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Small RNA coaR contributes to intestinal colonization in Vibrio cholerae via the two-component system EnvZ/OmpR.
Environmental Microbiology ( IF 4.3 ) Pub Date : 2019-12-23 , DOI: 10.1111/1462-2920.14906
Daoyi Xi 1, 2, 3, 4 , Yujia Li 1, 2, 3, 4 , Junxiang Yan 1, 2, 3, 4 , Yuehua Li 1, 2, 3, 4 , Xiaochen Wang 1, 2, 3, 4 , Boyang Cao 1, 2, 3, 4
Affiliation  

Vibrio cholerae is a waterborne bacterium responsible for worldwide outbreaks of acute and fatal cholera. Recently, small regulatory RNAs (sRNAs) have become increasingly recognized as important regulators of virulence gene expression in response to environmental signals. In this study, we determined that two‐component system EnvZ/OmpR was required for intestinal colonization in V. cholerae O1 EI Tor strain E12382. Analysis of the characteristics of OmpR revealed a potential binding site in the intergenic region between vc1470 and vc1471, and qRT‐PCR showed that expression of the intergenic region increased 5.3‐fold in the small intestine compared to LB medium. Race and northern blot assays were performed and demonstrated a new sRNA, coaR (cholerae osmolarity and acidity related regulatory RNA). A ΔcoaR mutant showed a deficient colonization ability in small intestine with CI of 0.15. We identified a target of coaR, tcpI, a negative regulator of the major pilin subunit of TcpA. The ΔtcpI mutant has an increased colonization with CI of 3.16. The expression of coaR increased 2.8‐fold and 3.3‐fold under relative acidic and hypertonic condition. In summary, coaR was induced under the condition of high osmolarity and acid stress via EnvZ/OmpR and explained that tcpI relieves pH‐mediated repression of toxin co‐regulated pilus synthesis.

中文翻译:

小RNA coaR通过两组分系统EnvZ / OmpR有助于霍乱弧菌的肠道定居。

霍乱弧菌是一种导致全球范围内急性和致命霍乱暴发的水生细菌。近来,小调节RNA(sRNA)已被越来越多地认为是响应于环境信号的毒力基因表达的重要调节剂。在这项研究中,我们确定霍乱弧菌O1 EI Tor菌株E12382的肠道定植需要两组分系统EnvZ / OmpR 。对OmpR特征的分析揭示了vc1470vc1471之间的基因间区域中潜在的结合位点,而qRT-PCR显示,与LB培养基相比,小肠中基因间区域的表达增加了5.3倍。进行了种族和Northern印迹分析,并证明了一种新的sRNA,coaR(霍乱渗透压和酸度相关的调节性RNA)。甲Δ COAR突变体显示在小肠0.15 CI一个缺陷殖能力。我们确定了coaR tcpI的目标,tcpITcpA主要菌毛素亚单位的负调节剂。该Δ TCPI突变体具有与3.16 CI增加的定植。在相对酸性和高渗条件下,coaR的表达分别增加了2.8倍和3.3倍。总之,在高渗透压和酸性胁迫下,通过EnvZ / OmpR诱导了coaR的产生,并解释了tcpI减轻了pH介导的毒素对共调节菌毛合成的抑制。
更新日期:2019-12-23
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