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Published 2 August 2004. doi:10.1083/jcb.200405016
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 166, Number 3, 311-316
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 Yeast cell death during DNA damage arrest is independent of caspase or reactive oxygen species

Robert Wysocki and Stephen J. Kron

Center for Molecular Oncology and Department of Molecular Genetics and Cell Biology, The University of Chicago, Chicago, Illinois 60637

Address correspondence to Stephen J. Kron, Center for Molecular Oncology, The University of Chicago, 924 E. 57th Street, Rm. R320, Chicago, IL 60637. Tel.: (773) 834-0250. Fax: (773) 702-4394. email: skron{at}uchicago.edu


Abstract
CDC13 encodes a telomere-binding protein that prevents degradation of telomeres. cdc13-1 yeast grown at the nonpermissive temperature undergo G2/M arrest, progressive chromosome instability, and subsequent cell death. Recently, it has been suggested that cell death in the cdc13-1 mutant is an active process characterized by phenotypic hallmarks of apoptosis and caspase activation. In this work, we show that cell death triggered by cdc13-1 is independent of the yeast metacaspase Yca1p and reactive oxygen species but related to cell cycle arrest per se. Inactivating YCA1 or depleting reactive oxygen species does not increase viability of cdc13-1 cells. In turn, caspase activation does not precede cell death in the cdc13-1 mutant. Yca1p activity assayed by cell binding of mammalian caspase inhibitors is confounded by artifactual labeling of dead yeast cells, which nonspecifically bind fluorochromes. We speculate that during a prolonged cell cycle arrest, cdc13-1 cells reach a critical size and die by cell lysis.

Key Words: FITC-VAD-FMK; apoptosis; CDC13; YCA1; Saccharomyces cerevisiae

Abbreviations used in this paper: DHR123, dihydrorhodamine 123; FMK, fluoromethyl ketone; NAC, N-acetyl-cysteine; PI, propidium iodide; ROS, reactive oxygen species; VAD, valyl-alanyl-aspartyl.


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