Quorum sensing is a regulatory process used by bacteria for controlling gene expression in response to increasing cell density.¹ This regulatory process manifests itself with a variety of phenotypes including biofilm formation and virulence factor production.² Coordinated gene expression is achieved by the production, release, and detection of small diffusible signal molecules called autoinducers. The N-acylated homoserine lactones (AHLs) comprise one such class of autoinducers, each of which generally consists of a fatty acid coupled with homoserine lactone (HSL). AHLs vary in acyl group length (C₄-C₁₈), in the substitution of C3 (hydrogen, hydroxyl, or oxo group) and in the presence or absence of one or more carbon-carbon double bonds in the fatty acid chain. These differences confer signal specificity through the affinity of transcriptional regulators of the LuxR family.³ C₁₆:1-Δ⁹-(L)-HSL is a long-chain AHL that functions as a quorum sensing signaling molecule in strains of S. meliloti.^4,5,6,7 Regulating bacterial quorum sensing signaling can be used to inhibit pathogenesis and thus, represents a new approach to antimicrobial therapy in the treatment of infectious diseases.⁸

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