Hu Z, Nehlin J O, Ronne H, Michels C A
Department of Biology, Queens College and the Graduate School of CUNY, Flushing 11367, USA.
Curr Genet. 1995 Aug;28(3):258-66. doi: 10.1007/BF00309785.
Glucose repression is a global regulatory system in Saccharomyces cerevisiae controlling carbon-source utilization, mitochondrial biogenesis, gluconeogenesis and other metabolic pathways. Mig1p, a zinc-finger class of DNA-binding protein, is a transcriptional repressor regulating GAL and SUC gene expression in response to glucose. This report demonstrates that Mig1 protein represses transcription of the MAL61 and MAL62 structural genes and also the MAL63 gene, which encodes the Mal-activator. Mig1p DNA-binding sites were identified upstream of all three MAL genes. Both of the Mig1p-binding sites found in the bidirectional MAL61-MAL62 promoter were shown to function in the Mig1p-dependent glucose repression. Studies using constitutive Mal-activator alleles suggest that glucose regulation of inducer availability is a second major contributing factor in glucose repression of MAL gene expression and is even stronger than the Mig1p-dependent component of repression. Moreover, our results also suggest the contribution of other minor mechanisms in glucose regulation of MAL gene expression.
葡萄糖阻遏是酿酒酵母中的一种全局调控系统，可控制碳源利用、线粒体生物发生、糖异生及其他代谢途径。Mig1p是一种锌指类DNA结合蛋白，是一种转录阻遏物，可响应葡萄糖调节GAL和SUC基因的表达。本报告表明，Mig1蛋白可抑制MAL61和MAL62结构基因以及编码Mal激活剂的MAL63基因的转录。在所有三个MAL基因的上游都鉴定出了Mig1p DNA结合位点。在双向MAL61 - MAL62启动子中发现的两个Mig1p结合位点均显示在Mig1p依赖性葡萄糖阻遏中发挥作用。使用组成型Mal激活剂等位基因的研究表明，葡萄糖对诱导剂可用性的调节是MAL基因表达葡萄糖阻遏中的第二个主要促成因素，甚至比Mig1p依赖性阻遏成分更强。此外，我们的结果还表明了其他次要机制在MAL基因表达葡萄糖调节中的作用。
