The expression of virulence factors in many enteric bacterial pathogens is dependent upon a regulatory protein from a family of homologous virulence regulators. Rns is a representative member of this family and is required for the expression of adherent CS1 pili in enterotoxigenic strains of Escherichia coli, a common cause of diarrhea in humans. Rns may regulate the expression of adherent pili in response to environmental conditions that mimic the gastrointestinal tract of the host because CS1 pili are not expressed constitutively and Rns is homologous to the ligand dependent regulator AraC. Alternatively, Rns may be a constitutive activator whose effects are modulated through other regulatory pathways. This study will use in vivo and in vitro analysis of Rns and its DNA binding sites to determine if the activity of Rns is directly or indirectly affected by environmental conditions. The definitive elaboration of the Rns regulatory pathway may present new avenues for disease prevention by illuminating potential therapeutic targets required for the expression of virulence factors in enteric bacterial pathogens.
