首页> 外文期刊>Journal of Molecular Biology >The Xp10 Bacteriophage Protein P7 Inhibits Transcription by the Major and Major Variant Forms of the Host RNA Polymerase via a Common Mechanism
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The Xp10 Bacteriophage Protein P7 Inhibits Transcription by the Major and Major Variant Forms of the Host RNA Polymerase via a Common Mechanism

机译:Xp10噬菌体蛋白P7通过共同机制通过宿主RNA聚合酶的主要和主要变体形式抑制转录。

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摘要

The a factor is a functionally obligatory subunit of the bacterial transcription machinery, the RNA polymerase. Bacteriophage-encoded small proteins that either modulate or inhibit the bacterial RNAP to allow the temporal regulation of bacteriophage gene expression often target the activity of the major bacterial sigma factor, sigma(70). Previously, we showed that during Xanthomonas oryzae phage Xp10 infection, the phage protein P7 inhibits the host RNAP by preventing the productive engagement with the promoter and simultaneously displaces the sigma(70) factor from the RNAP. In this study, we demonstrate that P7 also inhibits the productive engagement of the bacterial RNAP containing the major variant bacterial sigma factor, sigma(54), with its cognate promoter. The results suggest for the first time that the major variant form of the host RNAP can also be targeted by bacteriophage-encoded transcription regulatory proteins. Since the major and major variant sigma factor interacting surfaces in the RNAP substantially overlap, but different regions of sigma(70) an and sigma(54) are used for binding to the RNAP, our results further underscore the importance of the sigma-RNAP interface in bacterial RNAP function and regulation and potentially for intervention by antibacterials. (C) 2016 The Authors. Published by Elsevier Ltd. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
机译:一个因素是细菌转录机制的功能必需亚基,RNA聚合酶。噬菌体编码的小蛋白可以调节或抑制细菌RNAP,以实现对噬菌体基因表达的时间调控,通常靶向主要细菌sigma因子sigma(70)的活性。以前,我们表明在米氏黄单胞菌噬菌体Xp10感染期间,噬菌体蛋白P7通过阻止与启动子的有效结合而抑制了宿主RNAP,同时从RNAP置换了sigma(70)因子。在这项研究中,我们证明P7还抑制包含主要变异细菌sigma因子sigma(54)及其同源启动子的细菌RNAP的生产性结合。结果首次表明,宿主RNAP的主要变异形式也可以被噬菌体编码的转录调节蛋白靶向。由于RNAP中主要和主要变异的sigma因子相互作用表面基本重叠,但是使用sigma(70)an和sigma(54)的不同区域来结合RNAP,因此我们的结果进一步强调了sigma-RNAP界面的重要性在细菌RNAP的功能和调节中发挥作用,并可能通过抗菌药物干预。 (C)2016作者。由Elsevier Ltd.发行。这是CC BY许可下的开放访问文章(http://creativecommons.org/licenses/by/4.0/)。

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