Open AccessPotassium deprivation is sufficient to induce a cell death program in Saccharomyces cerevisiae
Author(s) -
Lauff Diana Beatríz,
SantaMaría Guillermo E.
Publication year - 2010
Publication title -
fems yeast research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.991
H-Index - 92
eISSN - 1567-1364
pISSN - 1567-1356
DOI - 10.1111/j.1567-1364.2010.00628.x
Subject(s) - biology , programmed cell death , propidium iodide , saccharomyces cerevisiae , microbiology and biotechnology , vacuole , apoptosis , calcium , fragmentation (computing) , biochemistry , yeast , chemistry , cytoplasm , ecology , organic chemistry
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 trk1 Δ trk2 Δ 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.