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

LAUFF DB; SANTA MARIA G.E.

FEMS YEAST RESEARCH

WILEY-BLACKWELL PUBLISHING, INC

Año: 2010 vol. 10 p. 497 - 507

1567-1356

Cell culture in low potassium (K1) media has been associated to programmed celldeath (PCD) in metazoans. In this study, deprivation of K1 led Saccharomycescerevisiae cells to a death process that involved phosphatidylserine externalization,changes in chromatin condensation, DNA and vacuole fragmentation as well asenhanced accumulation of reactive oxygen species. During the course of K1starvation, plasma membrane hyperpolarization and increased accumulation ofcalcium (Ca21) took place. The presence of rubidium (Rb1), a K1-analogueelement, in the K1-deprived medium was accompanied by Rb1 accumulation butdid not fully prevent the appearance of PCD markers. This argues for a specificeffect of K1 on the course of cell death. While the absence of the YCA1 metacaspasedid not have a major effect, the absence of TRK (transport of K1) K1-transportersled to changes in the pattern of annexin V/propidium iodide labeling. This changeparalleled a fast accumulation of Ca21. Addition of ethylene glycol tetraacetic acidimproved growth and reduced cell death in trk1Dtrk2D cells. These findings revealthat K1 deprivation is sufficient to induce PCD in a cell-walled eukaryoticorganism and suggest that the phenotype attributed to the lack of TRK genes ispartially due to the effect of the encoded transporters on Ca21 homeostasis.