaptation to DNA damage checkpoint in senescent telomerase-negative cells promotes genome instability.Genes & development · 2018Article
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1 author at 1 institution in 1 country.
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Abstract
In many somatic human tissues, telomeres shorten progressively because of the DNA-end replication problem. Consequently, cells cease to proliferate and are maintained in a metabolically viable state called replicative senescence. These cells are characterized by an activation of DNA damage checkpoints stemming from eroded telomeres, which are bypassed in many cancer cells. Hence, replicative senescence has been considered one of the most potent tumor suppressor pathways. However, the mechanism through which short telomeres trigger this cellular response is far from being understood. When telomerase is removed experimentally in Saccharomyces cerevisiae, telomere shortening also results in a gradual arrest of population growth, suggesting that replicative senescence also occurs in this unicellular eukaryote. In this review, we present the key steps that have contributed to the understanding of the mechanisms underlying the establishment of replicative senescence in budding yeast. As in mammals, signals stemming from short telomeres activate the DNA damage checkpoints, suggesting that the early cellular response to the shortest telomere(s) is conserved in evolution. Yet closer analysis reveals a complex picture in which the apparent single checkpoint response may result from a variety of telomeric alterations expressed in the absence of telomerase. Accordingly, the DNA replication of eroding telomeres appears as a critical challenge for senescing budding yeast cells and the easy manipulation of S. cerevisiae is providing insights into the way short telomeres are integrated into their chromatin and nuclear environments. Finally, the loss of telomerase in budding yeast triggers a more general metabolic alteration that remains largely unexplored. Thus, telomerase-deficient S. cerevisiae cells may have more common points than anticipated with somatic cells, in which telomerase depletion is naturally programed, thus potentially inspiring investigations in mammalian cells.
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