Treitel M A, Carlson M
Department of Genetics and Development, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.
Proc Natl Acad Sci U S A. 1995 Apr 11;92(8):3132-6. doi: 10.1073/pnas.92.8.3132.
The SSN6-TUP1 protein complex represses transcription of diversely regulated genes in the yeast Saccharomyces cerevisiae. Here we present evidence that MIG1, a zinc-finger protein in the EGR1/Zif268 family, recruits SSN6-TUP1 to glucose-repressed promoters. DNA-bound LexA-MIG1 represses transcription of a target gene in glucose-grown cells, and repression requires SSN6 and TUP1. We also show that MIG1 and SSN6 fusion proteins interact in the two-hybrid system. Unexpectedly, we found that LexA-MIG1 activates transcription strongly in an ssn6 mutant and weakly in a tup1 mutant. Finally, LexA-MIG1 does not repress transcription in glucose-deprived cells, and MIG1 is differentially phosphorylated in response to glucose availability. We suggest a role for phosphorylation in regulating repression.
SSN6-TUP1蛋白复合物可抑制酿酒酵母中多种受调控基因的转录。在此，我们提供证据表明，EGR1/Zif268家族中的锌指蛋白MIG1可将SSN6-TUP1招募至受葡萄糖抑制的启动子区域。与DNA结合的LexA-MIG1可抑制葡萄糖培养细胞中靶基因的转录，且这种抑制作用需要SSN6和TUP1。我们还表明，MIG1和SSN6融合蛋白在双杂交系统中相互作用。出乎意料的是，我们发现LexA-MIG1在ssn6突变体中强烈激活转录，而在tup1突变体中则微弱激活转录。最后，LexA-MIG1在葡萄糖缺乏的细胞中不抑制转录，并且MIG1会根据葡萄糖的可利用性发生差异磷酸化。我们认为磷酸化在调节抑制作用中发挥作用。
