P 型 ATP 酶 PA1429 调控群体感应系统和细菌毒力。
The P-Type ATPase PA1429 Regulates Quorum-Sensing Systems and Bacterial Virulence.
作者信息
Zhang Yani, Qin Jing, Tan Boren, Kong Weina, Chen Gukui, Zhang Chao, Liang Haihua
机构信息
Key Laboratory of Resources Biology and Biotechnology in Western China, Ministry of Education, College of Life Sciences, Northwest University, Xi'an, China.
Western Reserve Academy, Hudson, OH, United States.
出版信息
Front Microbiol. 2017 Dec 7;8:2449. doi: 10.3389/fmicb.2017.02449. eCollection 2017.
is becoming an increasingly prevalent pathogen, capable of causing numerous life threatening infections in immunocompromised patients. The three hierarchically arranged quorum sensing (QS) systems, namely , and play key roles in coordinating virulence expression in . However, the regulatory mechanisms of the system have not been fully elucidated. To identify new genes involved in synthesis of the quinolone signal (PQS), a transposon mutagenesis library was constructed. PA1429 was found to inhibit PQS biosynthesis. The PA1429 deletion mutant also exhibited increased bacterial motility, biofilm formation, and virulence in a mouse model of acute lung infection. Interestingly, it also displayed reduced tolerance to oxidative stress. Mutated in the PA1429 deletion background restored bacterial susceptibility to HO. In addition, our data showed that PA1429 repressed the expression of and systems. Overall, these results provide new insights into the complex regulatory networks of quorum-sensing and virulence expression in
正成为一种日益普遍的病原体，能够在免疫功能低下的患者中引起众多危及生命的感染。三种层次排列的群体感应（QS）系统，即 、 和 ，在协调 中的毒力表达方面发挥着关键作用。然而， 系统的调控机制尚未完全阐明。为了鉴定参与喹诺酮信号（PQS）合成的新基因，构建了一个转座子诱变文库。发现PA1429抑制PQS生物合成。PA1429缺失突变体在急性肺部感染小鼠模型中还表现出细菌运动性、生物膜形成增加以及毒力增强。有趣的是，它对氧化应激的耐受性也降低。在PA1429缺失背景下突变的 恢复了细菌对HO的敏感性。此外，我们的数据表明PA1429抑制了 和 系统的表达。总体而言，这些结果为群体感应和毒力表达的复杂调控网络提供了新的见解。
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