Extracellular pH and high concentration of potassium regulate the primary necrosis in the yeast Saccharomyces cerevisiae.

Extracellular pH and concentration of K+ as well as their gradient across the plasma membrane have a significant impact on the physiology of the yeast cell, but their role in cell death has not been thoroughly investigated. Here we observed that increasing extracellular pH, as well as supplementing with K+ ions had a mitigating effect on cell death in yeast occurring under several conditions. The first is sugar induced cell death (SICD), and the second is death caused by several specific gene deletions, which have been recently identified in a systematic screen. It was shown that in both cases, primary necrosis is suppressed at neutral pH. SICD was also inhibited by the protonophore dinitrophenol (DNP) and 150 mM extracellular K+, with the latter condition also benefiting survival of cell dying due to gene mutations. In the case of SICD, these effects could not be mitigated by perturbing known pH-dependent signaling pathways, and thus are likely to be realized via direct effects on the plasma membrane potential. Thus, (a)-we show that stabilization of external pH at a neutral level can suppress different types of primary necrosis, and (b)-we suggest that changes to the cellular membrane potential can play a central role in yeast cell death caused by different factors.

Glucose causes primary necrosis in exponentially grown yeast Saccharomyces cerevisiae.

In this paper, we present data on sugar-induced cell death (SICD) in the yeast Saccharomyces cerevisiae in the exponential phase of growth. We suggest that the nature of SICD in exponentially grown yeast is primary necrosis, in contrast to cells in the stationary growth phase, which exhibit apoptotic SICD. The following findings confirm this conclusion: (i) the process rate; (ii) the impairments of plasma membrane integrity; (iii) the drastic morphological changes in the intracellular content; (iv) the absence of chromatin condensation; (v) the absence of externalization of phosphotidylserine (PS) on the outer leaflet of plasma membrane and (vi) the insensitivity of the SICD process to cycloheximide (CHX). Research shows that SICD occurs in a subpopulation of cells in the S-phase.