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  current news   Press   selected story    
     
  25th April 2011  
 

Anti-activator QslA defines the quorum sensing threshold and response in Pseudomonas aeruginosa.

 
 




Authors
Qihui Seet and Lian-Hui Zhang.

Published in Molecular Microbiology, 22 March 2011. (Epub ahead of print.)

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.

 
 

 
 


Figure Legend : A schematic model showing the role of QslA in raising the QS threshold. QS-dependent gene expression level is plotted against 3-oxo-C12-HSL concentration for wild-type strain (solid line) and mutant ΔqslA (dotted line). The 3-oxo-C12-HSL concentration at which QS occurs in wild type or ΔqslA is indicated by the line with double arrows. QslA increases QS threshold through sequestering LasR by formation of QslA-LasR complex.

For more information on Lianhui ZHANG’s laboratory, please click here.