Recent studies in our laboratory have demonstrated that P. aeruginosa produces a small messenger molecule that induces the disaggregation of biofilm cell clusters and results in a switch from a biofilm to a planktonic lifestyle. Preliminary results have demonstrated that these dispersed bacteria are significantly more susceptible to antibiotic treatment when compared to biofilm bacteria that have not been induced to disperse. We wish to characterize the mechanism of signal transduction in the biofilm dispersion response mediated by cis-2-decenoic acid. In performing this work we propose to identify the components of the system that are responsible for signal transduction in the biofilm dispersion response and to identify those genes that are regulated by this signaling system. In performing this work we will use molecular approaches to characterize the interactions of the sensors, response regulators and target DNA, and analyze protein-protein interactions and DNA interactions in the presence and absence of signal.
The current application proposes work that will yield important information leading to an understanding of the mechanism of the biofilm dispersion response in P. aeruginosa. Findings from the proposed research are expected to lead to novel and improved strategies for the treatment of bacterial biofilm infections. The potential for artificial induction of dispersion in biofilms includes enhanced treatment of biofilm infections, improved treatment of burns, improved removal of biofilm from surfaces, and novel mechanisms for disease prevention in clinical, household and industrial settings.
|Marques, Cláudia N H; Davies, David G; Sauer, Karin (2015) Control of Biofilms with the Fatty Acid Signaling Molecule cis-2-Decenoic Acid. Pharmaceuticals (Basel) 8:816-35|
|Amari, Diana T; Marques, Cláudia N H; Davies, David G (2013) The putative enoyl-coenzyme A hydratase DspI is required for production of the Pseudomonas aeruginosa biofilm dispersion autoinducer cis-2-decenoic acid. J Bacteriol 195:4600-10|