Jasmine Lee1,*, Jien Wu1,*, Yinyue Deng1, Jing Wang1, Chao Wang1, Jianhe Wang1, Changqing Chang1, Yihu Dong1, Paul Williams2 & Lian-Hui Zhang1.
1- Institute of Molecular and Cell Biology, Singapore
2- University of Nottingham, Nottingham, U.K.
*: Co-first authors
Published online in Nature Chemical Biology on 31 March 2013.
Pseudomonas aeruginosa uses a hierarchical quorum sensing (QS) network consisting of las, pqs and rhl regulatory elements to coordinate the expression of bacterial virulence genes. However, clinical isolates frequently contain loss-of-function mutations in the central las system. This motivated us to search for a mechanism that may functionally substitute las. Here we report identification of a new QS signal, IQS. Disruption of IQS biosynthesis paralyzes the pqs and rhl QS systems and attenuates bacterial virulence. Production of IQS is tightly controlled by las under normal culture conditions but is also activated by phosphate limitation, a common stressor that bacteria encounter during infections. Thus, these results have established an integrated QS system that connects the central las system and phosphate-stress response mechanism to the downstream pqs and rhl regulatory systems. Our discovery highlights the complexity of QS signaling systems and extends the gamut of QS and stress-response mechanisms.
Production of QS signals C4HSL and PQS is dependent on IQS. (a,b) The production of C4HSL(a) and PQS (b) in deletion mutant ΔambBsupplemented with 0 nM, 10 nM or 100 nM of IQS. The levels of two QS signals in strain PAO1 were determined as a control. The experiments were repeated four times, and the data represent mean values ± s.d. The amount of PQS produced by PAO1 was arbitrarily set at 100%.
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