Vallier L G, Carlson M
Department of Genetics, College of Physicians and Surgeons, Columbia University, New York, New York 10032.
Genetics. 1994 May;137(1):49-54. doi: 10.1093/genetics/137.1.49.
In the yeast Saccharomyces cerevisiae, glucose repression of SUC2 transcription requires the SSN6-TUP1 repressor complex. It has been proposed that the DNA-binding protein MIG1 secures SSN6-TUP1 to the SUC2 promoter. Here we show that a mig1 deletion does not cause nearly as dramatic a loss of repression as ssn6: glucose-grown mig1 mutants display 20-fold lower SUC2 expression than ssn6 mutants. Thus, repression by SSN6-TUP1 is not mediated solely by MIG1, but also involves MIG1-independent mechanisms. We report that mig1 partially restores SUC2 expression in mutants lacking the SNF1 protein kinase and show that mig1 is allelic to ssn1, a mutation selected as a suppressor of snf1. Other SSN genes identified in this selection were therefore candidates for a role in repression of SUC2. We show that mig1 acts synergistically with ssn2 through ssn5, ssn7, and ssn8 to relieve glucose repression of SUC2 and to suppress the requirement for SNF1. These findings indicate that the SSN proteins contribute to repression of SUC2, and the pleiotropic phenotypes of the ssn mutants suggest global roles in repression. Finally, the regulated SUC2 expression observed in snf1 mig1 mutants indicates that signals regarding glucose availability can be transmitted independently of the SNF1 protein kinase.
在酿酒酵母中，SUC2转录的葡萄糖阻遏需要SSN6-TUP1阻遏复合物。有人提出，DNA结合蛋白MIG1将SSN6-TUP1固定在SUC2启动子上。在此我们表明，mig1缺失所导致的阻遏丧失程度远不及ssn6：在葡萄糖培养基中生长的mig1突变体的SUC2表达水平比ssn6突变体低20倍。因此，SSN6-TUP1介导的阻遏并非仅由MIG1介导，还涉及不依赖MIG1的机制。我们报道，mig1可部分恢复缺乏SNF1蛋白激酶的突变体中的SUC2表达，并表明mig1与ssn1等位，ssn1是作为snf1的一个抑制子而筛选出的突变。因此，在此筛选中鉴定出的其他SSN基因是参与SUC2阻遏作用的候选基因。我们表明，mig1通过ssn5、ssn7和ssn8与ssn2协同作用，以解除对SUC2的葡萄糖阻遏并抑制对SNF1的需求。这些发现表明，SSN蛋白参与了对SUC2的阻遏作用，并且ssn突变体的多效性表型提示其在阻遏作用中具有全局作用。最后，在snf1 mig1突变体中观察到的受调控的SUC2表达表明，有关葡萄糖可用性的信号可以独立于SNF1蛋白激酶进行传递。
