SummaryDuring the last years, several reports described an apoptosis-like programmed cell death process in yeast in response to different environmental aggressions. Here, evidence is presented that hyperosmotic stress caused by high glucose or sorbitol concentrations in culture medium induces in Saccharomyces cerevisiae a cell death process accompanied by morphological and biochemical indicators of apoptotic programmed cell death, namely chromatin condensation along the nuclear envelope, mitochondrial swelling and reduction of cristae number, production of reactive oxygen species and DNA strand breaks, with maintenance of plasma membrane integrity. Disruption of AIF1 had no effect on cell survival, but lack of Yca1p drastically reduced metacaspase activation and decreased cell death indicating that this death process was associated to activation of this protease. Supporting the involvement of mitochondria and cytochrome c in caspase activation, the mutant strains cyc1 Δ Δ Δ Δ cyc7 Δ Δ Δ Δ and cyc3 Δ Δ Δ Δ , both lacking mature cytochrome c , displayed a decrease in caspase activation associated to increased cell survival when exposed to hyperosmotic stress. These findings indicate that hyperosmotic stress triggers S. cerevisiae into an apoptosis-like programmed cell death that is mediated by a caspase-dependent mitochondrial pathway partially dependent on cytochrome c .

Cell walls determine the shape of fungal cells and are essential for their integrity. They consist mainly of carbohydrates, some free and some linked to protein. The main components of the yeast cell wall are a (133)-␤-D-glucan (50%) that also contains some (136)-␤-linked branches (5%) (11) and a mannoprotein, most of which is carbohydrate. A (136)-␤-D-glucan, also containing some (133)-␤-linked branches (14%), is a relatively minor constituent (15%), and chitin (0.6 to 9%) is present at an even lower level (18). The latter is concentrated in the bud-scar region (18). The role of cell surface polysaccharides as receptors for proteins in many cell events is widely accepted, but the mechanism of their action is poorly understood. As well as acting as receptors for bacteria, viruses, and toxins, surface polysaccharides may be involved in cell interactions, such as cell associations, distribution, and turnover (15).Killer yeasts act on sensitive yeasts by liberating killer toxins that are either proteins or glycoproteins. The K1 killer toxin of Saccharomyces cerevisiae acts in two steps (20). First, the toxin is adsorbed by a glucan of the cell wall. Then, the toxin is bound to a receptor in the cell membrane, damaging the membrane and releasing K ϩ , ATP, and other metabolites and destroying the pH gradient of the membrane (8). Binding of toxin to the wall receptor appears to be a necessary prelude to cell killing (1, 4). Previous workers (1, 5) defined a specific cell wall receptor for killer toxin by measuring binding of toxin to sensitive cells and to resistant mutants with defective receptors. The receptor, probably a polysaccharide or glycoprotein, was solubilized from yeast cell walls by an endo-(133)-␤-D-glucanase action and is heat and pronase resistant but periodate sensitive (1).Various primary receptors for other killer toxins have been reported. (133) (33), and chitin is a receptor for Kluyveromyces lactis killer toxin (41). Thus, any of the principal components of the cell wall could be the primary receptor for a killer toxin.The phenomenon of killer activity in yeast was originally observed with Saccharomyces (23) and was later found in other genera (19,27). Recently, interest in the development of bacteriocins as food preservatives (14) and in the use of the killer factors for industrial applications has increased (7,13,29,30). However, the role that killer activity may have as a mechanism of antagonism among yeasts in natural environments is not clear, and the conditions governing their behavior in various niches are mostly unknown. In spite of this lack of knowledge, the use of killer toxins to control yeast populations during fermentations has been postulated for beer and wine (7).In previous work (22,25,26), members of this group found that Pichia membranifaciens, the dominant species of yeast isolated from spontaneously fermenting olive brines, had killer characteristics. We also found that sodium chloride, in concentrations similar to those found in the brines, enhanced the apparent toxicity of...

Yeasts were isolated from spontaneous fermentations of olives in brines. Ascomycetous species dominated the yeast flora (>90%) and among them Pichia membranae‐faciens and related species. Some components of the olives were tested as substrates for growth. Killer activity was observed in approximately half of the isolates, and the wider spectra were displayed by strains of Pichia anomala.

Aims: In this work the microflora present in kefir, a fermented milk product, was studied together with the effect of kefir administration on different groups of indigenous bacteria of mouse bowel. Methods and Results: Kefir microflora was composed of lactic acid bacteria, acetic acid bacteria and yeasts. Yeast population was composed of Saccharomyces cerevisiae, S. unisporus, Candida kefir, Kluyveromyces marxianus and K. lactis. The streptococci levels in kefir treated mice increased by 10‐fold and the levels of sulfite‐reducing clostridia decreased by 100‐fold. The number of lactic acid bacteria increased significantly. Conclusions: The administration of kefir significantly increased the lactic acid bacteria counts in the mucosa of the bowel. Ingestion of kefir specifically lowered microbial populations of Enterobacteriaceae and clostridia. Significance and Impact of the Study: This is the first long‐term study about the effects of the kefir administration on the intestinal microflora of mice.

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