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      Identification of new quorum sensing autoinducer binding partners in Pseudomonas aeruginosa using photoaffinity probes†

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          Abstract

          Design, synthesis and application of PQS and HHQ probes for investigating quinolone quorum sensing pathways using photoaffinity labeling.

          Abstract

          Many bacterial species, including the human pathogen Pseudomonas aeruginosa, employ a mechanism of intercellular communication known as quorum sensing (QS), which is mediated by signalling molecules termed autoinducers. The Pseudomonas Quinolone Signal (PQS) and 2-Heptyl-3 H-4-Quinolone (HHQ) are autoinducers in P. aeruginosa, and they are considered important factors in the progress of infections by this clinically relevant organism. Herein, we report the development of HHQ and PQS photoaffinity-based probes for chemical proteomic studies. Application of these probes led to the identification of previously unsuspected putative HHQ and PQS binders, thereby providing new insights into QS at a proteomic level and revealing potential new small molecule targets for virulence attenuation strategies. Notably, we found evidence that PQS binds RhlR, the cognate receptor in the Rhl QS sub-system of P. aeruginosa. This is the first indication of interaction between the Rhl and PQS systems at the protein/ligand level, which suggests that RhlR should be considered a highly attractive target for antivirulence strategies.

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          Establishment of Pseudomonas aeruginosa infection: lessons from a versatile opportunist.

          J Lyczak, C. L. Cannon, G B Pier (2000)
          Pseudomonas aeruginosa is an ubiquitous pathogen capable of infecting virtually all tissues. A large variety of virulence factors contribute to its importance in burn wounds, lung infection and eye infection. Prominent factors include pili, flagella, lipopolysaccharide, proteases, quorum sensing, exotoxin A and exoenzymes secreted by the type III secretion system.
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            The multiple signaling systems regulating virulence in Pseudomonas aeruginosa.

            Pol Nadal Jimenez, Gudrun Koch, Jessica Thompson … (2012)
            Cell-to-cell communication is a major process that allows bacteria to sense and coordinately react to the fluctuating conditions of the surrounding environment. In several pathogens, this process triggers the production of virulence factors and/or a switch in bacterial lifestyle that is a major determining factor in the outcome and severity of the infection. Understanding how bacteria control these signaling systems is crucial to the development of novel antimicrobial agents capable of reducing virulence while allowing the immune system of the host to clear bacterial infection, an approach likely to reduce the selective pressures for development of resistance. We provide here an up-to-date overview of the molecular basis and physiological implications of cell-to-cell signaling systems in Gram-negative bacteria, focusing on the well-studied bacterium Pseudomonas aeruginosa. All of the known cell-to-cell signaling systems in this bacterium are described, from the most-studied systems, i.e., N-acyl homoserine lactones (AHLs), the 4-quinolones, the global activator of antibiotic and cyanide synthesis (GAC), the cyclic di-GMP (c-di-GMP) and cyclic AMP (cAMP) systems, and the alarmones guanosine tetraphosphate (ppGpp) and guanosine pentaphosphate (pppGpp), to less-well-studied signaling molecules, including diketopiperazines, fatty acids (diffusible signal factor [DSF]-like factors), pyoverdine, and pyocyanin. This overview clearly illustrates that bacterial communication is far more complex than initially thought and delivers a clear distinction between signals that are quorum sensing dependent and those relying on alternative factors for their production.
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              Look who's talking: communication and quorum sensing in the bacterial world.

              Paul Williams, Klaus Winzer, Weng C. Chan … (2007)
              For many years bacteria were considered primarily as autonomous unicellular organisms with little capacity for collective behaviour. However, we now appreciate that bacterial cells are in fact, highly communicative. The generic term 'quorum sensing' has been adopted to describe the bacterial cell-to-cell communication mechanisms which co-ordinate gene expression usually, but not always, when the population has reached a high cell density. Quorum sensing depends on the synthesis of small molecules (often referred to as pheromones or autoinducers) that diffuse in and out of bacterial cells. As the bacterial population density increases, so does the synthesis of quorum sensing signal molecules, and consequently, their concentration in the external environment rises. Once a critical threshold concentration has been reached, a target sensor kinase or response regulator is activated (or repressed) so facilitating the expression of quorum sensing-dependent genes. Quorum sensing enables a bacterial population to mount a co-operative response that improves access to nutrients or specific environmental niches, promotes collective defence against other competitor prokaryotes or eukaryotic defence mechanisms and facilitates survival through differentiation into morphological forms better able to combat environmental threats. Quorum sensing also crosses the prokaryotic-eukaryotic boundary since quorum sensing-dependent signalling can be exploited or inactivated by both plants and mammals.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Chem Sci
                Journal ID (iso-abbrev): Chem Sci
                Title: Chemical Science
                Publisher: Royal Society of Chemistry
                ISSN (Print): 2041-6520
                ISSN (Electronic): 2041-6539
                Publication date (Print): 1 November 2017
                Publication date (Electronic): 29 August 2017
                Volume: 8
                Issue: 11
                Pages: 7403-7411
                Affiliations
                [a ] Department of Chemistry , University of Cambridge , Lensfield Road , Cambridge , CB2 1EW , UK . Email: spring@ 123456ch.cam.ac.uk
                [b ] Leiden Institute of Chemistry , Leiden University , Einsteinweg 55 , 2333 CC Leiden , The Netherlands
                [c ] Department of Biochemistry , University of Cambridge , 80 Tennis Court Road , Cambridge , CB2 1GA , UK . Email: mw240@ 123456cam.ac.uk
                Author notes

                ‡Present address Y.R.B.: Department of Chemistry, Physical and Theoretical Chemistry Laboratory, South Parks Road, Oxford OX1 3QZ, UK.

                §Present address J.T.H.: Department of Chemistry, University of Leicester, Leicester LE1 7RH, UK.

                ¶Present address E.A.: Institute of Chemical Research of Catalonia (ICIQ), Barcelona Institute of Science and Technology, Av. Països Catalans 16, 43007, Tarragona, Spain.

                Author information
                http://orcid.org/0000-0002-0266-771X
                http://orcid.org/0000-0001-7355-2824
                Article
                Publisher ID: c7sc01270e
                DOI: 10.1039/c7sc01270e
                PMC ID: 5674140
                PubMed ID: 29163891
                SO-VID: 657f2c6a-429e-42d7-8e4e-2214c7d94c5a
                Copyright © This journal is © The Royal Society of Chemistry 2017
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution 3.0 Unported License ( http://creativecommons.org/licenses/by/3.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 21 March 2017
                Date accepted : 26 August 2017
                Categories
                Subject: Chemistry

                Notes

                †Electronic supplementary information (ESI) available. See DOI: 10.1039/c7sc01270e


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