Potassium deprivation is sufficient to induce a cell death program in Saccharomyces cerevisiae

• Published in: FEMS yeast research Vol. 10; no. 5; pp. 497 - 507
• Main Authors: Lauff, Diana Beatríz, Santa-María, Guillermo E
• Format: Journal Article
• Language: English
• Published: Oxford, UK Oxford, UK : Blackwell Publishing Ltd 01-08-2010; Blackwell Publishing Ltd; Oxford University Press
• Subjects: Annexin V; Apoptosis; Calcium - metabolism; Calcium homeostasis; Cation Transport Proteins - genetics; Cation Transport Proteins - metabolism; Cell culture; Cell Death; Cell Membrane - chemistry; Cell Membrane - physiology; Chromatin; Chromatin - metabolism; DNA Fragmentation; Ethylene glycol; Gene Deletion; Homeostasis; Hyperpolarization; Phenotypes; Phosphatidylserine; Phosphatidylserines - analysis; Potassium; Potassium - metabolism; potassium transport; programmed cell death; Propidium iodide; Reactive oxygen species; Reactive Oxygen Species - metabolism; Rubidium; Rubidium - metabolism; Saccharomyces cerevisiae; Saccharomyces cerevisiae - chemistry; Saccharomyces cerevisiae - cytology; Saccharomyces cerevisiae - metabolism; Saccharomyces cerevisiae Proteins - genetics; Saccharomyces cerevisiae Proteins - metabolism; TRK; Yeast; apoptosis; programmed cell death; TRK; potassium transport
• ISSN: 1567-1356; 1567-1364
• DOI: 10.1111/j.1567-1364.2010.00628.x

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.