Effect of sdiA on Biosensors of N -Acylhomoserine Lactones

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Abstract
Many gram-negative bacteria synthesize N-acylhomoserine lactones (AHLs) and then use transcription factors of the LuxR family to sense and respond to AHL accumulation in the environment; this phenomenon is termed quorum sensing. Bacteria produce a variety of AHLs, and numerous bacterial reporter strains, or biosensors, that can detect subsets of these molecules have been constructed. Many of these are based on Escherichia coli because this species does not produce AHLs. However, both Escherichia and Salmonella spp. contain a LuxR homolog named SdiA that can detect exogenous AHL synthesized by other microbial species. In this study we have determined that sdiA of E. coli and Salmonella spp. can activate an RhlR-based biosensor plasmid in response to AHLs other than what the biosensor was designed to detect. SdiA does not activate LuxR-, LasR-, or AhyR-based biosensor plasmids, although the presence of sdiA in E. coli does interfere with the function of the AhyR-based biosensor. Because sdiA interferes with the function of two of the four reporters, we have constructed a set of E. coli biosensor strains that lack sdiA. The set includes control reporters that allow the luxR dependence of responses to be determined.