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肠出血性大肠杆菌 LEE1 调控区的一个隐秘启动子:富含 AT 的基因调控区中的启动子特异性。

A cryptic promoter in the LEE1 regulatory region of enterohaemorrhagic Escherichia coli: promoter specificity in AT-rich gene regulatory regions.

机构信息

School of Biosciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK.

出版信息

Biochem J. 2011 Jun 15;436(3):681-6. doi: 10.1042/BJ20110260.

Abstract

Transcription of the LEE1 operon in the locus of enterocyte effacement of enterohaemorrhagic Escherichia coli is due to the P1 promoter. Mutational and biochemical analyses reveal the existence of an overlapping promoter, designated P1A, which can drive transcript initiation 10 bp upstream of the P1 promoter transcript start point. Because of the overlap between P1 and P1A, P1A activity is unmasked only when the P1 promoter is inactivated by mutation. In the present paper, we report that mutation of the P1-10 element is less effective in unmasking P1A promoter activity than mutation of the P1-35 element. This suggests that the P1 promoter -35 element, which corresponds to the consensus, can sequester RNA polymerase even when P1 is inactive and thereby prevent RNA polymerase from serving the P1A promoter. We propose that such promoter elements may play a role in enforcing specificity in bacterial regulatory regions that contain alternative possible promoters.

摘要

肠出血性大肠杆菌菌体脱落相关 locus 中 LEE1 操纵子的转录归因于 P1 启动子。通过突变和生化分析揭示了一个重叠的启动子,命名为 P1A,它可以在 P1 启动子转录起始点上游 10bp 处驱动转录起始。由于 P1 和 P1A 之间存在重叠,只有当 P1 启动子发生突变失活时,P1A 启动子的活性才会被揭示出来。在本文中,我们报告称,与 P1-35 元件的突变相比,P1-10 元件的突变在揭示 P1A 启动子活性方面的效果较差。这表明 P1 启动子 -35 元件与共有序列相对应,即使 P1 处于非活性状态,它也可以使 RNA 聚合酶失活,从而阻止 RNA 聚合酶为 P1A 启动子服务。我们提出,在含有替代可能启动子的细菌调控区域中,这种启动子元件可能发挥作用,以强制执行特异性。

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