Gaudin H M, Silverman P M
Program in Molecular and Cell Biology, Oklahoma Medical Research Foundation, Oklahoma 73104.
Mol Microbiol. 1993 Apr;8(2):335-42. doi: 10.1111/j.1365-2958.1993.tb01577.x.
Expression of the F plasmid traY promoter in vivo requires both host (E. coli) and plasmid encoded proteins. As judged by transcript size and primer extension analyses, the F plasmid traY promoter was utilized in vitro by purified E. coli sigma 70 RNA polymerase in the absence of other proteins. However, in vitro transcription required supercoiled templates. Endonuclease protection experiments showed that RNA polymerase is unable to form a stable complex at the traY promoter in linear or relaxed circular templates. In vitro transcription with linear templates could be elicited by altering the traY -10 and -35 hexamers to the consensus sequences. Alterations that reduced the effect of template supercoiling on apparent promoter strength in vitro also reduced the effect of the F plasmid TraJ protein on traY expression in vivo. Apparent traY promoter strength in vitro, estimated in template competition experiments, was unaltered by deletion of tra DNA normally upstream of the promoter, a change in promoter context that elicited high levels of promoter activity in TraJ- cells. These data suggest a model for regulated traY promoter activity in which a nucleoprotein complex involving tra DNA immediately upstream locally relaxes traY promoter DNA. TraJ and perhaps other activators could disrupt the complex, allowing promoter DNA to equilibrate at the prevailing negative superhelical density and thereby eliciting transcription initiation.
F质粒traY启动子在体内的表达需要宿主(大肠杆菌)和质粒编码的蛋白质。根据转录本大小和引物延伸分析判断,在没有其他蛋白质的情况下,纯化的大肠杆菌σ70 RNA聚合酶在体外可利用F质粒traY启动子。然而,体外转录需要超螺旋模板。核酸内切酶保护实验表明,RNA聚合酶无法在线性或松弛环状模板的traY启动子处形成稳定的复合物。通过将traY -10和-35六聚体改变为共有序列,可以引发线性模板的体外转录。降低模板超螺旋对体外表观启动子强度影响的改变,也降低了F质粒TraJ蛋白对体内traY表达的影响。在模板竞争实验中估计的体外traY启动子表观强度,不会因缺失启动子上游正常的tra DNA而改变,这种启动子环境的变化会在TraJ-细胞中引发高水平的启动子活性。这些数据提示了一种调控traY启动子活性的模型,其中涉及紧邻上游tra DNA的核蛋白复合物会局部松弛traY启动子DNA。TraJ以及可能的其他激活剂可以破坏该复合物,使启动子DNA在普遍的负超螺旋密度下达到平衡,从而引发转录起始。