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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Repression by SSN6-TUP1 is directed by MIG1, a repressor/activator protein.
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Repression by SSN6-TUP1 is directed by MIG1, a repressor/activator protein.

机译：SSN6-TUP1的阻遏作用是由MIG1（一种阻遏物/激活物蛋白）控制的。

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摘要

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.
机译：SSN6-TUP1蛋白复合物可抑制酵母酿酒酵母中多种调控基因的转录。在这里我们提供证据，MIG1，EGR1 / Zif268家族中的锌指蛋白，招募SSN6-TUP1到葡萄糖抑制的启动子。 DNA结合的LexA-MIG1抑制葡萄糖生长细胞中靶基因的转录，而抑制则需要SSN6和TUP1。我们还显示，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不会抑制葡萄糖剥夺的细胞中的转录，并且MIG1响应于葡萄糖的可用性而被差异磷酸化。我们建议磷酸化调节镇压中的作用。

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