Editor: André Goffeau
Potassium deprivation is sufficient to induce a cell death program in Saccharomyces cerevisiae
Article first published online: 7 APR 2010
© 2010 Federation of European Microbiological Societies. Published by Blackwell Publishing Ltd. All rights reserved
FEMS Yeast Research
Volume 10, Issue 5, pages 497–507, August 2010
How to Cite
Lauff, D. B. and Santa-María, G. E. (2010), Potassium deprivation is sufficient to induce a cell death program in Saccharomyces cerevisiae. FEMS Yeast Research, 10: 497–507. doi: 10.1111/j.1567-1364.2010.00628.x
- Issue published online: 9 JUL 2010
- Article first published online: 7 APR 2010
- Received 7 December 2009; revised 29 March 2010; accepted 31 March 2010.Final version published online 11 May 2010.
- programmed cell death;
- potassium transport;
- Saccharomyces cerevisiae;
Cell culture in low potassium (K+) media has been associated to programmed cell death (PCD) in metazoans. In this study, deprivation of K+ led Saccharomyces cerevisiae cells to a death process that involved phosphatidylserine externalization, changes in chromatin condensation, DNA and vacuole fragmentation as well as enhanced accumulation of reactive oxygen species. During the course of K+ starvation, plasma membrane hyperpolarization and increased accumulation of calcium (Ca2+) took place. The presence of rubidium (Rb+), a K+-analogue element, in the K+-deprived medium was accompanied by Rb+ accumulation but did not fully prevent the appearance of PCD markers. This argues for a specific effect of K+ on the course of cell death. While the absence of the YCA1 metacaspase did not have a major effect, the absence of TRK (transport of K+) K+-transporters led to changes in the pattern of annexin V/propidium iodide labeling. This change paralleled a fast accumulation of Ca2+. Addition of ethylene glycol tetraacetic acid improved growth and reduced cell death in trk1Δtrk2Δ cells. These findings reveal that K+ deprivation is sufficient to induce PCD in a cell-walled eukaryotic organism and suggest that the phenotype attributed to the lack of TRK genes is partially due to the effect of the encoded transporters on Ca2+ homeostasis.