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RpoS和吲哚信号传导控制鳗弧菌对无菌海鲈(欧洲鲈)幼体的毒力。

RpoS and indole signaling control the virulence of Vibrio anguillarum towards gnotobiotic sea bass (Dicentrarchus labrax) larvae.

作者信息

Li Xuan, Yang Qian, Dierckens Kristof, Milton Debra L, Defoirdt Tom

机构信息

Laboratory of Aquaculture and Artemia Reference Center, Ghent University, Ghent, Belgium.

Southern Research Institute, Birmingham, Alabama, United States of America; Department of Molecular Biology, Umeå University, Umeå, Sweden.

出版信息

PLoS One. 2014 Oct 31;9(10):e111801. doi: 10.1371/journal.pone.0111801. eCollection 2014.

Abstract

Quorum sensing, bacterial cell-to-cell communication with small signal molecules, controls the virulence of many pathogens. In contrast to other vibrios, neither the VanI/VanR acylhomoserine lactone quorum sensing system, nor the three-channel quorum sensing system affects virulence of the economically important aquatic pathogen Vibrio anguillarum. Indole is another molecule that recently gained attention as a putative signal molecule. The data presented in this study indicate that indole signaling and the alternative sigma factor RpoS have a significant impact on the virulence of V. anguillarum. Deletion of rpoS resulted in increased expression of the indole biosynthesis gene tnaA and in increased production of indole. Both rpoS deletion and the addition of exogenous indole (50-100 µM) resulted in decreased biofilm formation, exopolysaccharide production (a phenotype that is required for pathogenicity) and expression of the exopolysaccharide synthesis gene wbfD. Further, indole inhibitors increased the virulence of the rpoS deletion mutant, suggesting that indole acts downstream of RpoS. Finally, in addition to the phenotypes found to be affected by indole, the rpoS deletion mutant also showed increased motility and decreased sensitivity to oxidative stress.

摘要

群体感应,即细菌通过小分子信号分子进行细胞间通讯,控制着许多病原体的毒力。与其他弧菌不同,VanI/VanR酰基高丝氨酸内酯群体感应系统和三通道群体感应系统均不影响经济上重要的水生病原体鳗弧菌的毒力。吲哚是另一种最近作为假定信号分子而受到关注的分子。本研究中呈现的数据表明,吲哚信号传导和替代西格玛因子RpoS对鳗弧菌的毒力有重大影响。rpoS的缺失导致吲哚生物合成基因tnaA的表达增加以及吲哚产量增加。rpoS缺失和添加外源性吲哚(50 - 100 µM)均导致生物膜形成减少、胞外多糖产生(一种致病性所需的表型)以及胞外多糖合成基因wbfD的表达降低。此外,吲哚抑制剂增加了rpoS缺失突变体的毒力,表明吲哚在RpoS的下游起作用。最后,除了发现受吲哚影响的表型外,rpoS缺失突变体还表现出运动性增加和对氧化应激的敏感性降低。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33d0/4216140/7db680b0521d/pone.0111801.g001.jpg

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