Independent mechanisms for acquired salt tolerance versus growth resumption induced by mild ethanol pretreatment inSaccharomyces cerevisiae

Abstract

27All living organisms must recognize and respond to various environmental stresses 28 throughout their lifetime. In natural environments, cells frequently encounter fluctuating 29 concentrations of different stressors that can occur in combination or sequentially. Thus, the 30 ability to anticipate an impending stress is likely ecologically relevant. One possible mechanism 31 for anticipating future stress is acquired stress resistance, where cells pre-exposed to a mild 32 sub-lethal dose of stress gain the ability to survive an otherwise lethal dose of stress. We have 33 been leveraging wild strains of Saccharomyces cerevisiae to investigate natural variation in the 34 yeast ethanol stress response and its role in acquired stress resistance. Here, we report that a 35 wild vineyard isolate possesses ethanol-induced cross-protection against severe concentrations 36 of salt. Because this phenotype correlates with ethanol-dependent induction of the ENA genes, 37 which encode sodium efflux pumps already associated with salt resistance, we hypothesized 38 that variation in ENA expression was responsible for differences in acquired salt tolerance 39 across strains. Surprisingly, we found that the ENA genes were completely dispensable for 40 ethanol-induced survival of high salt concentrations in the wild vineyard strain. Instead, the ENA 41 genes were necessary for the ability to resume growth on high concentrations of salt following a 42 mild ethanol pretreatment. Surprisingly, this growth acclimation phenotype was also shared by 43 the lab yeast strain despite lack of ENA induction under this condition. This study underscores 44 that cross protection can affect both viability and growth through distinct mechanisms, both of 45 which likely confer fitness effects that are ecologically relevant. 46 47 48

Gene-by-environment interactions influence the fitness cost of gene copy-number variation in yeast

“…Remarkably, the other strains all induced ENA1 expression to within 2-fold of BY4743 mRNA levels, albeit with delayed kinetics. While induction of ENA1 may help with the acclimation to continued salt stress (76), it is likely that the basal expression levels influence the immediate survival after rapid-onset salt stress. Thus, we propose that although strains retain the ability to induce ENA1 expression after stress, the low starting mRNA levels likely contribute to variations in the ability to survive the initial NaCl exposure -this likely also explains differences in the fitness cost of other OE genes, including OE of other sodium transporters and ion-response regulators whose duplication provides a major benefit to wild strains but has no effect in BY4743 (see Discussion).…”