Background Freezing stress is the key factor that affecting the cell activity and fermentation performance of baker’s yeast in frozen dough production. Generally, cells protect themselves from injury and maintain metabolism by regulating gene expression and modulating metabolic patterns in stresses. The Snf1 protein kinase is an important regulator of yeast in response to stresses. In this study, we aim to study the role of the catalytic subunit of Snf1 protein kinase in the cell tolerance and dough leavening ability of baker’s yeast during freezing. Furthermore, the effects of SNF1 overexpression on the global gene expression and metabolite profile of baker’s yeast before and after freezing were analysed using RNA-sequencing and untargeted UPLC − QTOF-MS/MS, respectively. Results The results suggest that overexpression of SNF1 was effective in enhancing the cell tolerance and fermentation capacity of baker’s yeast in freezing, which may be related to the upregulated proteasome, altered metabolism of carbon sources and protectant molecules, and changed cell membrane components. SNF1 overexpression altered the level of leucin, proline, serine, isoleucine, arginine, homocitrulline, glycerol, palmitic acid, lysophosphatidylcholine (LysoPC), and lysophosphatidylethanolamine (LysoPE) before freezing, conferring cells resistance in freezing. After freezing, relative high level of proline, lysine, and glycerol maintained by SNF1 overexpression with increased content of LysoPC and LysoPE. Conclusions This study will increase the knowledge of the cellular response of baker’s yeast cells to freezing and provide new opportunities for the breeding of low-temperature resistant strains.

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The uncontrolled natural pre-fermentation process of coconut water represents great hidden safety hazards, unstable production, and impact on the quality of nata de coco–the trade name of bacterial cellulose (BC) in food industry. In this study, BC production from Komagataeibacter nataicola Q2 was conducted in the media of coconut water (50%, v/v) pre-fermented by 11 coconut-sourced yeast strains in static. Results suggested that coconut water pre-fermented by different yeast strains had varied effects on the production of BC. Compared with the use of fresh coconut water, the use of coconut water pre-fermented by Saccharomyces cerevisiae SC7 increased the BC yield by 165%. Both natural pre-fermentation and SC7 pre-fermentation altered the concentrations of amino acids in fresh coconut water. The addition of selected amino acids aspartic acid, glutamic acid, serine, methionine, threonine, isoleucine, phenylalanine, and proline at different concentrations had varied effects on the production of BC. The yield of BC was the highest when adding 3.0% (w/v) methionine. Moreover, adding 3.0% methionine allowed the production of BC with larger loops of looser aggregated microfibers, increased the crystallinity of BC from 64.8% to 69.4%, but decreased the temperature of maximum weight loss rate, hardness, and adhesiveness from 223 °C, 8.68 kg, and 92.8 g.sec to 212 °C, 7.01 kg, and 58.5 g.sec, respectively, in the test condition.

Glucose repression is a key regulatory system controlling the metabolism of non-glucose carbon source in yeast. Glucose represses the utilization of maltose, the most abundant fermentable sugar in lean dough and wort, thereby negatively affecting the fermentation efficiency and product quality of pasta products and beer. In this study, the focus was on the role of three kinases, Elm1, Tos3, and Sak1, in the maltose metabolism of baker’s yeast in lean dough. The results suggested that the three kinases played different roles in the regulation of the maltose metabolism of baker’s yeast with differential regulations on MAL genes. Elm1 was necessary for the maltose metabolism of baker’s yeast in maltose and maltose-glucose, and the overexpression of ELM1 could enhance the maltose metabolism and lean dough fermentation ability by upregulating the transcription of MALx1 (x is the locus) in maltose and maltose-glucose and MALx2 in maltose. The native level of TOS3 and SAK1 was essential for yeast cells to adapt glucose repression, but the overexpression of TOS3 and SAK1 alone repressed the expression of MALx1 in maltose-glucose and MALx2 in maltose. Moreover, the three kinases might regulate the maltose metabolism via the Snf1-parallel pathways with a carbon source-dependent manner. These results, for the first time, suggested that Elm1, rather than Tos3 and Sak1, might be the dominant regulator in the maltose metabolism of baker’s yeast. These findings provided knowledge about the glucose repression of maltose and gave a new perspective for breeding industrial yeasts with rapid maltose metabolism.

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