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      Why yeast cells can undergo apoptosis: death in times of peace, love, and war

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          Abstract

          The purpose of apoptosis in multicellular organisms is obvious: single cells die for the benefit of the whole organism (for example, during tissue development or embryogenesis). Although apoptosis has also been shown in various microorganisms, the reason for this cell death program has remained unexplained. Recently published studies have now described yeast apoptosis during aging, mating, or exposure to killer toxins (Fabrizio, P., L. Battistella, R. Vardavas, C. Gattazzo, L.L. Liou, A. Diaspro, J.W. Dossen, E.B. Gralla, and V.D. Longo. 2004. J. Cell Biol. 166:1055–1067; Herker, E., H. Jungwirth, K.A. Lehmann, C. Maldener, K.U. Frohlich, S. Wissing, S. Buttner, M. Fehr, S. Sigrist, and F. Madeo. 2004. J. Cell Biol. 164:501–507, underscoring the evolutionary benefit of a cell suicide program in yeast and, thus, giving a unicellular organism causes to die for.

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          The chronological life span of Saccharomyces cerevisiae.

          Paola Fabrizio, Ana Longo (2003)
          Simple model systems have played an important role in the discovery of fundamental mechanisms of aging. Studies in yeast, worms and fruit flies have resulted in the identification of proteins and signalling pathways that regulate stress resistance and longevity. New findings indicate that these pathways may have evolved to prevent damage and postpone aging during periods of starvation and may be conserved from yeast to mammals. We will review the yeast S. cerevisiae model system with emphasis on the chronological life span as a model system to study aging and the regulation of stress resistance in eukaryotes.
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            Bakers' yeast, a model for fungal biofilm formation.

            G Fink, Hannah T. Reynolds (2001)
            Biofilms are formed by the aggregation of microorganisms into multicellular structures that adhere to surfaces. Here we show that bakers' yeast Saccharomyces cerevisiae can initiate biofilm formation. When grown in low-glucose medium, the yeast cells adhered avidly to a number of plastic surfaces. On semi-solid (0.3% agar) medium they formed "mats": complex multicellular structures composed of yeast-form cells. Both attachment to plastic and mat formation require Flo11p, a member of a large family of fungal cell surface glycoproteins involved in adherence. The ability to study biofilm formation in a tractable genetic system may facilitate the identification of new targets for antifungal therapy.
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              Chronological aging leads to apoptosis in yeast

              Eva Herker, Helmut Jungwirth, Katharina Lehmann … (2004)
              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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                Author and article information

                Journal
                Journal ID (nlm-ta): J Cell Biol
                Journal ID (publisher-id): jcb
                Title: The Journal of Cell Biology
                Publisher: The Rockefeller University Press
                ISSN (Print): 0021-9525
                ISSN (Electronic): 1540-8140
                Publication date (Print): 20 November 2006
                Volume: 175
                Issue: 4
                Pages: 521-525
                Affiliations
                [1 ]Institute of Molecular Biosciences, University of Graz, 8010 Graz, Austria
                [2 ]Gladstone Institute of Virology and Immunology, San Francisco, CA 94158
                [3 ]Apoptosis, Cancer, and Immunity Unit, Institut Gustave Roussy, Faculté Paris Sud-Université, Institut National de la Santé et de la Recherche Médicale, Paris XI, France
                Author notes

                Correspondence to Frank Madeo: frank.madeo@ 123456uni-graz.at

                Article
                Publisher ID: 200608098
                DOI: 10.1083/jcb.200608098
                PMC ID: 2064587
                PubMed ID: 17101700
                SO-VID: ee65664b-9345-489e-9dff-5d86de2caa90
                Copyright © Copyright © 2006, The Rockefeller University Press
                History
                Date received : 16 August 2006
                Date accepted : 13 October 2006
                Categories
                Subject: Reviews
                Subject: Mini-Review

                ScienceOpen disciplines: Cell biology
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                ScienceOpen disciplines: Cell biology

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