Contribution of σ and σ Factors to Expression of Class II in Neisseria meningitidis.

expresses multicomponent organelles called type four pili (Tfp), which are key virulence factors required for attachment to human cells during carriage and disease. Pilin (PilE) is the main component of Tfp, and isolates either have a class I locus and express pilins that undergo antigenic variation or have a class II locus and express invariant pilins. The transcriptional regulation of class I has been studied in both and , while the control of expression of class II has been elucidated in the nonpathogenic species However, the factors that govern the regulation of the class II gene in are not known. In this work, we have bioinformatically and experimentally identified the class II promoter. We confirmed the presence of conserved σ and σ-dependent promoters upstream of in a collection of meningococcal genomes and demonstrated that class II expression initiates from the σ family-dependent promoter. By deletion or overexpression of sigma factors, we showed that σ, σ, and σ do not affect class II pilin expression. These findings are consistent with a role of the housekeeping σ in expression of this important component of Tfp. Taken together, our data indicate that the σ-dependent network responsible for the expression of class II has been selected to maintain expression, consistent with the essential roles of Tfp in colonization and pathogenesis. The type four pilus (Tfp) of contributes to fundamental processes such as adhesion, transformation, and disease pathology. Meningococci express one of two distinct classes of Tfp (class I or class II), which can be distinguished antigenically or by the major subunit () locus and its genetic context. The factors that govern transcription of the class II gene are not known, even though it is present in isolates that cause epidemic disease. Here we show that the transcription of class II is maintained throughout growth and under different stress conditions and is driven by a σ-dependent promoter. This is distinct from Tfp regulation in nonpathogenic spp. and may confer an advantage during host-cell interaction and infection.