Department of Biochemistry, University of Wisconsin-Madison, Madison, Wisconsin, USA.
Department of Biochemistry, University of Wisconsin-Madison, Madison, Wisconsin, USA
J Bacteriol. 2019 Apr 9;201(9). doi: 10.1128/JB.00804-18. Print 2019 May 1.
Biofilm formation is a complex process that requires a number of transcriptional, proteomic, and physiological changes to enable bacterial survival. The lipid membrane presents a barrier to communication between the machinery within bacteria and the physical and chemical features of their extracellular environment, and yet little is known about how the membrane influences biofilm development. We found that depleting the anionic phospholipid cardiolipin reduces biofilm formation in cells by as much as 50%. The absence of cardiolipin activates the regulation of colanic acid synthesis (Rcs) envelope stress response, which represses the production of flagella, disrupts initial biofilm attachment, and reduces biofilm growth. We demonstrate that a reduction in the concentration of cardiolipin impairs translocation of proteins across the inner membrane, which we hypothesize activates the Rcs pathway through the outer membrane lipoprotein RcsF. Our study demonstrates a molecular connection between the composition of membrane phospholipids and biofilm formation in and suggests that altering lipid biosynthesis may be a viable approach for altering biofilm formation and possibly other multicellular phenotypes related to bacterial adaptation and survival. There is a growing interest in the role of lipid membrane composition in the physiology and adaptation of bacteria. We demonstrate that a reduction in the anionic phospholipid cardiolipin impairs biofilm formation in cells. Depleting cardiolipin reduced protein translocation across the inner membrane and activated the Rcs envelope stress response. Consequently, cardiolipin depletion produced cells lacking assembled flagella, which impacted their ability to attach to surfaces and seed the earliest stage in biofilm formation. This study provides empirical evidence for the role of anionic phospholipid homeostasis in protein translocation and its effect on biofilm development and highlights modulation of the membrane composition as a potential method of altering bacterial phenotypes related to adaptation and survival.
生物膜的形成是一个复杂的过程，需要许多转录、蛋白质组学和生理变化，以使细菌得以存活。脂质膜对细菌内部机制与细胞外环境的物理和化学特性之间的通讯构成了障碍，但人们对膜如何影响生物膜的发展知之甚少。我们发现，耗尽带负电荷的磷脂心磷脂会使 细胞的生物膜形成减少多达 50%。心磷脂的缺乏会激活调节菌毛酸合成（Rcs）的包膜应激反应，该反应会抑制鞭毛的产生，破坏初始生物膜附着，并减少生物膜的生长。我们证明，心磷脂浓度的降低会损害跨内膜的蛋白质易位，我们假设这通过外膜脂蛋白 RcsF 激活了 Rcs 途径。我们的研究表明，膜磷脂组成与 生物膜形成之间存在分子联系，并表明改变脂质生物合成可能是改变生物膜形成的可行方法，并且可能与与细菌适应和生存相关的其他多细胞表型有关。人们对脂质膜组成在细菌生理学和适应中的作用越来越感兴趣。我们证明，减少带负电荷的磷脂心磷脂会损害 细胞的生物膜形成。耗尽心磷脂会减少跨内膜的蛋白质易位，并激活 Rcs 包膜应激反应。因此，心磷脂的耗竭导致缺乏组装的菌毛的细胞，这影响了它们附着在表面并启动生物膜形成的最早阶段的能力。这项研究提供了阴离子磷脂动态平衡在蛋白质易位及其对生物膜发育影响的实证证据，并强调了调节膜组成作为改变与适应和生存相关的细菌表型的潜在方法。
