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Abstract BackgroundOrganisms frequently experience environmental stresses that occur in predictable patterns and combinations. For wildSaccharomyces cerevisiaeyeast growing in natural environments, cells may experience high osmotic stress when they first enter broken fruit, followed by high ethanol levels during fermentation, and then finally high levels of oxidative stress resulting from respiration of ethanol. Yeast have adapted to these patterns by evolving sophisticated “cross protection” mechanisms, where mild ‘primary’ doses of one stress can enhance tolerance to severe doses of a different ‘secondary’ stress. For example, in many yeast strains, mild osmotic or mild ethanol stresses cross protect against severe oxidative stress, which likely reflects an anticipatory response important for high fitness in nature. ResultsDuring the course of genetic mapping studies aimed at understanding the mechanisms underlying natural variation in ethanol-induced cross protection against H₂O₂, we found that a key H₂O₂scavenging enzyme, cytosolic catalase T (Ctt1p), was absolutely essential for cross protection in a wild oak strain. This suggested the absence of other compensatory mechanisms for acquiring H₂O₂resistance in that strain background under those conditions. In this study, we found surprising heterogeneity across diverse yeast strains in whetherCTT1function was fully necessary for acquired H₂O₂resistance. Some strains exhibited partial dispensability ofCTT1when ethanol and/or salt were used as mild stressors, suggesting that compensatory peroxidases may play a role in acquired stress resistance in certain genetic backgrounds. We leveraged global transcriptional responses to ethanol and salt stresses in strains with different levels ofCTT1dispensability, allowing us to identify possible regulators of these alternative peroxidases and acquired stress resistance in general. ConclusionsUltimately, this study highlights how superficially similar traits can have different underlying molecular foundations and provides a framework for understanding the diversity and regulation of stress defense mechanisms.