Shankar C S, Ramakrishnan M S, Umesh-Kumar S
Department of Food Microbiology, Central Food Technological Research Institute, Mysore, India.
Microbiology (Reading). 1996 Sep;142 ( Pt 9):2663-7. doi: 10.1099/00221287-142-9-2663.
MIG1, encoding a C2H2 zinc-finger repressor protein involved in carbon catabolite repression, was found to play a role in non-sexual flocculation of Saccharomyces cerevisiae. Disruption of MIG1 in a flocculent mutant strain of NCYC 227, resulted in a non-flocculent phenotype. Expression of MIG1 on a 2 mu pRS426 vector in a non-flocculent strain, YM 4134, caused flocculation; MIG1 on a high-copy-number LEU2-d plasmid caused intense flocculation in the same strain. Mutations in the SSN6 and TUP1 genes confer a flocculent phenotype in non-flocculent strains of S. cerevisiae, and it has been shown that Mig1 can tether the Ssn6p-Tup1p complex to the regulatory regions of glucose-repressible genes. Mutations in tup1 in a MIG1 background caused flocculation while double mutants of TUP1 and MIG1 did not flocculate. Based on these results, a model for the role of MIG1 in flocculation gene regulation is proposed.
MIG1编码一种参与碳代谢物阻遏的C2H2锌指阻遏蛋白,被发现参与酿酒酵母的非性絮凝过程。在絮凝突变株NCYC 227中破坏MIG1会导致非絮凝表型。在非絮凝菌株YM 4134中,将MIG1在2μm pRS426载体上表达会导致絮凝;MIG1在高拷贝数的LEU2-d质粒上会使同一菌株产生强烈絮凝。SSN6和TUP1基因的突变会使酿酒酵母的非絮凝菌株呈现絮凝表型,并且已经表明Mig1可以将Ssn6p-Tup1p复合物连接到葡萄糖可阻遏基因的调控区域。在MIG1背景下tup1的突变会导致絮凝,而TUP1和MIG1的双突变体则不会絮凝。基于这些结果,提出了一个MIG1在絮凝基因调控中作用的模型。