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Published 17 February 2004. doi:10.1083/jcb.200310014
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 164, Number 4, 501-507
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Chronological aging leads to apoptosis in yeast



Eva Herker1, Helmut Jungwirth1, Katharina A. Lehmann2, Corinna Maldener1, Kai-Uwe Fröhlich4, Silke Wissing1, Sabrina Büttner1, Markus Fehr3, Stephan Sigrist5, and Frank Madeo1

1 Institute for Physiological Chemistry, University of Tübingen, 72076 Tübingen, Germany
2 Wilhelm-Schickard Institute for Informatics, University of Tübingen, 72076 Tübingen, Germany
3 Department of Plant Biology, Carnegie Institution of Washington, Stanford University, Stanford, CA 94305
4 Institute of Molecular Biology, Biochemistry, and Microbiology, Karl-Franzens University, 8010 Graz, Austria
5 European Neuroscience Institute Göttingen, 37073 Göttingen, Germany

Address correspondence to Frank Madeo, Institute for Physiological Chemistry, University of Tübingen, Hoppe-Seyler-Strasse 4, 72076 Tübingen, Germany. Tel.: 49-7071-2974184. Fax: 49-7071-295565. email: frank.madeo{at}uni-tuebingen.de

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.

Key Words: aging; apoptosis; oxygen stress; Saccharomyces cerevisiae; YCA1

E. Herker and H. Jungwirth contributed equally to this paper.

Abbreviations used in this paper: DHR, dihydrorhodamine 123; ROS, reactive oxygen species; SC, synthetic complete.


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