Abstract
Many Proteobacteria govern responses to changes in cell density by using acyl-homoserine lactone (AHL) quorum-sensing (QS) signaling. Similar to the LuxI-LuxR system described in Vibrio fischeri, a minimal AHL QS circuit comprises a pair of genes, a luxI-type synthase gene encoding an enzyme that synthesizes an AHL and a luxR-type AHL-responsive transcription regulator gene. In most bacteria that utilize AHL QS, cognate luxI and luxR homologs are found in proximity to each other on the chromosome. However, a number of recent reports have identified luxR homologs that are not linked to luxI homologs; in some cases luxR homologs have been identified in bacteria that have no luxI homologs. A luxR homolog without a linked luxI homologs is termed an orphan or solo. One of the first reports of an orphan was on QscR in Pseudomonas aeruginosa. The qscR gene was revealed by whole genome sequencing and has been studied in some detail. P. aeruginosa encodes two AHL synthases and three AHL responsive receptors, LasI-LasR form a cognate synthase-receptor pair as do RhlI-RhlR. QscR lacks a linked synthase and responds to the LasI-generated AHL. QS regulation of gene expression in P. aeruginosa employs multiple signals and occurs in the context of other interconnected regulatory circuits that control diverse physiological functions. QscR affects virulence of P. aeruginosa, and although it shows sensitivity to the LasI-generated AHL, 3-oxo-dodecanoylhomoserine lactone, it's specificity is relaxed compared to LasR and can respond equally well to several AHLs. QscR controls a set of genes that overlaps the set regulated by LasR. QscR is comparatively easy to purify and study in vitro, and has become a model for understanding the biochemistry of LuxR homologs. In fact there is a crystal structure of QscR bound to the LasI-generated AHL. Here, we review the current state of research concerning QscR and highlight recent advances in our understanding of its structure and biochemistry.
Highlights
Reviewed by: Vittorio Venturi, International Centre for Genetic Engineering and Biotechnology, Italy Ralf Heermann, Ludwig-Maximilians-Universität München, Germany Joon-Hee Lee, Pusan National University, South Korea
Similar to the LuxI-LuxR system described in Vibrio fischeri, a minimal acyl-homoserine lactone (AHL) QS circuit comprises a pair of genes, a luxI-type synthase gene encoding an enzyme that synthesizes an AHL and a luxR-type AHL-responsive transcription regulator gene
P. aeruginosa QS is one of the best understood cell-cell signaling systems in bacteria. It has two synthase and receptor pairs that allow it to respond to self-generated AHL signals and a third orphan receptor with no cognate synthase
Summary
An evolving perspective on the Pseudomonas aeruginosa orphan quorum sensing regulator QscR. QscR affects virulence of P. aeruginosa, and it shows sensitivity to the LasI-generated AHL, 3-oxo-dodecanoylhomoserine lactone, it’s specificity is relaxed compared to LasR and can respond well to several AHLs. QscR controls a set of genes that overlaps the set regulated by LasR. The. QS regulatory circuit in P. aeruginosa comprises two sub-circuits, Las and Rhl, which utilize the N-acyl homoserine lactone signal molecules 3OC12-HSL and C4-HSL, respectively (Passador et al, 1993; Ochsner et al, 1994; Pearson et al, 1994, 1995; Ochsner and Reiser, 1995). Each circuit includes an AHL signal synthase gene (lasI or rhlI), and another gene (lasR or rhlR) encoding a cognate receptor, which regulates target gene expression. Unlike LasR and RhlR this homolog, later termed QscR, does not have an associated synthase gene
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