Necrosis in yeast

Abstract

Necrosis was long regarded as an accidental cell death process resulting from overwhelming cellular injury such as chemical or physical disruption of the plasma membrane. Such a definition, however, proved to be inapplicable to many necrotic scenarios. The discovery that genetic manipulation of several proteins either protected or enhanced necrotic cell death argued in favor of a regulated and hence programmed process, as it is the case for apoptosis. For more than a decade, yeast has served as a model for apoptosis research; recently, evidence accumulated that it also harbors a necrotic program. Here, we summarize the current knowledge about factors that control necrotic cell death in yeast. Mitochondria, aging and a low pH are positive regulators of this process while cellular polyamines (e.g. spermidine) and endonuclease G as well as homeostatic organelles like the vacuole or peroxisomes are potent inhibitors of necrosis. Physiological necrosis may stimulate intercellular signaling via the release of necrotic factors that promote viability of healthy cells and, thus, assure survival of the clone. Together, the data obtained in yeast argue for the existence of a necrotic program, which controls longevity and whose physiological function may thus be aging.

Autophagy proteins play cytoprotective and cytocidal roles in leucine starvation-induced cell death inSaccharomyces cerevisiae

“…Cell wall-permeabilized cells were then stained with 2 ml annexin-FITC (BioLegend, 640905) and 2 ml (500 mg/ml) PI (195458, MP Biomedicals, LLC) following our previously described protocol. 13 In these studies, approximately 90% of the annexin V-binding cells also accumulated PI indicating that they were either in secondary 26 or severe necrosis. Cell walls were not permeabilized when only propidium iodide uptake was tested.…”

“…1E). In this study we could not determine whether cells that stained with both dyes initiated a mixed cell death response from the very beginning of the stress, 24 or instead deteriorated through an apoptotic process known as secondary necrosis 26 that generated membrane holes large enough to let annexin V (MW = 35.8 kDa) as well as PI (MW = 0.67 kDa) enter. Mutational studies did little to distinguish between these alternatives.…”

Impact of multi-metals (Cd, Pb and Zn) exposure on the physiology of the yeast Pichia kudriavzevii

“…The exposure for 24 h to the action of multi-metals induced a loss of membrane integrity in the majority of cell population with the leakage of intracellular components (Fig. 1); this resembles a necrotic scenario (Eisenberg et al 2010). At this time (24 h), a dramatic loss of proliferation capacity and the ability of yeast cells to process FUN-1 occurred (Fig.…”

Effects of citrus limon essential oil (Citrus limon L.) on cytomorphometric changes of Candida albicans

“…Anti-fungal ingredients at low concentrations can lead to apoptosis, but at high concentrations can cause necrosis as a result of radical damage to the cellular structure and integrity. 13 A research conducted by Kim et al on the death process of C. albicans given Amphotericin B and flucytosine shows that the morphology of C. albicans cells undergo the process of death through cell membrane damage. 14 Similarly, a research conducted by Dai et al 12 finds that the administration of the root extract of Scutellaria baicaleinsis on C. albicans can trigger apoptosis in the cells of C. albicans, leading to death.…”