Zijderveld D C, d'Adda di Fagagna F, Giacca M, Timmers H T, van der Vliet P C
Laboratory for Physiological Chemistry, University of Utrecht, The Netherlands.
J Virol. 1994 Dec;68(12):8288-95. doi: 10.1128/JVI.68.12.8288-8295.1994.
Previous studies have shown that the sequence-independent adenovirus DNA binding protein (DBP) increases transcription from several promoters, notably from the adenovirus major late promoter (MLP) and the adeno-associated virus P5 promoter, both of which contain a USF/MLTF binding site. In order to study this mechanism, we have investigated the effects of DBP on the binding of USF/MLTF to MLP and on transcription from MLP by a reconstituted in vitro system. As shown by gel retardation and DNase I footprinting, upon saturation of DNA, DBP enhances the binding affinity of USF43 to the promoter three- to fourfold without changing the footprint pattern. In contrast, the binding of the TATA box binding protein to the promoter is not influenced by DBP. No protein-protein interactions between DBP and USF43 could be observed in the absence of DNA, suggesting that enhanced binding is caused by a change in DNA structure induced by the DBP-DNA complex. Employing a transcription system reconstituted with purified general transcription factors, we show that USF43 enhances basal transcription and that USF43-dependent transcription is further increased by DBP, while DBP alone does not have an effect on basal transcription. Our results suggest that transcription enhancement by DBP is based on a specific increase in the binding of a transcription factor to a promoter through subtle changes in DNA structure, similar to the mechanism by which DBP stimulates the initiation of DNA replication.
先前的研究表明,序列非依赖性腺病毒DNA结合蛋白(DBP)可增强多个启动子的转录,尤其是腺病毒主要晚期启动子(MLP)和腺相关病毒P5启动子,这两个启动子均含有一个USF/MLTF结合位点。为了研究这一机制,我们通过一个重组的体外系统,研究了DBP对USF/MLTF与MLP结合以及对MLP转录的影响。如凝胶阻滞和DNase I足迹实验所示,DNA饱和后,DBP可使USF43与启动子的结合亲和力提高三到四倍,而不改变足迹模式。相比之下,TATA盒结合蛋白与启动子的结合不受DBP影响。在没有DNA的情况下,未观察到DBP与USF43之间的蛋白质-蛋白质相互作用,这表明增强的结合是由DBP-DNA复合物诱导的DNA结构变化引起的。利用用纯化的通用转录因子重组的转录系统,我们发现USF43可增强基础转录,并且DBP可进一步提高USF43依赖性转录,而单独的DBP对基础转录没有影响。我们的结果表明,DBP增强转录是基于转录因子通过DNA结构的细微变化与启动子结合的特异性增加,这类似于DBP刺激DNA复制起始的机制。