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Published online 24 January 2005. doi:10.1083/jcb.200408071
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 168, Number 3, 353-358
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 Viral killer toxins induce caspase-mediated apoptosis in yeast

Jochen Reiter1, Eva Herker2, Frank Madeo2, and Manfred J. Schmitt1

1 Applied Molecular Biology, University of the Saarland, D-66041 Saarbrücken, Germany
2 Institute of Molecular Biosciences, Karl-Franzens University, A-8010 Graz, Austria

Correspondence to Manfred J. Schmitt: mjs{at}microbiol.uni-sb.de


Abstract
In yeast, apoptotic cell death can be triggered by various factors such as H2O2, cell aging, or acetic acid. Yeast caspase (Yca1p) and cellular reactive oxygen species (ROS) are key regulators of this process. Here, we show that moderate doses of three virally encoded killer toxins (K1, K28, and zygocin) induce an apoptotic yeast cell response, although all three toxins differ significantly in their primary killing mechanisms. In contrast, high toxin concentrations prevent the occurrence of an apoptotic cell response and rather cause necrotic, toxin-specific cell killing. Studies with {Delta}yca1 and {Delta}gsh1 deletion mutants indicate that ROS accumulation as well as the presence of yeast caspase 1 is needed for apoptosis in toxin-treated yeast cells. We conclude that in the natural environment of toxin-secreting killer yeasts, where toxin concentration is usually low, induction of apoptosis might play an important role in efficient toxin-mediated cell killing.

Abbreviations used in this paper: DHR, dihydrorhodamine; MBA, methylene blue agar plates; PS, phosphatidylserine; ROS, reactive oxygen species.


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