Structural basis for native agonist and synthetic inhibitor recognition by the Pseudomonas aeruginosa quorum sensing regulator PqsR (MvfR)

Bacterial populations co-ordinate gene expression collectively through quorum sensing (QS), a cell-to-cell communication mechanism employing diffusible signal molecules. The LysR-type transcriptional regulator (LTTR) protein PqsR (MvfR) is a key component of alkyl-quinolone (AQ)-dependent QS in Pseu...

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Main Authors: Ilangovan, Aravindan, Fletcher, Matthew, Rampioni, Giordano, Pustelny, Christian, Rumbaugh, Kendra, Heeb, Stephan, Cámara, Miguel, Truman, Alex, Chhabra, Siri Ram, Emsley, Jonas, Williams, Paul
Format: Article
Published: Public Library of Science 2013
Online Access:https://eprints.nottingham.ac.uk/2418/
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author Ilangovan, Aravindan
Fletcher, Matthew
Rampioni, Giordano
Pustelny, Christian
Rumbaugh, Kendra
Heeb, Stephan
Cámara, Miguel
Truman, Alex
Chhabra, Siri Ram
Emsley, Jonas
Williams, Paul
author_facet Ilangovan, Aravindan
Fletcher, Matthew
Rampioni, Giordano
Pustelny, Christian
Rumbaugh, Kendra
Heeb, Stephan
Cámara, Miguel
Truman, Alex
Chhabra, Siri Ram
Emsley, Jonas
Williams, Paul
author_sort Ilangovan, Aravindan
building Nottingham Research Data Repository
collection Online Access
description Bacterial populations co-ordinate gene expression collectively through quorum sensing (QS), a cell-to-cell communication mechanism employing diffusible signal molecules. The LysR-type transcriptional regulator (LTTR) protein PqsR (MvfR) is a key component of alkyl-quinolone (AQ)-dependent QS in Pseudomonas aeruginosa. PqsR is activated by 2-alkyl-4-quinolones including the Pseudomonas quinolone signal (PQS; 2-heptyl-3-hydroxy-4(1H)-quinolone), its precursor 2-heptyl-4- hydroxyquinoline (HHQ) and their C9 congeners, 2-nonyl-3-hydroxy-4(1H)-quinolone (C9-PQS) and 2-nonyl-4-hydroxyquinoline (NHQ). These drive the autoinduction of AQ biosynthesis and the up-regulation of key virulence determinants as a function of bacterial population density. Consequently, PqsR constitutes a potential target for novel antibacterial agents which attenuate infection through the blockade of virulence. Here we present the crystal structures of the PqsR co-inducer binding domain (CBD) and a complex with the native agonist NHQ. We show that the structure of the PqsR CBD has an unusually large ligand-binding pocket in which a native AQ agonist is stabilized entirely by hydrophobic interactions. Through a ligand-based design strategy we synthesized and evaluated a series of 50 AQ and novel quinazolinone (QZN) analogues and measured the impact on AQ biosynthesis, virulence gene expression and biofilm development. The simple exchange of two isosteres (OH for NH2) switches a QZN agonist to an antagonist with a concomitant impact on the induction of bacterial virulence factor production. We also determined the complex crystal structure of a QZN antagonist bound to PqsR revealing a similar orientation in the ligand binding pocket to the native agonist NHQ. This structure represents the first description of an LTTR-antagonist complex. Overall these studies present novel insights into LTTR ligand binding and ligand-based drug design and provide a chemical scaffold for further anti-P. aeruginosa virulence drug development by targeting the AQ receptor PqsR.
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spelling nottingham-24182020-05-04T16:37:46Z https://eprints.nottingham.ac.uk/2418/ Structural basis for native agonist and synthetic inhibitor recognition by the Pseudomonas aeruginosa quorum sensing regulator PqsR (MvfR) Ilangovan, Aravindan Fletcher, Matthew Rampioni, Giordano Pustelny, Christian Rumbaugh, Kendra Heeb, Stephan Cámara, Miguel Truman, Alex Chhabra, Siri Ram Emsley, Jonas Williams, Paul Bacterial populations co-ordinate gene expression collectively through quorum sensing (QS), a cell-to-cell communication mechanism employing diffusible signal molecules. The LysR-type transcriptional regulator (LTTR) protein PqsR (MvfR) is a key component of alkyl-quinolone (AQ)-dependent QS in Pseudomonas aeruginosa. PqsR is activated by 2-alkyl-4-quinolones including the Pseudomonas quinolone signal (PQS; 2-heptyl-3-hydroxy-4(1H)-quinolone), its precursor 2-heptyl-4- hydroxyquinoline (HHQ) and their C9 congeners, 2-nonyl-3-hydroxy-4(1H)-quinolone (C9-PQS) and 2-nonyl-4-hydroxyquinoline (NHQ). These drive the autoinduction of AQ biosynthesis and the up-regulation of key virulence determinants as a function of bacterial population density. Consequently, PqsR constitutes a potential target for novel antibacterial agents which attenuate infection through the blockade of virulence. Here we present the crystal structures of the PqsR co-inducer binding domain (CBD) and a complex with the native agonist NHQ. We show that the structure of the PqsR CBD has an unusually large ligand-binding pocket in which a native AQ agonist is stabilized entirely by hydrophobic interactions. Through a ligand-based design strategy we synthesized and evaluated a series of 50 AQ and novel quinazolinone (QZN) analogues and measured the impact on AQ biosynthesis, virulence gene expression and biofilm development. The simple exchange of two isosteres (OH for NH2) switches a QZN agonist to an antagonist with a concomitant impact on the induction of bacterial virulence factor production. We also determined the complex crystal structure of a QZN antagonist bound to PqsR revealing a similar orientation in the ligand binding pocket to the native agonist NHQ. This structure represents the first description of an LTTR-antagonist complex. Overall these studies present novel insights into LTTR ligand binding and ligand-based drug design and provide a chemical scaffold for further anti-P. aeruginosa virulence drug development by targeting the AQ receptor PqsR. Public Library of Science 2013-07-25 Article PeerReviewed Ilangovan, Aravindan, Fletcher, Matthew, Rampioni, Giordano, Pustelny, Christian, Rumbaugh, Kendra, Heeb, Stephan, Cámara, Miguel, Truman, Alex, Chhabra, Siri Ram, Emsley, Jonas and Williams, Paul (2013) Structural basis for native agonist and synthetic inhibitor recognition by the Pseudomonas aeruginosa quorum sensing regulator PqsR (MvfR). PLoS Pathogens, 9 (7). e1003508/1-e1003508/17. ISSN 1553-7366 http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1003508 doi:10.1371/journal.ppat.1003508 doi:10.1371/journal.ppat.1003508
spellingShingle Ilangovan, Aravindan
Fletcher, Matthew
Rampioni, Giordano
Pustelny, Christian
Rumbaugh, Kendra
Heeb, Stephan
Cámara, Miguel
Truman, Alex
Chhabra, Siri Ram
Emsley, Jonas
Williams, Paul
Structural basis for native agonist and synthetic inhibitor recognition by the Pseudomonas aeruginosa quorum sensing regulator PqsR (MvfR)
title Structural basis for native agonist and synthetic inhibitor recognition by the Pseudomonas aeruginosa quorum sensing regulator PqsR (MvfR)
title_full Structural basis for native agonist and synthetic inhibitor recognition by the Pseudomonas aeruginosa quorum sensing regulator PqsR (MvfR)
title_fullStr Structural basis for native agonist and synthetic inhibitor recognition by the Pseudomonas aeruginosa quorum sensing regulator PqsR (MvfR)
title_full_unstemmed Structural basis for native agonist and synthetic inhibitor recognition by the Pseudomonas aeruginosa quorum sensing regulator PqsR (MvfR)
title_short Structural basis for native agonist and synthetic inhibitor recognition by the Pseudomonas aeruginosa quorum sensing regulator PqsR (MvfR)
title_sort structural basis for native agonist and synthetic inhibitor recognition by the pseudomonas aeruginosa quorum sensing regulator pqsr (mvfr)
url https://eprints.nottingham.ac.uk/2418/
https://eprints.nottingham.ac.uk/2418/
https://eprints.nottingham.ac.uk/2418/