Potassium deprivation is sufficient to induce a cell death program in 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 (Ca(2+)) 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 Ca(2+). Addition of ethylene glycol tetraacetic acid improved growth and reduced cell death in trk1Deltatrk2Delta 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 Ca(2+) homeostasis.