Jani Sneha, Seely Andrew L, Peabody V George L, Jayaraman Arul, Manson Michael D
Department of Biology, 3258 TAMU, Texas A&M University, College Station, TX 77843-3258, USA.
Department of Chemical Engineering, 3122 TAMU, Texas A&M University, College Station, TX 77843-3122, USA.
Microbiology (Reading). 2017 Dec;163(12):1778-1790. doi: 10.1099/mic.0.000567.
Responses to the interspecies quorum-sensing signal autoinducer-2 (AI-2) regulate the patterns of gene expression that promote biofilm development. also senses AI-2 as a chemoattractant, a response that requires the periplasmic AI-2-binding protein LsrB and the chemoreceptor Tsr. Here, we confirm, as previously observed, that under static conditions highly motile cells self-aggregate and form surface-adherent structures more readily than cells lacking LsrB and Tsr, or than Δ cells unable to produce AI-2. This difference is observed both at 37 and 30 °C. Cells deleted for the genes encoding the operon repressor (Δ), or the AI-2 kinase (Δ), or an AI-2 uptake channel protein (Δ), or an AI-2 metabolism enzyme (Δ) are also defective in biofilm formation. The Δ and Δ cells are totally defective in AI-2 chemotaxis, whereas the other mutants show normal or near-normal chemotaxis to external gradients of AI-2. These data demonstrate that chemotaxis to external AI-2 is necessary but not sufficient to induce the full range of density-dependent behaviours that are required for optimal biofilm formation. We also demonstrate that, compared to other binding-protein-dependent chemotaxis systems in , low levels (on the order of ~250 molecules of periplasmic LsrB per wild-type cell and as low as ~50 molecules per cell in some mutants) are adequate for a strong chemotaxis response to external gradients of AI-2.
对种间群体感应信号自诱导物-2（AI-2）的应答调节着促进生物膜形成的基因表达模式。 还将AI-2感知为一种趋化剂，这种应答需要周质AI-2结合蛋白LsrB和化学感受器Tsr。在此，我们如先前观察到的那样证实，在静态条件下，高运动性细胞比缺乏LsrB和Tsr的细胞，或比无法产生AI-2的Δ细胞更容易自我聚集并形成表面附着结构。在37℃和30℃时均观察到这种差异。缺失编码操纵子阻遏物（Δ）、AI-2激酶（Δ）、AI-2摄取通道蛋白（Δ）或AI-2代谢酶（Δ）基因的细胞在生物膜形成方面也存在缺陷。Δ和Δ细胞在AI-2趋化性方面完全缺陷，而其他突变体对AI-2的外部梯度显示出正常或接近正常的趋化性。这些数据表明，对外部AI-2的趋化性是诱导最佳生物膜形成所需的全范围密度依赖性行为的必要条件，但不是充分条件。我们还证明，与 中其他依赖结合蛋白的趋化系统相比，低水平（野生型细胞中周质LsrB约为250个分子，某些突变体中低至每个细胞约50个分子）足以对AI-2的外部梯度产生强烈的趋化性应答。
