Exogenous Indole-3-Acetic Acid Induced Ethanol Tolerance in Phylogenetically Diverse Saccharomycetales Yeasts

Indole-3-acetic acid (IAA) is an exogenous growth regulatory signal that is produced by plants and various microorganisms. Microorganisms have been suggested to cross-communicate with each other through IAA-mediated signaling mechanisms. The IAA-induced tolerance response has been reported in several microorganisms, but has not yet been described in Saccharomycetales yeasts. In the present study, three common stressors (heat, osmotic pressure, and ethanol) were examined in relation to the influence of a pretreatment with IAA on stress tolerance in 12 different lineages of Saccharomyces cerevisiae. The pretreatment with IAA had a significant effect on the induction of ethanol tolerance by reducing the doubling time of S. cerevisiae growth without the pretreatment. However, the pretreatment did not significantly affect the induction of thermo- or osmotolerance. The IAA pretreatment decreased the lethal effects of ethanol on S. cerevisiae cells. Although yeasts produce ethanol to outcompete sympatric microorganisms, IAA is not a byproduct of this process. Nevertheless, the accumulation of IAA indicates an increasing number of microorganisms, and, thus, greater competition for resources. Since the wine trait is shared by both phylogenetically related and distinct lineages in Saccharomycetales, we conclude that IAA-induced ethanol tolerance is not specific to S. cerevisiae; it may be widely detected in both pre-whole genome duplication (WGD) and post-WGD yeasts belonging to several genera of Saccharomycetales.

Automated summary

This study investigated the impact of IAA on the stress tolerance of 12 different lineages of Saccharomyces cerevisiae. The results showed that pretreatment with IAA significantly increased the ethanol tolerance of S. cerevisiae, but had no significant effect on thermo- or osmotolerance. Furthermore, the pretreatment with IAA reduced the lethal effects of ethanol on S. cerevisiae cells.