Pando Jasmine M, Karlinsey Joyce E, Lara Jimmie C, Libby Stephen J, Fang Ferric C
Department of Microbiology, School of Medicine, University of Washington, Seattle, Washington, USA.
Department of Laboratory Medicine, School of Medicine, University of Washington, Seattle, Washington, USA.
mBio. 2017 Jun 6;8(3):e00808-17. doi: 10.1128/mBio.00808-17.
The Rcs phosphorelay and Psp (phage shock protein) systems are envelope stress responses that are highly conserved in gammaproteobacteria. The Rcs regulon was found to be strongly induced during metal deprivation of serovar Typhimurium lacking the Psp response. Nineteen genes activated by the RcsA-RcsB response regulator make up an operon responsible for the production of colanic acid capsular polysaccharide, which promotes biofilm development. Despite more than half a century of research, the physiological function of colanic acid has remained elusive. Here we show that Rcs-dependent colanic acid production maintains the transmembrane electrical potential and proton motive force in cooperation with the Psp response. Production of negatively charged exopolysaccharide covalently bound to the outer membrane may enhance the surface potential by increasing the local proton concentration. This provides a unifying mechanism to account for diverse Rcs/colanic acid-related phenotypes, including susceptibility to membrane-damaging agents and biofilm formation. Colanic acid is a negatively charged polysaccharide capsule produced by , , and other gammaproteobacteria. Research conducted over the 50 years since the discovery of colanic acid suggests that this exopolysaccharide plays an important role for bacteria living in biofilms. However, a precise physiological role for colanic acid has not been defined. In this study, we provide evidence that colanic acid maintains the transmembrane potential and proton motive force during envelope stress. This work provides a new and fundamental insight into bacterial physiology.
Rcs磷酸化信号转导和Psp（噬菌体休克蛋白）系统是γ-变形菌中高度保守的包膜应激反应。研究发现，在缺乏Psp反应的鼠伤寒血清型沙门氏菌金属缺乏期间，Rcs调控子被强烈诱导。由RcsA-RcsB反应调节因子激活的19个基因组成一个操纵子，负责产生促进生物膜形成的结肠酸荚膜多糖。尽管经过了半个多世纪的研究，结肠酸的生理功能仍然难以捉摸。在这里，我们表明，Rcs依赖性结肠酸的产生与Psp反应协同维持跨膜电势和质子动力。与外膜共价结合的带负电荷的胞外多糖的产生可能通过增加局部质子浓度来增强表面电势。这提供了一种统一的机制来解释各种与Rcs/结肠酸相关的表型，包括对膜损伤剂的敏感性和生物膜形成。结肠酸是由鼠伤寒沙门氏菌、大肠杆菌和其他γ-变形菌产生的带负电荷的多糖荚膜。自结肠酸发现以来的50年里进行的研究表明，这种胞外多糖对生活在生物膜中的细菌起着重要作用。然而，结肠酸的确切生理作用尚未明确。在这项研究中，我们提供证据表明，结肠酸在包膜应激期间维持跨膜电势和质子动力。这项工作为细菌生理学提供了新的基本见解。
