1. The α-hydroxyketone LAI-1 regulates motility, Lqs-dependent phosphorylation signalling and gene expression of Legionella pneumophila
- Author
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Schell, Ursula, Simon, Sylvia, Sahr, Tobias, Hager, Dominik, Albers, Michael F., Kessler, Aline, Fahrnbauer, Felix, Trauner, Dirk, Hedberg, Christian, Buchrieser, Carmen, Hilbi, Hubert, Max Von Pettenkofer Institute (MVP), Ludwig-Maximilians-Universität München (LMU), Institute of Medical Microbiology [Zurich], Universität Zürich [Zürich] = University of Zurich (UZH), Biologie des Bactéries intracellulaires - Biology of Intracellular Bacteria, Institut Pasteur [Paris]-Centre National de la Recherche Scientifique (CNRS), Department of Chemistry, LMU University of Munich, University of Munich, Chemical Biology Center (KBC), Umeå University, Work in the group of H.H. was supported by the German Research Foundation (DFG, HI 1511/2-1, HI 1511/5-1) and the Swiss National Science Foundation (SNF, 31003A_153200). Work in the C.B. laboratory was financed by the Institut Pasteur, the Institut Carnot-Pasteur MI, the French Region Ile de France (DIM Malinf),the grant N°ANR-10-LABX-62-IBEID, the Fondation pour la Recherche Médicale (FRM) grant N° DEQ20120323697 and the Pasteur-Weizmann consortium ‘The roles of non-codingRNAs in regulation of microbial life styles and virulence’. C.H. and M.F.A thank the Knut and Alice Wallenberg foundation (Sweden) for generous support, ANR-10-LABX-0062,IBEID,Integrative Biology of Emerging Infectious Diseases(2010), University of Zurich, Hilbi, Hubert, and Institut Pasteur [Paris] (IP)-Centre National de la Recherche Scientifique (CNRS) more...
- Subjects
MESH: Signal Transduction ,MESH: Gene Expression ,Movement ,viruses ,Gene Expression ,610 Medicine & health ,MESH: Ketones ,MESH: Movement ,[SDV.BC]Life Sciences [q-bio]/Cellular Biology ,MESH: Quorum Sensing ,Legionella pneumophila ,MESH: Gene Expression Profiling ,Cell Movement ,Alkanes ,1312 Molecular Biology ,Escherichia coli ,Phosphorylation ,Vibrio cholerae ,MESH: Cell Movement ,MESH: Gene Expression Regulation, Bacterial ,MESH: Phosphorylation ,10179 Institute of Medical Microbiology ,MESH: Escherichia coli ,Gene Expression Profiling ,2404 Microbiology ,MESH: Host-Pathogen Interactions ,Quorum Sensing ,Gene Expression Regulation, Bacterial ,MESH: Transcription Factors ,Ketones ,MESH: Legionella pneumophila ,MESH: Alkanes ,[SDV.MP]Life Sciences [q-bio]/Microbiology and Parasitology ,Host-Pathogen Interactions ,570 Life sciences ,biology ,MESH: Vibrio cholerae ,Signal Transduction ,Transcription Factors - Abstract
International audience; The causative agent of Legionnaires' disease, Legionella pneumophila, employs the autoinducer compound LAI-1 (3-hydroxypentadecane-4-one) for cell-cell communication. LAI-1 is produced and detected by the Lqs (Legionella quorum sensing) system, comprising the autoinducer synthase LqsA, the sensor kinases LqsS and LqsT, as well as the response regulator LqsR. Lqs-regulated processes include pathogen-host interactions, production of extracellular filaments and natural competence for DNA uptake. Here we show that synthetic LAI-1 promotes the motility of L. pneumophila by signalling through LqsS/LqsT and LqsR. Upon addition of LAI-1, autophosphorylation of LqsS/LqsT by [γ-(32) P]-ATP was inhibited in a dose-dependent manner. In contrast, the Vibrio cholerae autoinducer CAI-1 (3-hydroxytridecane-4-one) promoted the phosphorylation of LqsS (but not LqsT). LAI-1 did neither affect the stability of phospho-LqsS or phospho-LqsT, nor the dephosphorylation by LqsR. Transcriptome analysis of L. pneumophila treated with LAI-1 revealed that the compound positively regulates a number of genes, including the non-coding RNAs rsmY and rsmZ, and negatively regulates the RNA-binding global regulator crsA. Accordingly, LAI-1 controls the switch from the replicative to the transmissive growth phase of L. pneumophila. In summary, the findings indicate that LAI-1 regulates motility and the biphasic life style of L. pneumophila through LqsS- and LqsT-dependent phosphorylation signalling. more...
- Published
- 2016
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