REPRESSION BY SSN6-TUP1 IS DIRECTED BY MIG1, A REPRESSOR ACTIVATOR PROTEIN
REPRESSION BY SSN6-TUP1 IS DIRECTED BY MIG1, A REPRESSOR ACTIVATOR PROTEIN
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DOI：
10.1073/pnas.92.8.3132
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发表时间：
1995-04-11
影响因子：
11.1
通讯作者：
CARLSON, M
中科院分区：
文献类型：
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作者：
TREITEL, MA;CARLSON, M
在酿酒酵母中，SSN6-TUP1蛋白复合物可抑制多种调控基因的转录。本研究表明，EGR1/Zif268家族中的锌指蛋白MIG1可将SSN6-TUP1招募到葡萄糖抑制启动子中。dna结合的LexA-MIG1抑制葡萄糖生长细胞中靶基因的转录，这种抑制需要SSN6和TUP1。我们还发现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在葡萄糖可用性的反应中会发生差异磷酸化。我们认为磷酸化在调节抑制中起作用。
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.