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TATA结合蛋白与单纯疱疹病毒1型ICP4 DNA结合位点在复合物形成及转录抑制中的关系。

Relationship between TATA-binding protein and herpes simplex virus type 1 ICP4 DNA-binding sites in complex formation and repression of transcription.

作者信息

Kuddus R, Gu B, DeLuca N A

机构信息

Department of Molecular Genetics and Biochemistry, University of Pittsburgh School of Medicine, Pennsylvania 15261, USA.

出版信息

J Virol. 1995 Sep;69(9):5568-75. doi: 10.1128/JVI.69.9.5568-5575.1995.

Abstract

The herpes simplex virus (HSV) regulatory protein, infected-cell polypeptide 4 (ICP4), represses the transcription of promoters that have binding sites for ICP4 located near the transcription start site. It also been shown that ICP4 binds such promoter DNA cooperatively with the TATA-binding protein (TBP) and TFIIB to form a tripartite protein-DNA complex (C. Smith, P. Bates, R. Rivera-Gonzales, B. Gu, and N. A. DeLuca, J. Virol. 67:4676-4687, 1993). In this study, we analyzed the effects of position and orientation of the ICP4-binding site relative to the TATA box in the ICP4 promoter on transcriptional repression by ICP4 and on the ability of ICP4 to form tripartite complexes with TBP and TFIIB. The results of theis parallel study provide a strong correlation between tripartite complex formation and repression. Both tripartite-complex formation and transcriptional repression were efficient when the ICP4-binding site was downstream of the TATA box, within a short distance and in proper orientation. In addition, both tripartite-complex formation and repression were partially sensitive to the stereoaxial positioning of the ICP4-binding site relative to the TATA box. As a preliminary characterization of the tripartite complex, circular permutation analysis was performed to assess the distortion of the proximal promoter region in the tripartite complex. As previously reported, both TBP and ICP4 independently could bend DNA and the relative magnitude by which each of these proteins bent DNA in the tripartite complex was preserved. The results of this study suggest that the formation of tripartite complexes on a promoter is part of the mechanism of repression and that simple blocking as a sole result of ICP4 binding is not sufficient for full repression.

摘要

单纯疱疹病毒(HSV)调节蛋白感染细胞多肽4(ICP4)可抑制那些在转录起始位点附近含有ICP4结合位点的启动子的转录。研究还表明,ICP4与TATA结合蛋白(TBP)和TFIIB协同结合此类启动子DNA,形成三方蛋白质-DNA复合物(C.史密斯、P.贝茨、R.里维拉-冈萨雷斯、B.顾和N.A.德卢卡,《病毒学杂志》67:4676 - 4687,1993年)。在本研究中,我们分析了ICP4启动子中ICP4结合位点相对于TATA框的位置和方向对ICP4转录抑制作用以及ICP4与TBP和TFIIB形成三方复合物能力的影响。这项平行研究的结果表明三方复合物形成与抑制作用之间存在很强的相关性。当ICP4结合位点位于TATA框下游、距离较短且方向合适时,三方复合物形成和转录抑制都很有效。此外,三方复合物形成和抑制作用对ICP4结合位点相对于TATA框的立体定位都部分敏感。作为对三方复合物的初步表征,进行了环形置换分析以评估三方复合物中近端启动子区域的扭曲情况。如先前报道,TBP和ICP4均可独立使DNA弯曲,并且在三方复合物中每种蛋白质使DNA弯曲的相对幅度得以保留。本研究结果表明,启动子上三方复合物的形成是抑制机制的一部分,仅因ICP4结合导致的简单阻断不足以实现完全抑制。

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