Institute for Genetics, University of Cologne, Zuelpicher Str. 47a, Cologne, Germany.
Mol Microbiol. 2018 May;108(3):226-239. doi: 10.1111/mmi.13926. Epub 2018 Feb 23.
Nucleoid-associated protein H-NS represses transcription by forming extended DNA-H-NS complexes. Repression by H-NS operates mostly at the level of transcription initiation. Less is known about how DNA-H-NS complexes interfere with transcription elongation. In vitro H-NS has been shown to enhance RNA polymerase pausing and to promote Rho-dependent termination, while in vivo inhibition of Rho resulted in a decrease of the genome occupancy by H-NS. Here we show that transcription directed across H-NS binding regions relieves H-NS (and H-NS/StpA) mediated repression of promoters in these regions. Further, we observed a correlation of transcription across the H-NS-bound region and de-repression. The data suggest that the transcribing RNA polymerase is able to remodel the H-NS complex and/or dislodge H-NS from the DNA and thus relieve repression. Such an interference of transcription and H-NS mediated repression may imply that poorly transcribed AT-rich loci are prone to be repressed by H-NS, while efficiently transcribed loci escape repression.
类核相关蛋白 H-NS 通过形成延伸的 DNA-H-NS 复合物来抑制转录。H-NS 的抑制作用主要发生在转录起始水平。关于 DNA-H-NS 复合物如何干扰转录延伸,人们知之甚少。体外研究表明,H-NS 可以增强 RNA 聚合酶暂停,并促进 Rho 依赖性终止,而体内抑制 Rho 会导致 H-NS 在基因组上的占有率降低。在这里,我们表明,跨 H-NS 结合区域的转录可以缓解这些区域中 H-NS(和 H-NS/StpA)介导的启动子抑制。此外,我们观察到转录跨 H-NS 结合区域与去抑制之间存在相关性。这些数据表明,转录的 RNA 聚合酶能够重塑 H-NS 复合物并/或将 H-NS 从 DNA 上置换下来,从而缓解抑制。这种转录与 H-NS 介导的抑制之间的干扰可能意味着,转录较差的富含 AT 的基因座容易被 H-NS 抑制,而转录效率高的基因座则可以逃脱抑制。