Improvement of acetic acid tolerance and fermentation performance of Saccharomyces cerevisiae by disruption of the FPS1 aquaglyceroporin gene

Zhang, Junguo; Liu, Xiuying; He, Xiuping; Guo, Xiaoqian; Lu, Ying; Zhang, Borun

doi:10.1007/s10529-010-0433-3

Cited by 54 publications

(35 citation statements)

References 23 publications

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“…The intake of acetic acid produces cell acidiWcation and intracellular acetate anion (CH 3 COO ¡ ) accumulation, which is involved in inhibition of the glycolytic enzymes in yeast cells [14]. At the general culture temperature of yeast (30°C), the inhibitory eVect of acetic acid on cell growth is more eVective than on fermentation performance [22,30]. In this work, both cell growth and ethanol production of original strain CE25 at 37 and 40°C were hampered by acetic acid.…”

Section: Discussionmentioning

confidence: 96%

Improvement of robustness and ethanol production of ethanologenic Saccharomyces cerevisiae under co-stress of heat and inhibitors

Cheng

et al. 2012

Journal of Industrial Microbiology and Biotechnology

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Bioethanol is an attractive alternative to fossil fuels. Saccharomyces cerevisiae is the most important ethanol producer. However, yeast cells are challenged by various environmental stresses during the industrial process of ethanol production. The robustness under heat, acetic acid, and furfural stresses was improved for ethanologenic S. cerevisiae in this work using genome shuffling. Recombinant yeast strain R32 could grow at 45°C, and resist 0.55% (v/v) acetic acid and 0.3% (v/v) furfural at 40°C. When ethanol fermentation was conducted at temperatures ranging from 30 to 42°C, recombinant strain R32 always gave high ethanol production. After 42 h of fermentation at 42°C, 187.6 ± 1.4 g/l glucose was utilized by recombinant strain R32 to produce 81.4 ± 2.7 g/l ethanol, which were respectively 3.4 and 4.1 times those of CE25. After 36 h of fermentation at 40°C with 0.5% (v/v) acetic acid, 194.4 ± 1.2 g/l glucose in the medium was utilized by recombinant strain R32 to produce 84.2 ± 4.6 g/l of ethanol. The extent of glucose utilization and ethanol concentration of recombinant strain R32 were 6.3 and 7.9 times those of strain CE25. The ethanol concentration produced by recombinant strain R32 was 8.9 times that of strain CE25 after fermentation for 48 h under 0.2% (v/v) furfural stress at 40°C. The strong physiological robustness and fitness of yeast strain R32 support its potential application for industrial production of bioethanol from renewable resources such as lignocelluloses.

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Section: Discussionmentioning

confidence: 96%

Improvement of robustness and ethanol production of ethanologenic Saccharomyces cerevisiae under co-stress of heat and inhibitors

Cheng

et al. 2012

Journal of Industrial Microbiology and Biotechnology

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“…Thus, appropriate engineering to upregulate the sphingolipid pathway in situ may provide a readily accessible and rational means to enhance the acetic acid tolerance of industrially valuable S. cerevisiae strains, either alone or in combination with other genetic strategies that appear to improve the acetic acid tolerance of this organism [66–68]. …”

Section: Discussionmentioning

confidence: 99%

Sphingolipid biosynthesis upregulation by TOR complex 2–Ypk1 signaling during yeast adaptive response to acetic acid stress

Guerreiro

Muir

Ramachandran

et al. 2016

Biochemical Journal

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Acetic acid-induced inhibition of yeast growth and metabolism limits the productivity of industrial fermentation processes, especially when lignocellulosic hydrolysates are used as feedstock in industrial biotechnology. Tolerance to acetic acid of food spoilage yeasts is also a problem in the preservation of acidic foods and beverages. Thus, understanding the molecular mechanisms underlying adaptation and tolerance to acetic acid stress is increasingly important in industrial biotechnology and the food industry. Prior genetic screens for S. cerevisiae mutants with increased sensitivity to acetic acid identified loss-of-function mutations in the YPK1 gene, which encodes a protein kinase activated by the Target of Rapamycin (TOR) Complex 2 (TORC2). We show here by several independent criteria that TORC2-Ypk1 signaling is stimulated in response to acetic acid stress. Moreover, we demonstrate that TORC2-mediated Ypk1 phosphorylation and activation is necessary for acetic acid tolerance, and occurs independently of Hrk1, a protein kinase previously implicated in the cellular response to acetic acid. In addition, we show that TORC2-Ypk1-mediated activation of L-serine: palmitoyl-CoA acyltransferase, the enzyme complex that catalyzes the first committed step of sphingolipid biosynthesis, is required for acetic acid tolerance. Furthermore, analysis of the sphingolipid pathway using inhibitors and mutants indicates that it is production of certain complex sphingolipids that contributes to conferring acetic acid tolerance. Consistent with that conclusion, promoting sphingolipid synthesis by adding exogenous long-chain base precursor phytosphingosine to the growth medium enhanced acetic acid tolerance. Thus, appropriate modulation of the TORC2-Ypk1-sphingolipid axis in industrial yeast strains may have utility in improving fermentations of acetic acid-containing feedstocks.

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“…As www.intechopen.com mentioned above, knowledge on yeast stress mechanisms in response to acetic acid has already had an impact on the construction of industrial strains with improved performance in biotechnological processes (Zhang et al, 2011). However, most studies on stress response, including the latest on the evaluation of resistance to acetic acid at a genome-wide scale, have only been focused on the ability of yeast to divide and grow in the presence of toxic agents.…”

Section: Resultsmentioning

confidence: 99%

“…In another study, it was found that deletion of FPS1, coding for an aquaglyceroporin channel, abolishes acetic acid accumulation at low pH (Mollapour & Piper, 2007). This observation was explored to improve acetic acid resistance and fermentation performance of an ethanologenic industrial strain of S. cerevisiae through the disruption of FPS1 (Zhang et al, 2011). The acetic acid-tolerance phenotype of the disrupted mutant was mainly explained by the preservation of plasma membrane integrity, higher in vivo activity of the H + -ATPase, and lower oxidative damage after acetic acid treatment.…”

Section: Introductionmentioning

confidence: 99%

Stress and Cell Death in Yeast Induced by Acetic Acid

Sousa¹,

Ludovico²,

Rodrigues³

et al. 2012

Cell Metabolism - Cell Homeostasis and Stress Response

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Improvement of acetic acid tolerance and fermentation performance of Saccharomyces cerevisiae by disruption of the FPS1 aquaglyceroporin gene

Cited by 54 publications

References 23 publications

Improvement of robustness and ethanol production of ethanologenic Saccharomyces cerevisiae under co-stress of heat and inhibitors

Improvement of robustness and ethanol production of ethanologenic Saccharomyces cerevisiae under co-stress of heat and inhibitors

Sphingolipid biosynthesis upregulation by TOR complex 2–Ypk1 signaling during yeast adaptive response to acetic acid stress

Stress and Cell Death in Yeast Induced by Acetic Acid

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