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      Oxylipins mediate cell-to-cell communication in Pseudomonas aeruginosa

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          Abstract

          Oxygenated unsaturated fatty acids, known as oxylipins, are signaling molecules commonly used for cell-to-cell communication in eukaryotes. However, a role for oxylipins in mediating communication in prokaryotes has not previously been described. Bacteria mainly communicate via quorum sensing, which involves the production and detection of diverse small molecules termed autoinducers. Here we show that oleic acid-derived oxylipins produced by Pseudomonas aeruginosa function as autoinducers of a novel quorum sensing system. We found that this system controls the cell density-dependent expression of a gene subset independently of the quorum sensing systems thus far described in this bacterium. We identified a LysR-type transcriptional regulator as the primary receptor of the oxylipin signal. The discovery of this oxylipin-dependent quorum sensing system reveals that prokaryote-derived oxylipins also mediate cell-to-cell communication in bacteria.

          Abstract

          Eriel Martínez et al. report that the bacterial pathogen Pseudomonas aeruginosa can convert oleic acids into oxylipins for use in cell-cell communication. This quorum sensing system is regulated by the bacterial protein called oxylipin-dependent diol synthase regulator OdsR.

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          Bacterial quorum-sensing network architectures.

          Quorum sensing is a cell-cell communication process in which bacteria use the production and detection of extracellular chemicals called autoinducers to monitor cell population density. Quorum sensing allows bacteria to synchronize the gene expression of the group, and thus act in unison. Here, we review the mechanisms involved in quorum sensing with a focus on the Vibrio harveyi and Vibrio cholerae quorum-sensing systems. We discuss the differences between these two quorum-sensing systems and the differences between them and other paradigmatic bacterial signal transduction systems. We argue that the Vibrio quorum-sensing systems are optimally designed to precisely translate extracellular autoinducer information into internal changes in gene expression. We describe how studies of the V. harveyi and V. cholerae quorum-sensing systems have revealed some of the fundamental mechanisms underpinning the evolution of collective behaviors.
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            The hierarchy quorum sensing network in Pseudomonas aeruginosa

            Pseudomonas aeruginosa causes severe and persistent infections in immune compromised individuals and cystic fibrosis sufferers. The infection is hard to eradicate as P. aeruginosa has developed strong resistance to most conventional antibiotics. The problem is further compounded by the ability of the pathogen to form biofilm matrix, which provides bacterial cells a protected environment withstanding various stresses including antibiotics. Quorum sensing (QS), a cell density-based intercellular communication system, which plays a key role in regulation of the bacterial virulence and biofilm formation, could be a promising target for developing new strategies against P. aeruginosa infection. The QS network of P. aeruginosa is organized in a multi-layered hierarchy consisting of at least four interconnected signaling mechanisms. Evidence is accumulating that the QS regulatory network not only responds to bacterial population changes but also could react to environmental stress cues. This plasticity should be taken into consideration during exploration and development of anti-QS therapeutics.
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              Progress in and promise of bacterial quorum sensing research

              This Review highlights how we can build upon the relatively new and rapidly developing field of research into bacterial quorum sensing (QS). We now have a depth of knowledge about how bacteria use QS signals to communicate with each other and to coordinate their activities.
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                Author and article information

                Contributors
                emartinez-gutierrez@southernresearch.org
                jcampos-gomez@southernresearch.org
                Journal
                Commun Biol
                Commun Biol
                Communications Biology
                Nature Publishing Group UK (London )
                2399-3642
                15 February 2019
                15 February 2019
                2019
                : 2
                : 66
                Affiliations
                [1 ]ISNI 0000 0004 0376 8349, GRID grid.454225.0, Department of Infectious Diseases, Drug Discovery Division, , Southern Research, ; Birmingham, AL USA
                [2 ]ISNI 0000 0004 0376 8349, GRID grid.454225.0, Chemistry Department, Drug Discovery Division, , Southern Research, ; Birmingham, AL USA
                [3 ]ISNI 0000000106344187, GRID grid.265892.2, Mass Spectrometry/Proteomics (MSP) Shared Facility, School of Medicine, , University of Alabama at Birmingham, ; Birmingham, AL USA
                Author information
                http://orcid.org/0000-0002-2693-0885
                Article
                310
                10.1038/s42003-019-0310-0
                6377657
                30793044
                cfd73c7b-aa0a-4930-9f15-653b925e1422
                © The Author(s) 2019

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 13 June 2018
                : 15 January 2019
                Funding
                Funded by: University of Alabama at Birmingham Institutional Core System (Project # P30CA013148), and kind donation by Mr. Leon Edwards (Chevrolet)
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                © The Author(s) 2018

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