Neisseria gonorrhoeae is the etiologic agent for the sexually transmitted disease gonorrhea. The gonococcus is unusual in that the organism displays a remarkable propensity for changing its surface antigens, which allows the organism to escape the ravages of the human immune system. One such surface antigen that undergoes antigenic variation is pilin polypeptide, the major component of the pilus organelle. Previous work has established a strong correlation between piliation and the infective process, as non-piliated bacteria are non-infectious. Gonococci can become non-piliated either through aberrant recombination events during gene conversion, or, alternatively, presumably by turning off pilin synthesis. Little is known regarding transcriptional regulation, and what is known remains contentious. Pilin is transcribed from the pilE locus. Three functional promoters have been defined, of which two are functional in the gonococcus; the third was shown to be functional in a related organism. The regulation of transcription from these three promoters is poorly defined. This study addresses regulation of pilin synthesis in the gonococcus. A small DNA binding protein, integration host factor (IHF), was shown to be a transcriptional regulator for pilin synthesis. Furthermore, IHF synthesis was examined, and was shown to be unique when compared to similar studies in other organisms.
