Cited by 548Genetics, Aging, and Longevity in Model OrganismsCell death mechanisms and regulationFungal and yeast genetics research

Chronological aging leads to apoptosis in yeast

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Herker, Eva, Jungwirth, Helmut, Lehmann, Katharina A., Maldener, Corinna, Fröhlich, Kai-Uwe, Wissing, Silke, Büttner, Sabrina, Fehr, Markus +2 more·2004·The Journal of Cell Biology

Abstract

During the past years, yeast has been successfully established as a model to study mechanisms of apoptotic regulation. However, the beneficial effects of such a cell suicide program for a unicellular organism remained obscure. Here, we demonstrate that chronologically aged yeast cultures die exhibiting typical markers of apoptosis, accumulate oxygen radicals, and show caspase activation. Age-induced cell death is strongly delayed by overexpressing YAP1, a key transcriptional regulator in oxygen stress response. Disruption of apoptosis through deletion of yeast caspase YCA1 initially results in better survival of aged cultures. However, surviving cells lose the ability of regrowth, indicating that predamaged cells accumulate in the absence of apoptotic cell removal. Moreover, wild-type cells outlast yca1 disruptants in direct competition assays during long-term aging. We suggest that apoptosis in yeast confers a selective advantage for this unicellular organism, and demonstrate that old yeast cells release substances into the medium that stimulate survival of the clone.

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Crossref · 10.1083/jcb.200310014

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  • Features like superoxide levels and regrowth frequency are connected to PCD, an adaptive mechanism required for programmed aging through selective advantage at least in yeast.

    “Features like superoxide levels and regrowth frequency are connected to PCD, an adaptive mechanism required for programmed aging through selective advantage at least in yeast (Fabrizio et al., 2004; Herker et al., 2004).”

    From The Search for Antiaging Interventions: From Elixirs to Fasting Regimens (2014) · cites this paper as Herker et al., 2004

  • Genetic disruption of PCD-mediated cell removal improves short-term survival of aged cultures; however, the surviving cells lose their ability to re-grow, indicating an accumulation of damaged cells in the absence of PCD.

    “Genetic disruption of PCD-mediated cell removal improves short-term survival of aged cultures; however, the surviving cells lose their ability to re-grow, indicating an accumulation of damaged cells in the absence of PCD (Fabrizio et al., 2004; Herker et al., 2004).”

    From The Search for Antiaging Interventions: From Elixirs to Fasting Regimens (2014) · cites this paper as Herker et al., 2004

  • Within chronologically aged yeast cultures, single yeast cells induce programmed cell death (PCD) as a result of the accumulation of oxygen radicals and metacaspase activation.

    “Within chronologically aged yeast cultures, single yeast cells induce programmed cell death (PCD) as a result of the accumulation of oxygen radicals and metacaspase activation (Fabrizio et al., 2004; Herker et al., 2004).”

    From The Search for Antiaging Interventions: From Elixirs to Fasting Regimens (2014) · cites this paper as Herker et al., 2004

  • Strains with dysfunctional PCD have an initial advantage but are eventually overgrown and outcompeted by wild type cells.

    “Strains with dysfunctional PCD have an initial advantage but are eventually overgrown and outcompeted by wild type cells (Fabrizio et al., 2004; Herker et al., 2004).”

    From The Search for Antiaging Interventions: From Elixirs to Fasting Regimens (2014) · cites this paper as Herker et al., 2004

  • Deletion of the S. cerevisiae metacaspase YCA1 increased resistance to PCD caused by stressors such as hydrogen peroxide and also increased chronological life span.

    “Deletion of the Saccharomyces cerevisiae metacaspase YCA1 increased resistance to PCD caused by stressors such as hydrogen peroxide and also increased chronological life span (Herker et al., 2004; Madeo et al., 2002).”

    From Programmed cell death in aging (2015) · cites this paper as Herker et al., 2004

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Authors
Herker, E., Jungwirth, H., Lehmann, K. A., Maldener, C., Fröhlich, K.-U., Wissing, S., Büttner, S., Fehr, M., Sigrist, S., & Madeo, F.
Affiliations
  • University of Tübingen (DE)
  • 2Wilhelm-Schickard Institute for Informatics, University of Tübingen, 72076 Tübingen, Germany
  • 4Institute of Molecular Biology, Biochemistry, and Microbiology, Karl-Franzens University, 8010 Graz, Austria
  • 1Institute for Physiological Chemistry, University of Tübingen, 72076 Tübingen, Germany
  • Carnegie Institution for Science (US)
  • European Neuroscience Institute Göttingen (DE)
Corresponding author
Madeo, Frank
Venue
The Journal of Cell Biology
Published
2004-02-16
Volume
164
Issue
4
Pages
501-507
ISSN
  • 0021-9525 (ISSN-L)
  • 1540-8140
OpenAlex
W2067820742
Cited by
548
References
19
Citations by year
2026: 4 · 2025: 6 · 2024: 11 · 2023: 8 · 2022: 17 · 2021: 19 · 2020: 20 · 2019: 26 · 2018: 21 · 2017: 15 · 2016: 21 · 2015: 17 · 2014: 23 · 2013: 22 · 2012: 39
FWCI
13.37
Type
journal article
Language
en
Open access
Licence
cc-by-nc-sa
Locations
  • The Journal of Cell Biology (publishedVersion)
  • PubMed Central (publishedVersion, cc-by-nc-sa)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
Keywords
chronological aging, apoptosis, yeast, YAP, caspase activation, oxygen free radicals, cell suicide, clonal competition, unicellular organisms
MeSH terms
Aging, Cell Survival, Enzyme Activation, Saccharomyces cerevisiae, Transcription Factors, Biomarkers, Apoptosis, Reactive Oxygen Species, Caspases, Saccharomyces cerevisiae Proteins

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