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The capsular polysaccharide synthesis (cps) locus of Neisseria meningitidis is implicated in invasive meningococcal disease. The synthesis (synABCD) and transport (ctrABCD) operons are transcribed in opposite directions from a common intergenic region, and the expression is negatively regulated by the bacterial two-component system (TCS) misR/misS and thermosensitive RNA folding. However, these mechanisms do not fully explain the stationary phase responses, and the cis-acting elements remain to be fully characterized. Using the GFP reporter gene and site-directed mutagenesis, cis-regulatory elements in the 134 bp intergenic region, NmIR, were investigated. While confirming a known RpoD promoter, an additional potential promoter element and putative binding sites for the transcription factors fis and lexA were identified through sequence analysis. Deletion of the putative lexA binding site led to an increase in GFP fluorescence. The N. meningitidis genome carries only one lexA homolog, the helix-turn-helix regulator XRE family member (GenBank-NMB0910, HTH_XRE). Trans-complementation of the NmIR-GFP reporter with the N. meningitidis HTH_XRE expression plasmid led to increased fluorescence. Trans-complementation with either misR/misS or nusG decreased reporter gene expression. Consistent with previous reports, deletion of the RpoD promoter reduced expression by 50%, suggesting the redundancy of promoter elements in the intergenic region. Thus, the results confirm the functioning of an exogenous N. meningitidis capsule synthesis promoter in Escherichia coli and demonstrate its regulation through trans-complementation by misR/misS, HTH_XRE, and nusG.