Neisseria gonorrhoeae, the Gram-negative aetiological agent or gonorrhoea, is one of many mucosal pathogenes of man that expresses competence for natural transformation. Expression of this phenotype by gonococci appears to rely on the expression of type IV pili (Tip), but the mechanistic basis for this relationship remains unknown. During studies of gonococcal plus biogenesis, a homologue on the PilT family of proteins, required for Tip-dependent twitching motility in Pseudomonas aeruginosa and social gliding motility in Mytococcus xanthus, was discovered. Like the findings in these other species, we show here that gonococcal pilT mutants constructed in vitro no longer display twitching motility. In addition, we demonstrate that they have concurrently lost the ability to undergo natural transformation, despite the expression of structurally and morphologically normal Tfp. These results were confirmed by the findings that two classes of spontaneous mutants that failed to express twitching motility and transformability carried mutations in pilT. Piliated pilT mutants and a panel of pilus assembly mutants were found to be deficient in sequence-specific DNA uptake into the cell, the earliest demonstrable step in neisserial competence. The PilT-deficient strains represent the first genetically defined mutants that are defective in DNA uptake but retain Tfp expression.
ASJC Scopus subject areas
- Molecular Biology