Identification of Biofilm-Associated Cluster (bac) in Pseudomonas aeruginosa Involved in Biofilm Formation and Virulence

Abstract

Biofilms are prevalent in diseases caused by Pseudomonas aeruginosa, an opportunistic and nosocomial pathogen. By a proteomic approach, we previously identified a hypothetical protein of P. aeruginosa (coded by the gene pA3731) that was accumulated by biofilm cells. We report here that a ΔpA3731 mutant is highly biofilm-defective as compared with the wild-type strain. Using a mouse model of lung infection, we show that the mutation also induces a defect in bacterial growth during the acute phase of infection and an attenuation of the virulence. The pA3731 gene is found to control positively the ability to swarm and to produce extracellular rhamnolipids, and belongs to a cluster of 4 genes (pA3729–pA3732) not previously described in P. aeruginosa. Though the protein PA3731 has a predicted secondary structure similar to that of the Phage Shock Protein, some obvious differences are observed compared to already described psp systems, e.g., this unknown cluster is monocistronic and no homology is found between the other proteins constituting this locus and psp proteins. As E. coli PspA, the amount of the protein PA3731 is enlarged by an osmotic shock, however, not affected by a heat shock. We consequently named this locus bac for biofilm-associated cluster.

Intraclonal diversity of the Pseudomonas aeruginosa cystic fibrosis airway isolates TBCF10839 and TBCF121838: distinct signatures of transcriptome, proteome, metabolome, adherence and pathogenicity despite an almost identical genome sequence

“…PA0347 encodes a periplasmic glycerophosphoryl diester phosphodiesterase that hydrolyses glycerophosphodiesters into sn‐glycerol 3‐phosphate plus alcohol (Larson et al ., 1983). PA3729 is part of a monocistronic gene cluster (PA3729–PA3732) which positively controls swarming, extracellular rhamnolipid production and biofilm formation (Macé et al ., 2008). The three TBCF121838‐specific SNPs affected modulators of multidrug resistance, type III secretion (MexS/PA2491, R‐H exchange) and biofilm formation (DipA/PA5017, F‐L exchange; MifR/PA5511, D‐N exchange).…”

Quorum quenching quandary: resistance to antivirulence compounds

“…To investigate whether QQ-resistant bacterial mutants may arise in the presence of antivirulence compounds, we utilized the best studied bacterium for QS, P. aeruginosa, which is an opportunistic pathogen that is responsible for many infections, including those of ventilator-associated pneumonia, urinary and peritoneal dialysis, catheter infections, bacterial keratitis, otitis externa, burns, wound infections and those of the lung (Macé et al, 2008). Wild-type P. aeruginosa PA14 was used instead of PAO1 because PA14 is more virulent than PAO1 in diverse infection models (Harrison et al, 2010) and because of the availability of the complete mutant library (Liberati et al, 2006).…”

Tyrosine phosphatase TpbA controls rugose colony formation in Pseudomonas aeruginosa by dephosphorylating diguanylate cyclase TpbB

“…Pseudomonas aeruginosa is an opportunistic pathogen that is responsible for many biofilm infections including those associated with ventilator-associated pneumonia, urinary and peritoneal dialysis catheters, bacterial keratitis, otitis externa, burns, and lungs [1]. Persistence of this bacterium is linked to its ability to form biofilms [2] and rugose small-colony variants (RSCVs) [3] which are characterized by wrinkled, small colonies and an elevated capacity to form biofilms.…”