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Common and divergent features in transcriptional control of the homologous small RNAs GlmY and GlmZ in Enterobacteriaceae

机译:肠杆菌科中同源小RNA GlmY和GlmZ转录控制中的共同点和分歧点

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摘要

Small RNAs GlmY and GlmZ compose a cascade that feedback-regulates synthesis of enzyme GlmS in Enterobacteriaceae. Here, we analyzed the transcriptional regulation of glmY/glmZ from Yersinia pseudotuberculosis, Salmonella typhimurium and Escherichia coli, as representatives for other enterobacterial species, which exhibit similar promoter architectures. The GlmY and GlmZ sRNAs of Y. pseudotuberculosis are transcribed from Sigma(54)-promoters that require activation by the response regulator GlrR through binding to three conserved sites located upstream of the promoters. This also applies to glmY/glmZ of S. typhimurium and glmY of E. coli, but as a difference additional Sigma(70)-promoters overlap the Sigma(54)-promoters and initiate transcription at the same site. In contrast, E. coli glmZ is transcribed from a single Sigma(70)-promoter. Thus, transcription of glmY and glmZ is controlled by Sigma(54) and the two-component system GlrR/GlrK (QseF/QseE) in Y. pseudotuberculosis and presumably in many other Enterobacteria. However, in a subset of species such as E. coli this relationship is partially lost in favor of Sigma(70)-dependent transcription. In addition, we show that activity of the Sigma(54)-promoter of E. coli glmY requires binding of the integration host factor to sites upstream of the promoter. Finally, evidence is provided that phosphorylation of GlrR increases its activity and thereby sRNA expression.
机译:小RNA GlmY和GlmZ组成了一个级联,可反馈调节肠杆菌科细菌GlmS的合成。在这里,我们分析了来自假结核耶尔森氏菌,鼠伤寒沙门氏菌和大肠杆菌的glmY / glmZ的转录调控,作为其他肠杆菌种的代表,它们表现出相似的启动子结构。假结核耶尔森氏菌的GlmY和GlmZ sRNAs是从Sigma(54)启动子转录而来的,该启动子需要通过与启动子上游的三个保守位点结合而被反应调节因子GlrR激活。这也适用于鼠伤寒沙门氏菌的glmY / glmZ和大肠杆菌的glmY,但作为区别,其他Sigma(70)-启动子与Sigma(54)-启动子重叠,并在同一位点启动转录。相反,大肠杆菌glmZ是从单个Sigma(70)启动子转录的。因此,glmY和glmZ的转录受假结核耶尔森氏菌以及大概其他许多肠杆菌中的Sigma(54)和两组分系统GlrR / GlrK(QseF / QseE)控制。但是,在一部分物种(如大肠杆菌)中,这种关系部分丢失,有利于依赖Sigma(70)的转录。此外,我们显示大肠杆菌glmY的Sigma(54)启动子的活性需要整合宿主因子与启动子上游位点的结合。最后,提供证据表明GlrR的磷酸化增加了其活性,从而增加了sRNA的表达。

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