de Franciscis V, Brody E
J Biol Chem. 1982 Apr 25;257(8):4087-96.
We describe crude in vitro systems from T4-infected cells which reflect in vivo T4 regulation. Lysates from cells which had been infected in the presence of chloramphenicol manifest the same polarity of RNA synthesis as did the infected cells. Next, we describe a complementation system between lysates which have no RNA synthetic capacity and purified RNA polymerase; in this system, delayed early RNA synthesis in vitro depends on the presence of an active mot gene product. Mot activity controls middle mode gene expression in vivo. In vitro, not activity in the lysate directs RNA polymerase to initiate on regions of DNA that are otherwise inaccessible. This mot-dependent delayed early RNA synthesis in vitro is seen at 0.1 and 0.2 M KCl, but not at 0.05 M KCl. We present a model in which mot is a DNA melting protein necessary for recognition of a middle promoters by either Escherichia coli or T4-modified RNA polymerase which contains E. coli sigma subunit.
我们描述了来自T4感染细胞的原始体外系统,该系统反映了体内T4的调控情况。在氯霉素存在下感染的细胞裂解物表现出与感染细胞相同的RNA合成极性。接下来,我们描述了无RNA合成能力的裂解物与纯化的RNA聚合酶之间的互补系统;在该系统中,体外延迟早期RNA合成取决于活性mot基因产物的存在。Mot活性在体内控制中期模式基因表达。在体外,裂解物中的活性并非引导RNA聚合酶在其他情况下无法接近的DNA区域起始。这种体外依赖mot的延迟早期RNA合成在0.1和0.2 M KCl浓度下可见,但在0.05 M KCl浓度下则不可见。我们提出了一个模型,其中mot是一种DNA解链蛋白,对于大肠杆菌或含有大肠杆菌σ亚基的T4修饰RNA聚合酶识别中期启动子是必需的。