Garfinkel S, Thompson J A, Jacob W F, Cohen R, Safer B
Laboratory of Molecular Hematology, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892.
J Biol Chem. 1990 Jun 25;265(18):10309-19.
DNase I footprint analysis of the core adenovirus 2 (Ad2) major late promoter (MLP) has revealed distinct patterns of protection corresponding to the assembly of transcription components during transcriptional initiation (VanDyke, M. W., Sawadogo, M., and Roeder, R. G. (1989) Mol. Cell Biol. 7, 3371-3379). By using partially purified transcription factors, DNase I protection over the TATA box element and the CAP sequence was attributed to the binding of a single factor, TFIID. We have determined, however, that protection of the CAP region results from the binding of a novel factor, designated CAP-site binding factor (CBF), which is chromatographically and functionally distinct from TFIID. DNase I footprint analysis and gel electrophoresis mobility shift competition assays confirm that distinct polypeptides bind to the Ad2 MLP upstream promoter sequence, TATA box, and CAP sequences. When the CAP sequence is mutated, transcriptional activity of the Ad2 MLP is reduced both in vitro and in vivo. The decrease in transcriptional activity correlates with decreased CBF binding activity. Nuclear extracts depleted of CBF also exhibit reduced Ad2 MLP transcriptional activity. The addition of DNA affinity purified CBF, free of TFIID or major late transcription factor, restores the activity to control levels.
对腺病毒2型(Ad2)主要晚期启动子(MLP)核心区域进行的脱氧核糖核酸酶I足迹分析显示,在转录起始过程中,与转录组件组装相对应的保护模式明显不同(范戴克,M. W.,萨瓦多戈,M.,以及罗德,R. G.(1989年)《分子细胞生物学》7卷,3371 - 3379页)。通过使用部分纯化的转录因子,TATA盒元件和CAP序列上的脱氧核糖核酸酶I保护作用归因于单一因子TFIID的结合。然而,我们已经确定,CAP区域的保护作用是由一种新型因子的结合导致的,该因子被命名为CAP位点结合因子(CBF),它在色谱和功能上与TFIID不同。脱氧核糖核酸酶I足迹分析和凝胶电泳迁移率变动竞争试验证实,不同的多肽与Ad₂ MLP上游启动子序列、TATA盒和CAP序列结合。当CAP序列发生突变时,Ad2 MLP的转录活性在体外和体内均降低。转录活性的降低与CBF结合活性的降低相关。去除了CBF的核提取物也表现出Ad2 MLP转录活性降低。添加经DNA亲和纯化且不含TFIID或主要晚期转录因子的CBF可将活性恢复至对照水平。