Abstract
In Pseudomonas aeruginosa, acyl-homoserine-lactone quorum sensing (acyl-HSL QS) regulates the expression of virulence factors and biofilm formation in response to cell density. The RsaL protein represses transcription of the lasI gene, encoding the 3OC(12)-HSL signal synthase. The level of 3OC(12)-HSL is 10-fold higher in an rsaL mutant than in the wild type. In this work, we studied the effect of 3OC(12)-HSL overproduction caused by the rsaL mutation by comparing the transcriptional profiles and virulence-related phenotypes of a P. aeruginosa rsaL mutant and its wild-type parent. Results showed that the rsaL mutant overproduces secreted virulence factors (pyocyanin, elastase, hemolysins), displays increased twitching and swarming motility and is hypervirulent compared with the wild type. Interestingly, the rsaL mutant is impaired in biofilm formation. Taken together, these results suggest that RsaL could be important in the transition of P. aeruginosa from a planktonic to a sessile life style and in chronic infections, characterized by biofilm formation and limited virulence factor production.
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