ChpC controls twitching motility-mediated expansion of Pseudomonas aeruginosa biofilms in response to serum albumin, mucin and oligopeptides

Nolan, L. M., McCaughey, L. C. , Merjane, J., Turnbull, L. and Whitchurch, C. B. (2020) ChpC controls twitching motility-mediated expansion of Pseudomonas aeruginosa biofilms in response to serum albumin, mucin and oligopeptides. Microbiology, 166(7), pp. 669-678. (doi: 10.1099/mic.0.000911) (PMID:32478653) (PMCID:PMC7657506)

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Twitching motility-mediated biofilm expansion occurs via coordinated, multi-cellular collective behaviour to allow bacteria to actively expand across surfaces. Type-IV pili (T4P) are cell-associated virulence factors which mediate twitching motility via rounds of extension, surface attachment and retraction. The Chp chemosensory system is thought to respond to environmental signals to regulate the biogenesis, assembly and twitching motility function of T4P. In other well characterised chemosensory systems, methyl-accepting chemotaxis proteins (MCPs) feed environmental signals through a CheW adapter protein to the histidine kinase CheA to modulate motility. The Pseudomonas aeruginosa Chp system has an MCP PilJ and two CheW adapter proteins, PilI and ChpC, that likely interact with the histidine kinase ChpA to feed environmental signals into the system. In the current study we show that ChpC is involved in the response to host-derived signals serum albumin, mucin and oligopeptides. We demonstrate that these signals stimulate an increase in twitching motility, as well as in levels of 3′−5′-cyclic adenosine monophosphate (cAMP) and surface-assembled T4P. Interestingly, our data shows that changes in cAMP and surface piliation levels are independent of ChpC but that the twitching motility response to these environmental signals requires ChpC. Furthermore, we show that protease activity is required for the twitching motility response of P. aeruginosa to environmental signals. Based upon our data we propose a model whereby ChpC feeds these environmental signals into the Chp system, potentially via PilJ or another MCP, to control twitching motility. PilJ and PilI then modulate T4P surface levels to allow the cell to continue to undergo twitching motility. Our study is the first to link environmental signals to the Chp chemosensory system and refines our understanding of how this system controls twitching motility-mediated biofilm expansion in P. aeruginosa.

Item Type:Articles
Additional Information:L.M.N was supported by an Imperial College Research Fellowship. L.C.M was supported by a Sir Henry Wellcome Postdoctoral Fellowship (106064/Z/14/2). C.B.W. was supported by a National Health and Medical Research Council of Australia (NHMRC) Career Development Award and a Senior Research Fellowship (571905).This project was supported by NHMRC project grant (334076).
Glasgow Author(s) Enlighten ID:MCCAUGHEY, Dr LAURA
Authors: Nolan, L. M., McCaughey, L. C., Merjane, J., Turnbull, L., and Whitchurch, C. B.
College/School:College of Medical Veterinary and Life Sciences > School of Life Sciences
Journal Name:Microbiology
Publisher:Microbiology Society
ISSN (Online):1465-2080
Published Online:01 June 2020
Copyright Holders:Copyright © 2020 The Authors
First Published:First published in Microbiology 166(7): 669-678
Publisher Policy:Reproduced under a Creative Commons License

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