Majello B, Napolitano G, De Luca P, Lania L
Department of Genetics, Molecular and General Biology, University of Naples "Federico II," via Mezzocannone 8, 80134 Naples, Italy.
J Biol Chem. 1998 Jun 26;273(26):16509-16. doi: 10.1074/jbc.273.26.16509.
An increasing body of evidence suggests that eukaryotic activators stimulate polymerase II transcription by facilitating the assembly of the functional basal machinery at the promoter. Here we describe experiments that provide added support for the idea that recruitment of TATA-binding protein (TBP) is a rate-limiting step for transcription activation in mammalian cells. We found that, in human cell lines, recruitment of TBP to a promoter, as a GAL4-TBP fusion protein, can provide a substantial activation of transcription. Activation mediated by the hTBP, tethered to promoter DNA, is strictly dependent upon the presence of a functional TATA element, and it directs faithful transcription initiation. Interestingly, GAL4-hTBP activation was not observed from initiator (Inr) -dependent TATA-less promoters. These results suggest that TBP binding to DNA is not a rate-limiting step for the initial stages of TFIID recruitment to initiator-dependent TATA-less promoters. Finally, we provide evidence that synergy between GAL4-hTBP and defined transcription domains is restricted to activators, such as VP16 and Tat, which are likely to function at steps subsequent to the TFIID recruitment. These findings strengthen the idea that recruitment of TBP represents an important mechanism of activation of TATA-dependent promoters, and on the other hand, they suggest that TBP-DNA interactions are largely dispensable for specific transcription of initiator dependent TATA-less promoters.
越来越多的证据表明,真核激活因子通过促进启动子上功能性基础转录机制的组装来刺激聚合酶II转录。在此,我们描述了一些实验,这些实验为以下观点提供了更多支持,即TATA结合蛋白(TBP)的募集是哺乳动物细胞中转录激活的限速步骤。我们发现,在人类细胞系中,作为GAL4-TBP融合蛋白的TBP募集到启动子上可显著激活转录。与启动子DNA相连的hTBP介导的激活严格依赖于功能性TATA元件的存在,并指导准确的转录起始。有趣的是,从依赖起始子(Inr)的无TATA启动子中未观察到GAL4-hTBP激活。这些结果表明,TBP与DNA的结合不是TFIID募集到依赖起始子的无TATA启动子初始阶段的限速步骤。最后,我们提供证据表明,GAL4-hTBP与特定转录结构域之间的协同作用仅限于VP16和Tat等激活因子,这些激活因子可能在TFIID募集之后的步骤中发挥作用。这些发现强化了这样一种观点,即TBP的募集是TATA依赖启动子激活的重要机制,另一方面,它们表明TBP-DNA相互作用对于依赖起始子的无TATA启动子的特异性转录在很大程度上是不必要的。