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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >RovA, a global regulator of Yersinia pestis, specifically required for bubonic plague
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RovA, a global regulator of Yersinia pestis, specifically required for bubonic plague

机译：RovA，鼠疫耶尔森氏菌的全球监管者，鼠疫特别要求

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摘要

The pathogenic species of Yersinia contain the transcriptional regulator RovA. In Yersinia pseudotuberculosis and Yersinia en-terocolitica. RovA regulates expression of the invasion factor invasin (inv), which mediates translocation across the intestinal epithelium. A Y. enterocolitica rovA mutant has a significant decrease in virulence by LD_(50) analysis and an altered rate of dissemination compared with either wild type or an inv mutant, suggesting that RovA regulates multiple virulence factors. Here, we show the involvement of RovA in the virulence of Yersinia pestis, which naturally lacks a functional inv gene. A Y. pestis ΔrovA mutant is attenuated ≈80-fold by LD_(50) and is defective in dissemination/ colonization of spleens and lungs after s.c. inoculation. However, the ΔrovA mutant is only slightly attenuated when given via an intranasal or i.p. route, indicating a more important role for RovA in bubonic plague than pneumonic plague or systemic infection. Microarray analysis was used to define the RovA regulon. The psa locus was among the most highly down-regulated loci in the ΔrovA mutant. A ΔpsaA mutant had a significant dissemination defect after s.c. infection but only slight attenuation by the pneumonic-disease model, closely mimicking the virulence defect seen with the ΔrovA mutant. DNA-binding studies revealed that RovA specifically interacts with the psaE and psaA promoter regions, indicating a direct role for RovA in regulating this locus. Thus, RovA appears to be a global transcription factor in Y. pestis and, through its regulatory influence on genes such as psaEFABC, contributes to the virulence of Y. pestis.
机译：耶尔森氏菌的病原体包含转录调节剂RovA。在耶尔森氏菌假结核病和耶尔森氏菌病。 RovA调节入侵因子Invasin（inv）的表达，该因子介导跨肠上皮细胞的转运。与野生型或inv突变体相比，通过LD_（50）分析，小肠结肠炎耶尔森氏菌rovA突变体的毒力显着降低，并且传播速度发生了改变，这表明RovA调节了多种毒力因子。在这里，我们显示RovA参与了鼠疫耶尔森氏菌的毒力，自然缺乏功能性inv基因。鼠疫耶尔森氏菌rov突变体被LD_（50）衰减了约80倍，并且在s.c之后在脾脏和肺的扩散/定殖方面存在缺陷。接种。然而，当通过鼻内或腹膜内给予时，ΔrovA突变体仅略微减弱。这表明RovA在鼠疫鼠疫中的作用比肺鼠疫或全身感染更为重要。微阵列分析用于定义RovA调节剂。 psa基因座是ΔrovA突变体中被高度下调的基因座之一。皮下注射后，ΔpsaA突变体具有明显的传播缺陷。感染，但肺炎疾病模型仅略有减弱，非常类似于ΔrovA突变体所见的毒力缺陷。 DNA结合研究表明RovA与psaE和psaA启动子区域特异性相互作用，表明RovA在调节该基因座中具有直接作用。因此，RovA似乎是鼠疫耶尔森氏菌的一个全局转录因子，并且通过其对psaEFABC等基因的调控作用，有助于鼠疫耶尔森氏菌的毒性。

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