The CRISPR/Cas system in Neisseria meningitidis affects bacterial adhesion to human nasopharyngeal epithelial cells

Neisseria meningitidis, a commensal β-proteobacterium of the human nasopharynx, constitutes a worldwide leading cause of sepsis and epidemic meningitis. The molecular basis for their "accidental" pathogenicity is still not fully understood. Here, we show that knock-out strains lacking the Cas9 protein are impaired in the adhesion to human nasopharyngeal cells which constitutes a central step in the pathogenesis of invasive meningococcal disease. Transcriptome sequencing data suggest that meningococcal Cas9 does not affect the expression of classical surface adhesins but rather exerts its effect on cell adhesion in an indirect manner. Consequently, we speculate that the meningococcal type II-C CRISPR/Cas system exerts novel functions beyond its established role in defence against foreign DNA. 8 SAMPLES WITHOUT REPLICATES