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Molecular and Cellular Biology, September 2004, p. 7695-7706, Vol. 24, No. 17
0270-7306/04/$08.00+0 DOI: 10.1128/MCB.24.17.7695-7706.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
Sung Bae Lee, and
Hyen Sam Kang*
Department of Microbiology, School of Biological Sciences, Seoul National University, Seoul, Korea
Received 12 December 2003/ Returned for modification 2 February 2004/ Accepted 13 May 2004
In the yeast Saccharomyces diastaticus, expression of the STA1 gene, which encodes an extracellular glucoamylase, is negatively regulated by glucose. Here we demonstrate that glucose-dependent repression of STA1 expression is imposed by both Sfl1 and Nrg1, which serve as direct transcriptional repressors. We show that Nrg1 acts only on UAS1, and Sfl1 acts only on UAS2, in the STA1 promoter. When bound to its specific site, Sfl1 (but not Nrg1) prevents the binding to UAS2 of two transcriptional activators, Ste12 and Tec1, required for STA1 expression. We also found that Sfl1 contributes to STA1 repression by binding to the promoter and inhibiting the expression of FLO8, a gene that encodes a third transcriptional activator involved in STA1 expression. In addition, we show that the levels of Nrg1 and Sfl1 increase in glucose-grown cells, suggesting that the effects of glucose are mediated, at least in part, through an increase in the abundance of these repressors. NRG1 and SFL1 expression requires the Srb8-11 complex, and correspondingly, the Srb8-11 complex is also necessary for STA1 repression. However, our evidence indicates that the Srb8-11 complex does not associate with either the SFL1 or the NRG1 promoter and thus plays an indirect role in activating NRG1 and SFL1 expression.
Present address: Dobeel Corp., Byucksantechnopia I, 434-6, Sangdaewon-dong, Jungwon-gu, Seongnam-si 462-716, Korea.
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