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首页> 外文期刊>Journal of bacteriology >Thermoregulation of virB transcription in Shigella flexneri by sensing of changes in local DNA superhelicity.
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Thermoregulation of virB transcription in Shigella flexneri by sensing of changes in local DNA superhelicity.

机译：弗氏志贺氏菌中virB转录的温度调节，通过检测局部DNA超螺旋性的变化来实现。

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摘要

Transcription of the virB gene, a transcriptional regulator of invasion genes on the large plasmid of Shigella flexneri, is strictly regulated by growth temperature; when bacteria are grown at 37 degrees C, virB transcription is highly activated, while at 30 degrees C the level of virB transcription decreases to less than 5% of that at 37 degrees C. Transcription from the virB promoter is activated by VirF, which is encoded on the same plasmid, in a DNA superhelicity-dependent manner (T. Tobe, M. Yoshikawa, T. Mizuno, and C. Sasakawa, J. Bacteriol. 175:6142-6149, 1993). Here we provide evidence supporting the involvement of negative superhelicity in the thermoregulation of virB transcription. A local negatively supercoiled domain in the virB promoter region was created by activating a divergent transcription from the T7 RNA polymerase-dependent promoter, phi 10, which was placed upstream of the virB promoter in the opposite orientation. Transcription from the virB promoter was activated even at 30 degrees C by induction of divergent transcription. Levels of virB transcription correlated with levels of expressed T7 RNA polymerase. Transcriptional activation of virB by the system depended completely upon VirF function. The level of virB transcription achieved by introducing a negatively supercoiled domain was enough to give rise to expression of invasion capacity at 30 degrees C. These results indicated that the repression of virB transcription at 30 degrees C was caused by a reduction in negative superhelicity around the virB promoter region at 30 degrees C.
机译：virB基因的转录是弗氏志贺氏菌大质粒上侵袭基因的转录调节因子，受生长温度的严格控制。当细菌在37摄氏度下生长时，virB转录被高度激活，而在30摄氏度下virB转录水平下降到小于37摄氏度时的5％。virB启动子的转录被VirF激活。以超螺旋依赖的方式在同一质粒上编码（T.Tobe，M.Yoshikawa，T.Mizuno，和C.Sasakawa，J.Bacteriol.175：6142-6149，1993）。在这里，我们提供了支持负超螺旋参与virB转录温度调节的证据。通过激活来自T7 RNA聚合酶依赖性启动子phi 10的发散转录来创建virB启动子区域中的局部负超螺旋结构域，后者以相反的方向置于virB启动子的上游。甚至在30摄氏度，通过诱导差异转录，也激活了virB启动子的转录。 virB转录水平与表达的T7 RNA聚合酶水平相关。系统对virB的转录激活完全取决于VirF功能。通过引入负超螺旋结构域实现的virB转录水平足以在30摄氏度时引起侵袭能力的表达。这些结果表明，在30摄氏度时virB转录的抑制是由周围的负超螺旋度降低引起的。 virB启动子区在30摄氏度下。

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