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热休克蛋白70启动子处的协同与竞争性蛋白质相互作用。

Cooperative and competitive protein interactions at the hsp70 promoter.

作者信息

Mason P B, Lis J T

机构信息

Department of Biochemistry, Molecular and Cell Biology, Cornell University, Ithaca, New York 14853, USA.

出版信息

J Biol Chem. 1997 Dec 26;272(52):33227-33. doi: 10.1074/jbc.272.52.33227.

Abstract

Drosophila heat shock factor (HSF) binds to specific sequence elements of heat shock genes and can activate their transcription 200-fold. Though HSF has an acidic activation domain, the mechanistic details of heat shock gene activation remain undefined. Here we report that HSF interacts directly with the general transcription factor TBP (TATA-box binding protein), and these two factors bind cooperatively to heat shock promoters. A third factor that binds heat shock promoters, GAGA factor, also interacts with HSF and further stabilizes HSF binding to heat shock elements (HSEs). The interaction of HSF and TBP is explored in some detail here and is shown to be mediated by residues in both the amino- and carboxyl-terminal portions of HSF. This HSF/TBP interaction can be specifically disrupted by competition with the potent acidic transcriptional activator VP16. We further show that the acidic domain of the largest subunit of Drosophila RNA polymerase II (Pol II) associates with TBP in vitro and is specifically displaced from TBP upon addition of HSF. The region of TBP that mediates both HSF and Pol II acidic domain binding maps to the conserved carboxyl-terminal repeats and depends on at least one of the TBP residues known to be contacted by VP16 and to be critical for transcription activation. We discuss these findings in the context of a model in which HSF triggers hsp70 transcription by freeing the hsp70 promoter-paused Pol II from the constraints on elongation caused by the affinity of Pol II for general transcription factors.

摘要

果蝇热休克因子(HSF)与热休克基因的特定序列元件结合,并能将其转录激活200倍。尽管HSF具有一个酸性激活结构域,但热休克基因激活的机制细节仍不明确。在此我们报告,HSF直接与通用转录因子TBP(TATA盒结合蛋白)相互作用,并且这两个因子协同结合热休克启动子。另一个结合热休克启动子的因子,GAGA因子,也与HSF相互作用,并进一步稳定HSF与热休克元件(HSEs)的结合。本文对HSF与TBP的相互作用进行了较为详细的探讨,结果表明这种相互作用是由HSF氨基末端和羧基末端部分的残基介导的。HSF/TBP相互作用可通过与强效酸性转录激活因子VP16竞争而被特异性破坏。我们进一步表明,果蝇RNA聚合酶II(Pol II)最大亚基的酸性结构域在体外与TBP结合,并且在加入HSF后会从TBP上特异性解离。介导HSF和Pol II酸性结构域结合的TBP区域定位于保守的羧基末端重复序列,并且依赖于已知与VP16接触且对转录激活至关重要的至少一个TBP残基。我们在一个模型的背景下讨论这些发现,在该模型中,HSF通过使hsp70启动子暂停的Pol II从Pol II与通用转录因子亲和力所导致的延伸限制中释放出来,从而触发hsp70转录。

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