Tolerance and stress response to ethanol in the yeast Saccharomyces cerevisiae

Abstract

Eukaryotic cells have developed diverse strategies to combat the harmful effects of a variety of stress conditions. In the model yeast Saccharomyces cerevisiae, the increased concentration of ethanol, as the primary fermentation product, will influence the membrane fluidity and be toxic to membrane proteins, leading to cell growth inhibition and even death. Though little is known about the complex signal network responsible for alcohol stress responses in yeast cells, several mechanisms have been reported to be associated with this process, including changes in gene expression, in membrane composition, and increases in chaperone proteins that help stabilize other denatured proteins. Here, we review the recent progresses in our understanding of ethanol resistance and stress responses in yeast.

Saccharomyces cerevisiae KNU5377 Stress Response during High-Temperature Ethanol Fermentation

“…The high toxicity of endogenously produced ethanol reduces cell viability, growth rate, and fermentation rate. Many mechanisms have been developed to help organisms withstand and/or prevent ethanol-induced damage during fermentation, including crossstress protection; yeast hybrids based on enological characterization (Belloch et al, 2008); membrane remodeling via changes in membrane (palmitoleic acid, oleic acid, and ergosterol) and cell wall composition (fatty acid, lipid, and isoprenoid metabolism); accumulation of amino acids (proline and tryptophan) and storage solutes (trehalose and glycogen) (Zhao and Bai, 2009); expression of molecular chaperones; transcriptional activation of V-ATPase and peroxisomal functions; enhancement of NADPH regeneration and redox balance (Cebollero et al, 2007;Ding et al, 2009;Orozco et al, 2012); genetic improvement through sexual cycle, parasexual hybridization and genetic engineering; and transcriptome remodeling of transcription factors, stress-related genes, and genes involved in signal transduction (Gibson et al, 2007;Ma and Liu, 2010a;Stanley et al, 2010). However, this approach has the intrinsic limitation that yeast adapts to different metabolic environments such as a high concentration of ethanol during fermentation.…”

Mini-Review: The Role of Saccharomyces cerevisiae in the Production of Gin and Vodka

“…Interestingly, research has demonstrated that, under fermentation conditions, there was complete repression of heat shock proteins [61]. Ethanol stress has been extensively reviewed [60,62,63], and therefore the implications will not be discussed further here. However, the ethanol stress tolerance of strains of distilling yeast (both potable and fuel alcohol) have been determined to demonstrate strain specific responses when fermenting at very high gravities and are also influenced by the format in which the yeast is supplied [48].…”

Understanding and overcoming monoterpene toxicity in Saccharomyces cerevisia for the production of sustainable jet fuels

“…Traditionally used in the flavour and fragrance industry, monoterpenes, such as d-limonene, are now being sought after as potential chemopreventive agents 21,22 and precursors for light end components of "dropin" jet fuels 23,24 . Due to their structural complexity, chemical synthesis and extraction of isoprenoids from biological tissues suffer from low yields, impurities and high-cost 25 .…”

“…Cell viability and ethanol production by S. cerevisiae using enzymatically digested citrus peel waste was significantly reduced in the presence of 0.02-0.10% orange peel oil, which contains 95-97% limonene [18][19][20] . Although growth inhibition by orange peel oil, limonene and other nonsubstituted monoterpenes in yeast and bacteria is wellestablished 15,16,[20][21][22][23] , the exact mechanism remains poorly understood.…”

“…For a sparingly water-soluble solvent in equilibrium, the membrane concentration will be proportional to the solvent's aqueous concentration, and molecular toxicity is typically observed to increase proportionally with the solvent's aqueous concentration (21)(22)(23). With the membrane and aqueous phases in equilibrium, molecular toxicity must peak when the aqueous concentration has reached its solubility limit, since both phases are saturated at this point.…”