The intragenus and interspecies quorum-sensing autoinducers exert distinct control over Vibrio cholerae biofilm formation and dispersal
The intragenus and interspecies quorum-sensing autoinducers exert distinct control over Vibrio cholerae biofilm formation and dispersal
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DOI：
10.1371/journal.pbio.3000429
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发表时间：
2019-11-01
期刊：
影响因子：
9.8
通讯作者：
Bassler, Bonnie L.
中科院分区：
文献类型：
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作者：
Bridges, Andrew A.;Bassler, Bonnie L.
霍乱弧菌具有多种群体感应（QS）系统，控制毒力和生物膜形成等性状。在低细胞密度下，当不存在QS自诱导物时，霍乱弧菌形成生物膜。在高细胞密度下，当自诱导物积累时，生物膜形成被抑制，并且发生分散。在这里，我们专注于两个良好的特点QS自身诱导剂的作用，并行工作。一种称为霍乱弧菌自诱导物-1（CAI-1）的自诱导物用于测量弧菌丰度，另一种称为自诱导物-2（AI-2）的自诱导物由不同的细菌物种广泛产生，并推测使霍乱弧菌能够评估邻近群落的总细菌细胞密度。两个霍乱弧菌自诱导剂将信息汇集到共享的信号中继途径中。QS系统架构的这一特征使得人们很难理解如何从每个自诱导物中提取特定信息，自诱导物如何驱动不同的输出行为，以及细菌如何使用QS来区分细菌群落中的亲属和非亲属。我们开发了一种活细胞生物膜形成和分散试验，可以检查两种自诱导物在控制霍乱弧菌行为中的单独和组合作用。我们表明，QS系统作为一个符合检测器，其中两个autoinducers必须同时存在的生物膜形成的镇压发生。在该背景下，当仅存在少数霍乱弧菌细胞时，CAI-1 QS途径被激活，而AI-2途径仅在高得多的细胞密度下被激活。这种不对称性的结果是AI-2的外源性来源，而不是CAI-1，有助于满足符合检测器抑制生物膜形成和促进扩散。我们认为，霍乱弧菌在进入高细胞密度QS模式之前，使用CAI-1来验证它的一些亲属是否存在，但事实上，是广泛制造的自诱导物AI-2设定了霍乱弧菌QS计划的步伐。不同的霍乱弧菌自身诱导物的独特作用的第一份报告表明，检测亲属促进了与检测非亲属不同的结果。
Vibrio cholerae possesses multiple quorum-sensing (QS) systems that control virulence and biofilm formation among other traits. At low cell densities, when QS autoinducers are absent, V. cholerae forms biofilms. At high cell densities, when autoinducers have accumulated, biofilm formation is repressed, and dispersal occurs. Here, we focus on the roles of two well-characterized QS autoinducers that function in parallel. One autoinducer, called cholerae autoinducer-1 (CAI-1), is used to measure Vibrio abundance, and the other autoinducer, called autoinducer-2 (AI-2), is widely produced by different bacterial species and presumed to enable V. cholerae to assess the total bacterial cell density of the vicinal community. The two V. cholerae autoinducers funnel information into a shared signal relay pathway. This feature of the QS system architecture has made it difficult to understand how specific information can be extracted from each autoinducer, how the autoinducers might drive distinct output behaviors, and, in turn, how the bacteria use QS to distinguish kin from nonkin in bacterial communities. We develop a live-cell biofilm formation and dispersal assay that allows examination of the individual and combined roles of the two autoinducers in controlling V. cholerae behavior. We show that the QS system works as a coincidence detector in which both autoinducers must be present simultaneously for repression of biofilm formation to occur. Within that context, the CAI-1 QS pathway is activated when only a few V. cholerae cells are present, whereas the AI-2 pathway is activated only at much higher cell density. The consequence of this asymmetry is that exogenous sources of AI-2, but not CAI-1, contribute to satisfying the coincidence detector to repress biofilm formation and promote dispersal. We propose that V. cholerae uses CAI-1 to verify that some of its kin are present before committing to the high-cell-density QS mode, but it is, in fact, the broadly made autoinducer AI-2 that sets the pace of the V. cholerae QS program. This first report of unique roles for the different V. cholerae autoinducers suggests that detection of kin fosters a distinct outcome from detection of nonkin.