The effect of the N-acyl-homoserine lactonase on the properties of Pectobacterium betavasculorum

Bacteria use quorum sensing (QS) as a mechanism of cell to cell communication that enables them to coordinate essential behaviours. To study the role of QS regulation in directing the cellular processes and virulence of Pectobacterium betavasculorum, the effect of the aiiA gene on this bacterium was investigated. In this study, plasmid pVLT33/aiiA was introduced into bacterial cells to gain Pb/pVLT33/aiiA. The pVLT33/aiiA plasmid contains a heterologous aiiA gene (encoding AiiA enzyme), which catalyzes the degradation of QS signalling molecules of the of N-acyl-homoserine lactones (AHLs). An absence or reduction of AHLs in enclosed medium was assessed with the biosensor Chromobacterium violaceum CV026 in a co-culture assay. To evaluate the effects of AHL on virulence behaviour of the mutated P. betavasculorum, motility, biofilm formation and pathogenicity assays on potato tubers were performed. The results revealed that swimming motility and biofilm formation in the Pb/pVLT33/aiiA strain were significantly influenced, while the introduction of the aiiA gene had no effect on the hypersensitive response. The enzymatic bioassay revealed that the aiiA gene completely abolished secretion of pectate lyase (Pel) and polygalacturonase (Peh) enzymes, while the breakdown of cellulose was slightly reduced. Furthermore, aiiA expression in P. betavasculorum caused reduction of tissue maceration and pathogenicity on potato tubers and cactus. It can be concluded that the main virulence behaviours of P. betavasculorum are controlled by the QS system. Hence, application of anti-QS mechanisms is a promising strategy for the prevention of diseases in which virulence is regulated by QS.