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The RhlR quorum-sensing receptor controls Pseudomonas aeruginosa pathogenesis and biofilm development independently of its canonical homoserine lactone autoinducer.
PLoS Pathog. 2017 Jul; 13(7):e1006504.PP

Abstract

Quorum sensing (QS) is a bacterial cell-to-cell communication process that relies on the production, release, and response to extracellular signaling molecules called autoinducers. QS controls virulence and biofilm formation in the human pathogen Pseudomonas aeruginosa. P. aeruginosa possesses two canonical LuxI/R-type QS systems, LasI/R and RhlI/R, which produce and detect 3OC12-homoserine lactone and C4-homoserine lactone, respectively. Here, we use biofilm analyses, reporter assays, RNA-seq studies, and animal infection assays to show that RhlR directs both RhlI-dependent and RhlI-independent regulons. In the absence of RhlI, RhlR controls the expression of genes required for biofilm formation as well as genes encoding virulence factors. Consistent with these findings, ΔrhlR and ΔrhlI mutants have radically different biofilm phenotypes and the ΔrhlI mutant displays full virulence in animals whereas the ΔrhlR mutant is attenuated. The ΔrhlI mutant cell-free culture fluids contain an activity that stimulates RhlR-dependent gene expression. We propose a model in which RhlR responds to an alternative ligand, in addition to its canonical C4-homoserine lactone autoinducer. This alternate ligand promotes a RhlR-dependent transcriptional program in the absence of RhlI.

Authors+Show Affiliations

Princeton University, Department of Molecular Biology, Princeton, NJ, United States of America.Emory University School of Medicine, Children's Healthcare of Atlanta, Inc., Department of Pediatrics, and Center for Cystic Fibrosis and Airway Diseases Research, Atlanta, GA, United States of America.Princeton University, Department of Molecular Biology, Princeton, NJ, United States of America.Emory University School of Medicine, Children's Healthcare of Atlanta, Inc., Department of Pediatrics, and Center for Cystic Fibrosis and Airway Diseases Research, Atlanta, GA, United States of America.Princeton University, Department of Molecular Biology, Princeton, NJ, United States of America. Howard Hughes Medical Institute, Chevy Chase, MD, United States of America.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

28715477

Citation

Mukherjee, Sampriti, et al. "The RhlR Quorum-sensing Receptor Controls Pseudomonas Aeruginosa Pathogenesis and Biofilm Development Independently of Its Canonical Homoserine Lactone Autoinducer." PLoS Pathogens, vol. 13, no. 7, 2017, pp. e1006504.
Mukherjee S, Moustafa D, Smith CD, et al. The RhlR quorum-sensing receptor controls Pseudomonas aeruginosa pathogenesis and biofilm development independently of its canonical homoserine lactone autoinducer. PLoS Pathog. 2017;13(7):e1006504.
Mukherjee, S., Moustafa, D., Smith, C. D., Goldberg, J. B., & Bassler, B. L. (2017). The RhlR quorum-sensing receptor controls Pseudomonas aeruginosa pathogenesis and biofilm development independently of its canonical homoserine lactone autoinducer. PLoS Pathogens, 13(7), e1006504. https://doi.org/10.1371/journal.ppat.1006504
Mukherjee S, et al. The RhlR Quorum-sensing Receptor Controls Pseudomonas Aeruginosa Pathogenesis and Biofilm Development Independently of Its Canonical Homoserine Lactone Autoinducer. PLoS Pathog. 2017;13(7):e1006504. PubMed PMID: 28715477.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The RhlR quorum-sensing receptor controls Pseudomonas aeruginosa pathogenesis and biofilm development independently of its canonical homoserine lactone autoinducer. AU - Mukherjee,Sampriti, AU - Moustafa,Dina, AU - Smith,Chari D, AU - Goldberg,Joanna B, AU - Bassler,Bonnie L, Y1 - 2017/07/17/ PY - 2017/05/04/received PY - 2017/07/01/accepted PY - 2017/07/27/revised PY - 2017/7/18/pubmed PY - 2017/11/29/medline PY - 2017/7/18/entrez SP - e1006504 EP - e1006504 JF - PLoS pathogens JO - PLoS Pathog. VL - 13 IS - 7 N2 - Quorum sensing (QS) is a bacterial cell-to-cell communication process that relies on the production, release, and response to extracellular signaling molecules called autoinducers. QS controls virulence and biofilm formation in the human pathogen Pseudomonas aeruginosa. P. aeruginosa possesses two canonical LuxI/R-type QS systems, LasI/R and RhlI/R, which produce and detect 3OC12-homoserine lactone and C4-homoserine lactone, respectively. Here, we use biofilm analyses, reporter assays, RNA-seq studies, and animal infection assays to show that RhlR directs both RhlI-dependent and RhlI-independent regulons. In the absence of RhlI, RhlR controls the expression of genes required for biofilm formation as well as genes encoding virulence factors. Consistent with these findings, ΔrhlR and ΔrhlI mutants have radically different biofilm phenotypes and the ΔrhlI mutant displays full virulence in animals whereas the ΔrhlR mutant is attenuated. The ΔrhlI mutant cell-free culture fluids contain an activity that stimulates RhlR-dependent gene expression. We propose a model in which RhlR responds to an alternative ligand, in addition to its canonical C4-homoserine lactone autoinducer. This alternate ligand promotes a RhlR-dependent transcriptional program in the absence of RhlI. SN - 1553-7374 UR - https://www.unboundmedicine.com/medline/citation/28715477/The_RhlR_quorum_sensing_receptor_controls_Pseudomonas_aeruginosa_pathogenesis_and_biofilm_development_independently_of_its_canonical_homoserine_lactone_autoinducer_ L2 - http://dx.plos.org/10.1371/journal.ppat.1006504 DB - PRIME DP - Unbound Medicine ER -