Transcriptomic analysis reveals the role of RcsB in suppressing bacterial chemotaxis, flagellar assembly and infection in Yersinia enterocolitica
Transcriptomic analysis reveals the role of RcsB in suppressing bacterial chemotaxis, flagellar assembly and infection in Yersinia enterocolitica
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转录组分析揭示 RcsB 在抑制小肠结肠炎耶尔森氏菌细菌趋化、鞭毛组装和感染中的作用
DOI：
10.1007/s00294-020-01083-x
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发表时间：
2020-06-03
期刊：
影响因子：
2.5
通讯作者：
Chen, Jingyu
中科院分区：
文献类型：
--
作者：
Meng, Jiao;Bai, Jiaqi;Chen, Jingyu
确定肠杆菌科中的RCS(胶囊合成调节因子)调节子一直是最近几个研究的主要焦点。RCS系统在小肠结肠炎耶尔森菌中的整体作用在很大程度上是未知的。我们先前的研究表明，RCSB通过负性调节flhDC、hmsHFRS和hmsT的表达，抑制细胞的运动、生物被膜的形成和c-di-GMP的产生。为了鉴定RCSB调控的其他细胞功能，本研究利用RNA-Seq技术比较了野生型和Delta RCSB突变体的基因表达谱。共鉴定出132个受RCSB调控的差异表达基因，其中114个上调，18个下调。此外，对RNA测序的结果进行了讨论，重点讨论了RCSB在抑制细菌趋化、鞭毛组装和感染方面的预测作用。为了证实这些预测，我们在实验中验证了Delta RCSB突变体激活了趋化行为和鞭毛的生物合成，并显示出增强了小肠结肠炎耶尔森菌对Caco-2细胞的黏附和侵袭。尽管RCSB在很大程度上抑制了这些生理活性，但RCSB的存在对于优化小肠结肠炎耶尔森菌的生存仍然具有重要意义，我们以前的报告证明，RCSB对小肠结肠炎耶尔森菌中的阳离子抗菌肽多粘菌素B具有一定程度的抗性。总体而言，这项研究提供的信息补充了我们对RCS磷酸继电器在调节小肠结肠炎耶尔森菌致病性中的理解，同时也为RCS系统在肠杆菌科其他成员中的其他作用提供了线索。
Defining the Rcs (Regulator of Capsule Synthesis) regulon in Enterobacteriaceae has been the major focus of several recent studies. The overall role of the Rcs system in Yersinia enterocolitica is largely unknown. Our previous study showed that RcsB inhibits motility, biofilm formation and c-di-GMP production by negatively regulating flhDC, hmsHFRS and hmsT expression. To identify other cellular functions regulated by the RcsB, gene expression profiles of the wild type and Delta rcsB mutant were compared by RNA-Seq in this study. A total of 132 differentially expressed genes regulated by the RcsB have been identified, of which 114 were upregulated and 18 were downregulated. Further, the results of RNA sequencing were discussed with a focus on the predictive roles of RcsB in the inhibition of bacterial chemotaxis, flagellar assembly and infection. To confirm these predictions, we experimentally verified that the Delta rcsB mutant activated chemotactic behavior and flagella biosynthesis, and exhibited enhanced adhesion and invasion of Y. enterocolitica to Caco-2 cells. Although RcsB largely inhibits these physiological activities, the presence of RcsB is still of great significance for optimizing the survival of Y. enterocolitica as evidenced by our previous report that RcsB confers some level of resistance to the cationic antimicrobial peptide polymyxin B in Y. enterocolitica. Overall, the information provided in this study complements our understanding of Rcs phosphorelay in the regulation of Y. enterocolitica pathogenicity, and, simultaneously, provides clues to additional roles of the Rcs system in other members of family Enterobacteriaceae.