The Osmotic Hypersensitivity of the Yeast Saccharomyces cerevisiae is Strain and Growth Media Dependent: Quantitative Aspects of the Phenomenon

Abstract

Osmotic hypersensitivity is manifested as cellular death at magnitudes of osmotic stress that can support growth. Cellular capacity for survival when plated onto high NaCl media was examined for a number of laboratory and industrial strains of Saccharomyces cerevisiae. During respiro-fermentative growth in rich medium with glucose as energy and carbon source, the hypersensitivity phenomenon was fairly strain invariant with a threshold value of about 1 -NaCl; most strains fell within a 300 m range in LD 10 values (lethal dose yielding 10% survival). Furthermore, all but one of the strains displayed similar differential death responses above the threshold value, i.e. ten-fold decreased viability for every 250 m increase in salinity. Addition of small amounts of salt to the growth medium drastically improved tolerance and shifted the hypersensitivity threshold to higher NaCl concentrations. This salt-instigated tolerance could partly be reversed by washing in water. The washing procedure depleted cells of the glycerol that they had accumulated under saline growth, and the contribution from glycerol to the improved tolerance was about 50% in the two strains examined. Growth on derepressing carbon sources like galactose, ethanol or glycerol gave strain-dependent responses. The laboratory strain X2180-1A drastically improved tolerance while the bakers' yeast strain Y41 did so only marginally. It was concluded that all strains of S. cerevisiae display the osmotic hypersensitivity phenomenon in qualitative terms while the quantitative values differ. It was also proposed that growth rate does not dictate the level of osmotic hypersensitivity of S. cerevisiae.

Aquaporins in Saccharomyces

“…If control of the osmotic balance is important for mating, it may also be critical for processes like budding, pseudohyphal formation, or sporulation. It has been already shown that laboratory strains, industrial strains, and wild-type strains of yeast may have physiological differences in osmosensitivity, but the genetic explanation is not yet known (36). Our studies showing that wild-type and laboratory strains of S. cerevisiae contain distinct AQY1 sequences, resulting in major functional differences that may provide an explanation for these differences.…”

Intracellular Glycerol Levels Modulate the Activity of Sln1p, aSaccharomyces cerevisiae Two-component Regulator

“…For example, an increase in the osmolarity of the medium elicits an osmotic stress response that includes transient cell cycle arrest, restructuring of the actin cytoskeleton, and an elevation in the intracellular glycerol concentration (1)(2)(3)(4). Glycerol is produced intracellularly to partially offset the rise in external osmolarity thus preventing water loss that would lead to dehydration and eventual death (5)(6)(7)(8)(9). Although the exact mechanism by which cells sense a change in osmotic pressure is not known, components of the intracellular signaling pathway that responds to osmotic stress response have begun to be elucidated (10 -12).…”

Diversity of salt response among yeasts

“…The six strains belonging to three species included in the sensu stricto group of the genus Saccharomyces span from 1.7 and 2.3 M. Excluding the most resistant strain (DBVPG 6295), the other five cultures are very similar, ranging from 1.7 M to 1.9 M. These MIC values are in excellent agreement with the viability of S. cerevisiae colonies in NaCl containing plates (Blomberg, 1997).…”

“…The convenience of yeast as model of eukaryote cell for salt stress studies and as biotechnological microorganisms (Serrano et al, 1996;Prista et al, 1997;Huh et al, 2002;Lahav et al, 2002) has encouraged the search for biodiversity in salt tolerance and investigations on the physiological and genetic mechanisms underlying halotolerance (Ferrando et al, 1995;Blomberg, 1997;Mendizabal et al , 1998;Lages et al, 1999;Almagro et al, 2000;Calderon-Torres and Thome, 2001;Cosentino et al, 2001;Hansen et al, 2001;Prista et al, 2002;Ekendahl et al, 2003;Jansen et al, 2003;Schoondermark-Stolk et al, 2003;Turk et al, 2004).…”