Abstract
Quorum sensing (QS) in a bacterial population is activated when extracellular concentration of QS signal reaches a threshold, but how this threshold is determined remains largely unknown. In this study, we report the identification and characterization of a novel anti-activator encoded by qslA in Pseudomonas aeruginosa. The null mutation of qslA elevated AHL-dependent QS and PQS signalling, increased the expression of QS-dependent genes, and enhanced the virulence factor production and pathogenicity. We further present evidence that modulation of QS by QslA is due to protein-protein interaction with LasR, which prevents LasR from binding to its target promoter. QslA also influences the threshold concentration of QS signal needed for QS activation; in the absence of qslA, QS is activated by nine times less N-3-oxo-dodecanoyl-homoserine lactone (3-oxo-C12-HSL) than that in wild type. The findings from this study depict a new mechanism that governs the QS threshold in P. aeruginosa.
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