Suppr超能文献

SSN6-TUP1的抑制作用由MIG1介导,MIG1是一种阻遏物/激活蛋白。

Repression by SSN6-TUP1 is directed by MIG1, a repressor/activator protein.

作者信息

Treitel M A, Carlson M

机构信息

Department of Genetics and Development, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.

出版信息

Proc Natl Acad Sci U S A. 1995 Apr 11;92(8):3132-6. doi: 10.1073/pnas.92.8.3132.

Abstract

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.

摘要

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。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bc85/42119/fcba8264f136/pnas01492-0067-a.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验