首页> 外文期刊>Journal of Molecular Biology >A novel bacteriophage-encoded RNA polymerase binding protein inhibits transcription initiation and abolishes transcription termination by host RNA polymerase.
【24h】

A novel bacteriophage-encoded RNA polymerase binding protein inhibits transcription initiation and abolishes transcription termination by host RNA polymerase.

机译:一种新型的噬菌体编码的RNA聚合酶结合蛋白可抑制转录起始,并通过宿主RNA聚合酶消除转录终止。

获取原文
获取原文并翻译 | 示例
           

摘要

Xp10 is a lytic bacteriophage of Xanthomonas oryzae, a Gram-negative bacterium that causes rice blight. We purified an Xp10 protein, p7, that binds to and inhibits X. oryzae RNA polymerase (RNAP). P7 is a novel 73 amino acid-long protein; it does not bind to and hence does not affect transcription by Escherichia coli RNAP. Analysis of E. coli/X. oryzae RNAP hybrids locates the p7 binding site to the largest X. oryzae RNAP subunit, beta'. Binding of p7 to X. oryzae RNAP holoenzyme prevents large conformational change that places the sigma subunit region 4 into the correct position for interaction with the -35 promoter element. As a result, open promoter complex formation on the -10/-35 class promoters is inhibited. Inhibition of promoter complex formation on the extended -10 class promoters is less efficient. The p7 protein also abolishes factor-independent transcription termination by X. oryzae RNAP by preventing the release of nascent RNA at terminators. Further physiological and mechanistic studies of this novel transcription factor should provide additional insights into its biological role and the processes of promoter recognition and transcription termination. (c) 2002 Elsevier Science Ltd.
机译:Xp10是米氏黄单胞菌(Xanthomonas oryzae)的一种溶菌性噬菌体,这是一种引起水稻枯萎病的革兰氏阴性细菌。我们纯化了一个Xp10蛋白p7,该蛋白结合并抑制米曲霉RNA聚合酶(RNAP)。 P7是一种新型的73个氨基酸长的蛋白;它不结合,因此不影响大肠杆菌RNAP的转录。大肠杆菌/ X分析。稻米RNAP杂种将p7结合位点定位到最大的稻米X. RNAP亚基beta'。 p7与米曲霉RNAP全酶的结合防止了大的构象变化,该构象变化将sigma亚基区域4置于与-35启动子元件相互作用的正确位置。结果,在-10 / -35类启动子上开放的启动子复合物形成被抑制。在扩展的-10类启动子上抑制启动子复合物形成的效率较低。 p7蛋白还可以通过阻止终止子处新生RNA的释放来消除米曲霉RNAP的因子依赖性转录终止。此新型转录因子的进一步生理学和机制研究应提供对其生物学作用以及启动子识别和转录终止过程的更多见解。 (c)2002爱思唯尔科学有限公司。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号