Abstract
As well as their importance to nutrition, fatty acids (FA) represent a unique group of quorum sensing chemicals that modulate the behavior of bacterial population in virulence. However, the way in which full-length, membrane-bound receptors biochemically detect FA remains unclear. Here, we provide genetic, enzymological and biophysical evidences to demonstrate that in the phytopathogenic bacterium Xanthomonas campestris pv. campestris, a medium-chain FA diffusible signal factor (DSF) binds directly to the N-terminal, 22 amino acid-length sensor region of a receptor histidine kinase (HK), RpfC. The binding event remarkably activates RpfC autokinase activity by causing an allosteric change associated with the dimerization and histidine phosphotransfer (DHp) and catalytic ATP-binding (CA) domains. Six residues were found essential for sensing DSF, especially those located in the region adjoining to the inner membrane of cells. Disrupting direct DSF-RpfC interaction caused deficiency in bacterial virulence and biofilm development. In addition, two amino acids within the juxtamembrane domain of RpfC, Leu172 and Ala178, are involved in the autoinhibition of the RpfC kinase activity. Replacements of them caused constitutive activation of RpfC-mediated signaling regardless of DSF stimulation. Therefore, our results revealed a biochemical mechanism whereby FA activates bacterial HK in an allosteric manner, which will assist in future studies on the specificity of FA-HK recognition during bacterial virulence regulation and cell-cell communication.
Highlights
Quorum-sensing is a process that bacterial cells communicate with each other to elicit specific physiological responses, including virulence against hosts [1,2]
Fatty acids are part of the language of cell-cell communication known as quorum sensing for a decade
The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript
Summary
Quorum-sensing is a process that bacterial cells communicate with each other to elicit specific physiological responses, including virulence against hosts [1,2]. How single-celled bacteria detect and respond to population density is a fundamental question in studying quorum sensing. Previous studies have reported that a number of chemicals, such as acylated homoserine lactones, peptides, quinolones, and small molecular fatty acids (FA), were implicated in the “bacterial languages” that are usually recognized by bacterial sensor histidine kinases (HK) to elicit quorum sensing [1,3]. In the past three decades, the basic biochemical processes of protein phosphorylation and dephosphorylation during TCS regulation have been well documented, as the first event to trigger the cell-cell communication, only a few of ligand-HK interactions were experimentally investigated [5,6]. How HK recognizes various signals, especially in non-model bacteria, remains incompletely studied [7]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
