The function of SpnR and the inhibitory effects by halogenated furanone on quorum sensing in Serratia marcescens AS-1.
By secretion and detection of a series of signaling molecules, bacteria are able to coordinate gene expression as a community, to regulate a variety of important phenotypes, from virulence factor production to biofilm formation to symbiosis related behaviours such as bioluminescence. This widespread signaling mechanism is called quorum sensing. There are several quorum sensing systems described in Serratia. Serratia marcescens AS-1, isolated from soil, had the LuxI/LuxR homologues called SpnI/SpnR. S. marcescens AS-1 produced two kinds of N-acyl-L-homoserine lactones, N-hexanoyl-L-homoserine lactone and N-(3-oxohexanoyl)-L-homoserine lactone as signal molecules, which involved in quorum sensing to control the gene expression in response to increased cell density. By gene replacement method, the spnR mutant was constructed, named S. marcescens AS-1R. SpnR acted as a negative regulator for the production of prodigiosin, swarming motility and biofilm formation, which were regulated by quorum sensing. Halogenated furanone, known as a natural inhibitor of quorum sensing, could effectively inhibit the quorum sensing of S. marcescens AS-1 but without interrupting AHL-SpnR interaction. All results will be helpful to understand the mechanisms of halogenated furanone inhibition on quorum sensing and the potential application of halogenated furanone in effectively preventing infection disease caused by Serratia strains.