Effects of carbazole-degradative plasmid pCAR1 on biofilm morphology in Pseudomonas putida†KT2440.

Bacteria typically form biofilms under natural conditions. To elucidate the effect of the carriage of carbazole-degradative plasmid pCAR1 on biofilm formation by host bacteria, we compared the biofilm morphology, using confocal laser scanning microscopy, of three pCAR1-free and pCAR1-carrying Pseudomonas hosts: P. putida KT2440, P. aeruginosa PAO1 and P. fluorescens Pf0-1. Although pCAR1 did not significantly affect biofilm formation by PAO1 or Pf0-1, pCAR1-carrying KT2440 became filamentous and formed flat biofilms, whereas pCAR1-free KT2440 formed mushroom-like biofilms. pCAR1 contains three genes encoding nucleoid-associated proteins (NAPs), namely, Pmr, Pnd and Phu. The enhanced filamentous morphology was observed in two double mutants [KT2440(pCAR1ΔpmrΔpnd) and KT2440(pCAR1ΔpmrΔphu)], suggesting that these NAPs are involved in modulating the filamentous phenotype. Transcriptome analyses of the double mutants identified 32 candidate genes that may be involved in filamentation of KT2440. Overexpression of PP_2193 in KT2440 induced filamentation and overexpression of PP_0308 or PP_0309 in KT2440(pCAR1) enhanced filamentation of cells over time. This suggests that pCAR1 induces development of an abnormal filamentous morphology by KT2440 via a process involving overexpression of several genes, such as PP_2193. In addition, pCAR1-encoded NAPs partly suppress too much filamentation of KT2440(pCAR1) by repressing transcription of some genes, such as PP_0308 and PP_0309.

The Pseudomonas Quinolone Signal Inhibits Biofilm Development of Streptococcus mutans.

Bacteria often thrive in natural environments through a sessile mode of growth, known as the biofilm. Biofilms are well-structured communities and their formation is tightly regulated. However, the mechanisms by which interspecies interactions alter the formation of biofilms have not yet been elucidated in detail. We herein demonstrated that a quorum-sensing signal in Pseudomonas aeruginosa (the Pseudomonas quinolone signal; PQS) inhibited biofilm formation by Streptococcus mutans. Although the PQS did not affect cell growth, biofilm formation was markedly inhibited. Our results revealed a unique role for this multifunctional PQS and also indicated its application in the development of prophylactic agents against caries-causing S. mutans.

Inhibition of Pseudomonas aeruginosa swarming motility by 1-naphthol and other bicyclic compounds bearing hydroxyl groups.

Many bacteria convert bicyclic compounds, such as indole and naphthalene, to oxidized compounds, including hydroxyindoles and naphthols. Pseudomonas aeruginosa, a ubiquitous bacterium that inhabits diverse environments, shows pathogenicity against animals, plants, and other microorganisms, and increasing evidence has shown that several bicyclic compounds alter the virulence-related phenotypes of P. aeruginosa. Here, we revealed that hydroxyindoles (4- and 5-hydroxyindoles) and naphthalene derivatives bearing hydroxyl groups specifically inhibit swarming motility but have minor effects on other motilities, including swimming and twitching, in P. aeruginosa. Further analyses using 1-naphthol showed that this effect is also associated with clinically isolated hyperswarming P. aeruginosa cells. Swarming motility is associated with the dispersion of cells from biofilms, and the addition of 1-naphthol maintained biofilm biomass without cell dispersion. We showed that this 1-naphthol-dependent swarming inhibition is independent of changes of rhamnolipid production and the intracellular level of signaling molecule cyclic-di-GMP (c-di-GMP). Transcriptome analyses revealed that 1-naphthol increases gene expression associated with multidrug efflux and represses gene expression associated with aerotaxis and with pyochelin, flagellar, and pilus synthesis. In the present study, we showed that several bicyclic compounds bearing hydroxyl groups inhibit the swarming motility of P. aeruginosa, and these results provide new insight into the chemical structures that inhibit the specific phenotypes of P. aeruginosa.