A σ-core interaction of the RNA polymerase holoenzyme that enhances promoter escape
A σ-core interaction of the RNA polymerase holoenzyme that enhances promoter escape
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DOI：
10.1038/sj.emboj.7601612
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发表时间：
2007-03-21
期刊：
影响因子：
11.4
通讯作者：
Hochschild, Ann
中科院分区：
文献类型：
--
作者：
Leibman, Mark;Hochschild, Ann
细菌 RNA 聚合酶 (RNAP) 的 sigma 亚基是启动子特异性转录起始所必需的，并且还可以参与下游事件。大肠杆菌 sigma(70) 和核心酶 (alpha(2)beta beta'omega) 之间的几种功能上重要的亚基间相互作用已被定义。这些包括 sigma(70) 保守区 2 (sigma(2)) 和 beta' 卷曲螺旋结构域 (beta' 卷曲螺旋) 之间的相互作用，这是启动子开放复合物形成和 sigma(70) 依赖性早期延伸暂停期间 sigma(2) 和 DNA 之间序列特异性相互作用所必需的。在这里，我们描述了与 sigma(2) 相邻的 sigma(70) 区域（称为非保守区域（sigma(70) NCR））和 beta' N 端部分的区域之间先前未表征的相互作用，该区域似乎在功能上拮抗 sigma(2)/beta' 卷曲螺旋相互作用。具体来说，我们表明 sigma(70) NCR/beta' 相互作用促进启动子逃逸并阻碍早期延伸暂停，而 sigma(70)/beta' 卷曲螺旋相互作用则具有相反的效果。我们还证明，去除 sigma(70) NCR 会导致严重的生长缺陷；我们认为它对生长的重要性可能反映了它在启动子逃逸中的作用。
The sigma subunit of bacterial RNA polymerase ( RNAP) is required for promoter-specific transcription initiation and can also participate in downstream events. Several functionally important intersubunit interactions between Escherichia coli sigma(70) and the core enzyme (alpha(2)beta beta'omega) have been defined. These include an interaction between conserved region 2 of sigma(70) (sigma(2)) and the coiled-coil domain of beta' (beta' coiled-coil) that is required for sequence-specific interaction between sigma(2) and the DNA during both promoter open complex formation and sigma(70)-dependent early elongation pausing. Here, we describe a previously uncharacterized interaction between a region of sigma(70) adjacent to sigma(2) called the nonconserved region (sigma(70) NCR) and a region in the N-terminal portion of beta' that appears to functionally antagonize the sigma(2)/beta' coiled-coil interaction. Specifically, we show that the sigma(70) NCR/beta' interaction facilitates promoter escape and hinders early elongation pausing, in contrast to the sigma(70)/beta' coiled-coil interaction, which has opposite effects. We also demonstrate that removal of the sigma(70) NCR results in a severe growth defect; we suggest that its importance for growth may reflect its role in promoter escape.