Improved production of ethanol by deleting FPS1 and over-expressing GLT1 in Saccharomyces cerevisiae

To improve ethanol production in Saccharomyces cerevisiae, two yeast strains were constructed. In the mutant KAM-3, the FPS1 gene, which encodes a channel protein responsible for glycerol export, was deleted. The mutant KAM-11 had the GLT1 gene (encoding glutamate synthase) placed under the PGK1 pro...

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Bibliographic Details
Published in:Biotechnology letters 2006-12, Vol.28 (24), p.2033-2038
Main Authors: Kong, Qing-Xue, Gu, Ji-Guang, Cao, Li-Min, Zhang, Ai-Li, Chen, Xun, Zhao, Xue-Ming
Format: Article
Language:English
Subjects:
Biological and medical sciences
Biotechnology
Channel protein gene
Efficiency
Ethanol
Ethanol - metabolism
Fermentation
Fermentation - genetics
Fundamental and applied biological sciences. Psychology
Gene Deletion
Gene Expression Regulation, Fungal
Glutamate Synthase - genetics
Glutamate synthase gene
glycerol
Industrial Microbiology - methods
Membrane Proteins - genetics
Models, Biological
Organisms, Genetically Modified
Saccharomyces cerevisiae
Saccharomyces cerevisiae - genetics
Saccharomyces cerevisiae - metabolism
Saccharomyces cerevisiae Proteins - genetics
Up-Regulation
Yeast
Yeasts
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Summary:To improve ethanol production in Saccharomyces cerevisiae, two yeast strains were constructed. In the mutant KAM-3, the FPS1 gene, which encodes a channel protein responsible for glycerol export, was deleted. The mutant KAM-11 had the GLT1 gene (encoding glutamate synthase) placed under the PGK1 promoter while having the FPS1 deletion. Growth rate and biomass concentration remained virtually unchanged with the mutant KAM-11, compared to that of the parent. Over-expression of GLT1 by the PGK1 promoter along with FPS1 deletion resulted in a 14% higher ethanol production and a 30% lower glycerol formation compared to the parental strain under anaerobic fermentation conditions. Furthermore, acetate and pyruvic acid formation was also reduced in order for cells to maintain redox balance.
ISSN:0141-5492
1573-6776
DOI:10.1007/s10529-006-9185-5