Telesnitsky A P, Chamberlin M J
Department of Biochemistry University of California, Berkeley 94720.
J Mol Biol. 1989 Jan 20;205(2):315-30. doi: 10.1016/0022-2836(89)90343-4.
The efficiency of transcription termination at certain well-defined prokaryotic rho-independent terminators depends on the promoter unit from which transcription is initiated. Some promoter units allow substantial readthrough of strong termination signals, a phenomenon we term "factor-independent antitermination". This observation is not easily explained by current models for prokaryotic terminator function that consider the terminator to be a "cassette" involving only sequences and RNA transcript structures in the immediate region of the terminator or directly upstream. When transcription is carried out in vitro employing only purified Escherichia coli RNA polymerase, up to 20 times as many RNA polymerase molecules pass through a particular terminator when transcription is initiated from the E. coli tac promoter unit, as compared to transcription initiated from the T7A1 or rrnB P2 promoters. This effect cannot be attributed to antitermination factors separate from the core RNA polymerase. Similar differences in termination efficiency are found for the same promoters in vivo. These termination differences are affected by sequences just downstream from the start site for transcription, including those in the +25 region of the nascent transcript. These early transcribed sequences can confer factor-independent antitermination onto a heterologous promoter, but only when the sequences are precisely positioned relative to the start site for transcription. We have considered several possible models to explain how early transcribed sequences might affect termination, including those in which the 5' end of the transcript interacts with either the terminator RNA or the polymerase. We favor an alternative model in which these sequences interact with the core RNA polymerase to convert the enzyme from a termination-proficient state (T-state) to a conformation resistant to termination (R-state). Such enzyme conformations may be an important component of factor-dependent antitermination systems.
在某些明确界定的原核生物ρ因子非依赖性终止子处,转录终止的效率取决于转录起始的启动子单元。一些启动子单元允许强终止信号大量通读,我们将这种现象称为“因子非依赖性抗终止”。当前关于原核生物终止子功能的模型认为终止子是一个“盒式结构”,仅涉及终止子紧邻区域或直接上游的序列和RNA转录本结构,因此这一观察结果难以用这些模型来解释。当仅使用纯化的大肠杆菌RNA聚合酶进行体外转录时,与从T7A1或rrnB P2启动子起始转录相比,从大肠杆菌tac启动子单元起始转录时,通过特定终止子的RNA聚合酶分子数量多达20倍。这种效应不能归因于与核心RNA聚合酶分离的抗终止因子。在体内,相同的启动子也存在类似的终止效率差异。这些终止差异受到转录起始位点下游序列的影响,包括新生转录本+25区域的序列。这些早期转录的序列可以赋予异源启动子因子非依赖性抗终止能力,但前提是这些序列相对于转录起始位点的位置精确。我们考虑了几种可能的模型来解释早期转录序列如何影响终止,包括转录本5'端与终止子RNA或聚合酶相互作用的模型。我们倾向于另一种模型,即这些序列与核心RNA聚合酶相互作用,将酶从终止 proficient 状态(T状态)转变为抗终止的构象(R状态)。这种酶的构象可能是因子依赖性抗终止系统的重要组成部分。