Mechanisms of Acetate Ester Production and Control in Yeasts-Monograph.
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Accession number;01A0348430
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| Title;Mechanisms of Acetate Ester Production and Control in Yeasts-Monograph. |
| Author;
YOSHIMOTO HIROYUKI
(Kirin Brew. Co., Ltd., Res. and Dev. Div.)
FUJIWARA DAISUKE
(Kirin Brew. Co., Ltd., Res. and Dev. Div.)
BOUGAKI TAKAYUKI
(Ozeki Corp., Gen. Res. Lab.)
NAGASAWA NAOSHI
(Ozeki Corp., Gen. Res. Lab.)
FUJII TOSHIO
(Kirin Brew. Co., Ltd., Res. and Dev. Div.)
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Journal Title;Seibutsu Kogakkaishi
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Journal Code:G0440B
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ISSN:0919-3758
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VOL.79;NO.2;PAGE.33-40(2001)
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| Figure&Table&Reference;FIG.8, REF.40 |
| Pub. Country;Japan |
| Language;Japanese |
| Abstract;Acetate esters such as isoamyl acetate and ethyl acetate are major flavor components of yeast-fermented alcoholic beverages. These esters are synthesized by alcohol acetyltransferase (AATase) from acetyl CoA and the corresponding alcohols. The production of acetate esters is influenced by many factors, including aeration, the concentrations of unsaturated fatty acids, the precursor concentration, and the proportion of the nitrogen source. However, the mechanisms through which these factors influence acetate ester production remain unclear. To investigate the underlying cellular mechanisms of the effects of such factors, we cloned and characterized the ATF genes encoding AATase from the sake yeast Saccharomyces cerevisiae and the bottom fermenting yeast Saccharomyces pastorianus. Results of genetic and biochemical studies suggested that the reduction in the production of acetate esters arising from aeration or the addition of unsaturated fatty acids is due to a reduction in enzyme synthesis resulting from transcriptional repression of the ATF1 genes responsible for most AATase activity. Further studies demonstrated that changes in isoamyl acetate production caused by the nitrogen source depend on both the yield of precursor isoamyl alcohol and ATF transcription. Analysis of the ATF1 gene promoter region identified an 18-bp element containing a binding consensus sequence of transcription factor Rap1p, which is essential for transcriptional activation and repression by unsaturated fatty acids. Oxygen repressed an ATF1 transcript through the Rox1p-Tup1p-Ssn6p hypoxic repressor complex at the binding consensus sequence of Rox1p. ATF1 expression is activated by the nitrogen source through a protein kinase, Sch9p. Our study provides a model for investigating ATF1 transcriptional regulation by oxygen, unsaturated fatty acids, and nitrogen. (author abst.) |
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