Department of Human Physiology with Community Health, Vidyasagar University, Midnapore, West Bengal, 721102, India.
Department of Chemistry and Chemical Technology, Vidyasagar University, Midnapore, West Bengal, 721102, India.
Microb Ecol. 2019 Apr;77(3):616-630. doi: 10.1007/s00248-018-1262-5. Epub 2018 Sep 14.
Vibrio cholerae, the Gram-negative bacterium causing lethal diarrheal disease cholera, forms biofilm on solid surfaces to gain adaptive advantage for successful survival in aquatic reservoirs. Expression of exopolysaccharide (EPS), an extracellular matrix material, has been found critical for biofilm-based environmental persistence. In a subset of epidemic-causing V. cholerae, absence of flagellum but not motility was identified to induce elevated exopolysaccharide expression. Identification of the role played by quorum sensing autoinducer molecules, i.e., cholera autoinducer 1 (CAI-1) and autoinducer 2 (AI-2) as well as central regulator LuxO on EPS expression in the subset was explored. Deletion mutations were introduced in vital genes responsible for synthesizing CAI-1 (cqsA), AI-2 (luxS), flagellum (flaA), LuxO (luxO), flagellar motor (motX), and VpsR (vpsR) in the model strain MO10. Subsequent phenotypic alterations in terms of colony morphology, EPS expression, biofilm formation, and transcription level of relevant genes were analyzed. Autoinducer cross-feeding experiment confirmed the role of autoinducers in EPS signaling. Results reveal that autoinducers and flagellum are the two major EPS signaling units in this subset where one unit becomes predominant for EPS production in absence of the other. Moreover, either unit exerts negative influence on EPS induction by the other. Both the EPS signaling cascades are independent of LuxO contribution and essentially involve sodium-driven flagellar motor and VpsR. A cell density and flagellum-mediated, but LuxO-independent, EPS signaling mechanism is considered to be functional in these organisms that confers their survival fitness.
霍乱弧菌是一种革兰氏阴性细菌，会导致致命的腹泻病霍乱，它会在固体表面形成生物膜，从而在水生储层中获得成功生存的适应优势。已发现，细胞外基质物质外多糖 (EPS) 的表达对于基于生物膜的环境持久性至关重要。在引起流行的霍乱弧菌亚群中，鉴定出鞭毛缺失而不是运动性缺失会诱导 EPS 表达升高。探索了群体感应自动诱导分子（即霍乱自动诱导物 1 (CAI-1) 和自动诱导物 2 (AI-2) 以及中央调节剂 LuxO）在该亚群中对 EPS 表达的作用。在模型菌株 MO10 中，引入了负责合成 CAI-1 (cqsA)、AI-2 (luxS)、鞭毛 (flaA)、LuxO (luxO)、鞭毛马达 (motX) 和 VpsR (vpsR) 的关键基因的缺失突变。随后分析了菌落形态、EPS 表达、生物膜形成和相关基因转录水平的表型变化。自动诱导物交叉喂养实验证实了自动诱导物在 EPS 信号传递中的作用。结果表明，自动诱导物和鞭毛是该亚群中 EPS 信号传递的两个主要单元，其中一个单元在另一个单元缺失的情况下成为 EPS 产生的主要单元。此外，一个单元对另一个单元的 EPS 诱导施加负面影响。这两个 EPS 信号级联都独立于 LuxO 的贡献，并且本质上涉及钠离子驱动的鞭毛马达和 VpsR。认为这些生物体中存在一种细胞密度和鞭毛介导的、但不依赖 LuxO 的 EPS 信号机制，这使其具有生存适应性。
