Abstract
DspI, a putative enoyl-coenzyme A (CoA) hydratase/isomerase, was proposed to be involved in the synthesis of cis-2-decenoic acid (CDA), a quorum sensing (QS) signal molecule in the pathogen Pseudomonas aeruginosa (P. aeruginosa). The present study provided a structural basis for the dehydration reaction mechanism of DspI during CDA synthesis. Structural analysis reveals that Glu126, Glu146, Cys127, Cys131 and Cys154 are important for its enzymatic function. Moreover, we show that the deletion of dspI results in a remarkable decreased in the pyoverdine production, flagella-dependent swarming motility, and biofilm dispersion as well as attenuated virulence in P. aeruginosa PA14. This study thus unravels the mechanism of DspI in diffusible signal factor (DSF) CDA biosynthesis, providing vital information for developing inhibitors that interfere with DSF associated pathogenicity in P. aeruginosa.
Highlights
DspI, a putative enoyl-coenzyme A (CoA) hydratase/isomerase, was proposed to be involved in the synthesis of cis-2-decenoic acid (CDA), a quorum sensing (QS) signal molecule in the pathogen Pseudomonas aeruginosa (P. aeruginosa)
The fatty acid messenger CDA produced by P. aeruginosa is a new member of the diffusible signal factor (DSF) family, mediating interand intra-species communication
The increasing appreciation of its great potential clinical applications raises the requirement for understanding CDA synthesis and the signal transduction mechanism[7,37,38,39]
Summary
DspI, a putative enoyl-coenzyme A (CoA) hydratase/isomerase, was proposed to be involved in the synthesis of cis-2-decenoic acid (CDA), a quorum sensing (QS) signal molecule in the pathogen Pseudomonas aeruginosa (P. aeruginosa). This study unravels the mechanism of DspI in diffusible signal factor (DSF) CDA biosynthesis, providing vital information for developing inhibitors that interfere with DSF associated pathogenicity in P. aeruginosa. In response to cell density or confinement to niches, P. aeruginosa adopts various signal molecules to mediate virulence factors biosynthesis and/or biofilm formation. Inhibiting these signaling pathways represents attractive strategies for developing novel therapeutics against P. aeruginosa infection[1,2,3,4]. The detailed molecular mechanism of CDA biosynthesis mediated by DspI and the relationship between DspI and P. aeruginosa pathogenicity remains unclear
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