| Popis: |
Many bacterial species use the secondary messenger, c-di-GMP, to promote the production of biofilm matrix components. In Pseudomonas aeruginosa, c-di-GMP production is stimulated upon initial surface contact and generally remains high throughout biofilm growth. Transcription of several gene clusters, including the Sia signal transduction system, are induced in response to high cellular levels of c-di-GMP. The output of this system is SiaD, a diguanylate cyclase whose activity is induced in the presence of the detergent SDS. Previous studies demonstrated that Sia-mediated cellular aggregation is a key feature of P. aeruginosa growth in the presence of SDS. Here, we show that the Sia system is important for producing low levels of c-di-GMP when P. aeruginosa is growing planktonically. In addition, we show that Sia activity is important for maintaining cell-associated Psl in planktonic populations. We also demonstrate that Sia mutant strains have reduced cell-associated Psl and a surface attachment-deficient phenotype. The Sia system also appears to posttranslationally impact cell-associated Psl levels. Collectively, our findings suggest a novel role for the Sia system and c-di-GMP in planktonic populations by regulating levels of cell-associated Psl. IMPORTANCE The biofilm matrix of the opportunistic pathogen Pseudomonas aeruginosa is composed of exopolysaccharides (EPS), proteins, and nucleic acids. In P. aeruginosa, an increase in the small molecule c-di-GMP causes an increase in biofilm matrix production both transcriptionally and posttranslationally. C-di-GMP is synthesized by diguanylate cyclases (DGCs), and P. aeruginosa encodes many DGCs which are active under different conditions and influence specific pathways. Here, we demonstrate that the DGC SiaD, specifically, posttranslationally regulates production of the cell-associated form of the EPS Psl. Since cell-associated Psl is essential for attachment to surfaces, mutants lacking SiaD activity do not attach robustly to surfaces. Our findings reveal a novel mechanism for regulating production of an EPS important for colonization of infection sites. |
