Vibrio cholerae is a Gram-negative bacterium found in aquatic environments and a human pathogen of global significance. Its transition between host-associated and environmental lifestyles involves the tight regulation of niche-specific phenotypes such as motility, biofilm formation, and virulence. V. cholerae's transition from the host to environmental dispersal usually involves suppression of virulence and dispersion of biofilm communities. In contrast to this naturally occurring transition, bacterial aggregation by cationic polymers triggers a unique response, which is to suppress virulence gene expression while also triggering biofilm formation by V. cholerae, an artificial combination of traits that is potentially very useful to bind and neutralize the pathogen from contaminated water. Here, we set out to uncover the mechanistic basis of this polymer-triggered bacterial behavior. We found that bacteria-polymer aggregates undergo rapid autoinduction and achieve quorum sensing at bacterial densities far below those required for autoinduction in the absence of polymers. We demonstrate this induction of quorum sensing is due both to a rapid formation of autoinducer gradients and local enhancement of autoinducer concentrations within bacterial clusters as well as the stimulation of CAI-1 and AI-2 production by aggregated bacteria. We further found that polymers cause an induction of the biofilm-specific regulator VpsR and the biofilm structural protein RbmA, bypassing the usual suppression of biofilm during autoinduction. Overall, this study highlights that synthetic materials can be used to cross-wire natural bacterial responses to achieve a combination of phenotypes with potentially useful applications.

中文翻译：

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阳离子聚合物对霍乱弧菌的聚集作用增强了群体感应能力，但覆盖了对自感应的生物膜耗散。

霍乱弧菌是在水生环境中发现的革兰氏阴性细菌，是具有全球意义的人类病原体。它在寄主相关生活方式和环境生活方式之间的过渡涉及对利基特异性表型（例如运动性，生物膜形成和毒力）的严格调节。霍乱弧菌从宿主向环境扩散的转变通常涉及抑制生物膜群落的毒力和扩散。与这种自然发生的转变相反，阳离子聚合物引起的细菌聚集触发了独特的反应，即抑制毒力基因表达，同时也触发了霍乱弧菌的生物膜形成，霍乱弧菌是一种人工结合的性状，对结合和中和该性状非常有用。来自污染水的病原体。这里，我们着手揭示这种聚合物触发的细菌行为的机理基础。我们发现细菌-聚合物聚集体会经历快速的自动诱导，并且在细菌密度远低于不存在聚合物的情况下自动诱导所需的细菌密度下实现群体感应。我们证明了这种群体感应的诱导是由于细菌簇内快速形成的自诱导物梯度和局部增强的自诱导物浓度，以及由于聚集细菌对CAI-1和AI-2产生的刺激。我们进一步发现，聚合物引起生物膜特异性调节剂VpsR和生物膜结构蛋白RbmA的诱导，绕过了在自动诱导过程中通常对生物膜的抑制作用。全面的，