ArticleG3 (Bethesda, Md.)2011
Genome-wide analysis to identify pathways affecting telomere-initiated senescence in budding yeast.
Article in G3 (Bethesda, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- The canonical RPA complex interacts with Est3 to regulate yeast telomerase activity.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Mathematical model linking telomeres to senescence in Saccharomyces cerevisiae reveals cell lineage versus population dynamics.Nature communications · 2025Article
- SUNny Ways: The Role of the SUN-Domain Protein Mps3 Bridging Yeast Nuclear Organization and Lipid Homeostasis.Frontiers in genetics · 2020Review
- Quantitative assessment of changes in cell growth, size and morphology during telomere-initiated cellular senescence in Saccharomyces cerevisiae.Experimental cell research · 2019Article
- Molecular characterization ofLife science alliance · 2019Article
- A subtelomeric region affects telomerase-negative replicative senescence in Saccharomyces cerevisiae.Scientific reports · 2019Article
- Functional characterisation of long intergenic non-coding RNAs through genetic interaction profiling in Saccharomyces cerevisiae.BMC biology · 2016Article
- Nutrigenomics at the Interface of Aging, Lifespan, and Cancer Prevention.The Journal of nutrition · 2016Review
- Exploring Quantitative Yeast Phenomics with Single-Cell Analysis of DNA Damage Foci.Cell systems · 2016Article
- DNA Replication Stress Phosphoproteome Profiles Reveal Novel Functional Phosphorylation Sites on Xrs2 in Saccharomyces cerevisiae.Genetics · 2016Article
- Tryptophan-Dependent Control of Colony Formation After DNA Damage via Sea3-Regulated TORC1 Signaling in Saccharomyces cerevisiae.G3 (Bethesda, Md.) · 2015Article
- Genome-wide studies of telomere biology in budding yeast.Microbial cell (Graz, Austria) · 2014Review
- Multiple genetic pathways regulate replicative senescence in telomerase-deficient yeast.Aging cell · 2013Article
- Saccharomyces cerevisiae as a Model to Study Replicative Senescence Triggered by Telomere Shortening.Frontiers in oncology · 2013Article
- Rif2 promotes a telomere fold-back structure through Rpd3L recruitment in budding yeast.PLoS genetics · 2012Article
- Deregulated telomere transcription causes replication-dependent telomere shortening and promotes cellular senescence.Nucleic acids research · 2012Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
In telomerase-deficient yeast cells, like equivalent mammalian cells, telomeres shorten over many generations until a period of senescence/crisis is reached. After this, a small fraction of cells can escape senescence, principally using recombination-dependent mechanisms. To investigate the pathways that affect entry into and recovery from telomere-driven senescence, we combined a gene deletion disrupting telomerase (est1Δ) with the systematic yeast deletion collection and measured senescence characteristics in high-throughput assays. As expected, the vast majority of gene deletions showed no strong effects on entry into/exit from senescence. However, around 200 gene deletions behaving similarly to a rad52Δest1Δ archetype (rad52Δ affects homologous recombination) accelerated entry into senescence, and such cells often could not recover growth. A smaller number of strains similar to a rif1Δest1Δ archetype (rif1Δ affects proteins that bind telomeres) accelerated entry into senescence but also accelerated recovery from senescence. Our genome-wide analysis identifies genes that affect entry into and/or exit from telomere-initiated senescence and will be of interest to those studying telomere biology, replicative senescence, cancer, and ageing. Our dataset is complementary to other high-throughput studies relevant to telomere biology, genetic stability, and DNA damage responses.
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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.