Richard Cynthia L, Tandon Animesh, Kranz Robert G
Department of Biology, Washington University, St. Louis, Missouri 63130, USA.
J Bacteriol. 2004 Feb;186(3):740-9. doi: 10.1128/JB.186.3.740-749.2004.
It was previously shown that the Rhodobacter capsulatus NtrC enhancer-binding protein activates the R. capsulatus housekeeping RNA polymerase but not the Escherichia coli RNA polymerase at the nifA1 promoter. We have tested the hypothesis that this activity is due to the high G+C content of the -10 sequence. A comparative analysis of R. capsulatus and other alpha-proteobacterial promoters with known transcription start sites suggests that the G+C content of the -10 region is higher than that for E. coli. Both in vivo and in vitro results obtained with nifA1 promoters with -10 and/or -35 variations are reported here. A major conclusion of this study is that alpha-proteobacteria have evolved a promiscuous sigma factor and core RNA polymerase that can transcribe promoters with high-GC -10 regions in addition to the classic E. coli Pribnow box. To facilitate studies of R. capsulatus transcription, we cloned and overexpressed all of the RNA polymerase subunits in E. coli, and these were reconstituted in vitro to form an active, recombinant R. capsulatus RNA polymerase with properties mimicking those of the natural polymerase. Thus, no additional factors from R. capsulatus are necessary for the recognition of high-GC promoters or for activation by R. capsulatus NtrC. The addition of R. capsulatus sigma(70) to the E. coli core RNA polymerase or the use of -10 promoter mutants did not facilitate R. capsulatus NtrC activation of the nifA1 promoter by the E. coli RNA polymerase. Thus, an additional barrier to activation by R. capsulatus NtrC exists, probably a lack of the proper R. capsulatus NtrC-E. coli RNA polymerase (protein-protein) interaction(s).
先前的研究表明,荚膜红细菌NtrC增强子结合蛋白可激活荚膜红细菌管家RNA聚合酶,但不能在nifA1启动子处激活大肠杆菌RNA聚合酶。我们已经验证了这一活性是由于-10序列的高G+C含量这一假设。对荚膜红细菌和其他具有已知转录起始位点的α-变形菌属启动子的比较分析表明,-10区域的G+C含量高于大肠杆菌。本文报道了使用具有-10和/或-35变异的nifA1启动子在体内和体外获得的结果。这项研究的一个主要结论是,α-变形菌属已经进化出一种混杂的σ因子和核心RNA聚合酶,除了经典的大肠杆菌Pribnow框外,它们还可以转录具有高GC -10区域的启动子。为了便于对荚膜红细菌转录进行研究,我们在大肠杆菌中克隆并过表达了所有RNA聚合酶亚基,并在体外将它们重组形成一种活性重组荚膜红细菌RNA聚合酶,其性质与天然聚合酶相似。因此,识别高GC启动子或由荚膜红细菌NtrC激活不需要来自荚膜红细菌的其他因子。将荚膜红细菌σ70添加到大肠杆菌核心RNA聚合酶中或使用-10启动子突变体并不能促进大肠杆菌RNA聚合酶对荚膜红细菌NtrC激活nifA1启动子。因此,存在荚膜红细菌NtrC激活的另一个障碍,可能是缺乏适当的荚膜红细菌NtrC-大肠杆菌RNA聚合酶(蛋白质-蛋白质)相互作用。