Glucose repression of STA1 expression is mediated by the NRG1 and Sfl1 repressors and the Srb8-11 complex
Glucose repression of STA1 expression is mediated by the NRG1 and Sfl1 repressors and the Srb8-11 complex
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DOI：
10.1128/mcb.24.17.7695-7706.2004
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发表时间：
2004-09-01
影响因子：
5.3
通讯作者：
Kang, HS
中科院分区：
文献类型：
--
作者：
Kim, TS;Lee, SB;Kang, HS
在酵母中，编码胞外糖化酶的STA1基因的表达受葡萄糖的负调控。在这里，我们证明了糖依赖的STA1表达的抑制是由SFL1和Nrg1共同实施的，这两个基因作为直接转录抑制因子。我们发现，在STA1启动子中，Nrg1只作用于UAS1，SFL1只作用于UAS2。当Sill(但不是Nrg1)与其特定位点结合时，会阻止STA1表达所需的两个转录激活剂STE12和Tec1与UAS2的结合。我们还发现SFL1通过与启动子结合并抑制FLO8的表达而参与STA1的抑制，FLO8是一个编码参与STA1表达的第三转录激活因子的基因。此外，我们发现在葡萄糖培养的细胞中，Nrg1和SFL1的水平增加，这表明葡萄糖的影响至少部分是通过这些抑制物丰度的增加来介导的。NRG1和SFL1的表达需要Srb8-11复合体，相应地，Srb8-11复合体也是抑制STA1所必需的。然而，我们的证据表明，Srb8-11复合体既不与SFL1启动子结合，也不与NRG1启动子结合，因此在激活NRG1和SFL1表达方面发挥了间接作用。
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, Sill (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.