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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 gene regulation 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.

Quorum sensing is a widespread phenomenon in the microbial world that has important implications in the coordination of population-wide responses in several bacterial pathogens. In Group A Streptococcus (GAS), many questions surrounding quorum sensing systems remain to be solved pertaining to their function and their contribution to the GAS lifestyle in the host. The quorum sensing systems of GAS described to date can be categorized into four groups: Rgg, Sil, lantibiotic systems and LuxS/AI-2. The Rgg family of proteins, a conserved group of transcription factors that modify their activity in response to signaling peptides, has been shown to regulate genes involved in virulence, biofilm formation and competence. The sil locus, whose expression is regulated by the activity of signaling peptides and a putative two-component system, has been implicated on regulating genes involved with invasive disease in GAS isolates. Lantibiotic regulatory systems are involved in the production of bacteriocins and their autoregulation, and some of these genes have been shown to target both bacterial organisms as well as processes of survival inside the infected host. Finally AI-2 (dihydroxy pentanedione, DPD), synthesized by the LuxS enzyme in several bacteria including GAS, has been proposed to be a universal bacterial communication molecule. In this review we discuss the mechanisms of these four systems, the putative functions of their targets, and pose critical questions for future studies.