Abstract 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.
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|Evidence ID||Analyze ID||Gene||Gene Systematic Name||Phenotype||Experiment Type||Experiment Type Category||Mutant Information||Strain Background||Chemical||Details||Reference|
|Evidence ID||Analyze ID||Regulator||Regulator Systematic Name||Target||Target Systematic Name||Experiment||Conditions||Strain||Source||Reference|