Suppression of an absolute defect in type IV pilus biogenesis by loss-of-function mutations in pilT, a twitching motility gene in Neisseria gonorrhoeae.
Type IV pili of Neisseria gonorrhoeae, the Gram-negative etiologic agent of gonorrhea, facilitate colonization of the human host. Gonococcal PilT, a protein belonging to a large family of molecules sharing a highly conserved nucleotide binding domain motif, has been shown to be dispensable for organelle biogenesis but essential for twitching motility and competence for genetic transformation. Here, we show that the defect in pilus biogenesis resulting from mutations in the pilC gene, encoding a putative pilus-associated adhesin for human tissue, can be suppressed by the absence of functional PilT. These data conclusively demonstrate that PilT influences the Type IV pilus biogenesis pathway and strongly suggest that organelle expression is a dynamic process. In addition, these findings imply that PilT antagonizes the process of organelle biogenesis and provide the basis for a model for how the counteractive roles of PilT and PilC might relate mechanistically to the phenomenon of twitching motility.
Wolfgang
M
M
Department of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI 48109-0620, USA.
Park
H S
HS
Hayes
S F
SF
van Putten
J P
JP
Koomey
M
M
D000251:Adenosine Triphosphatases; D018829:Adhesins, Bacterial / Q000235:genetics*; D001426:Bacterial Proteins / Q000235:genetics*; D036781:Fimbriae Proteins; D015964:Gene Expression Regulation, Bacterial; D006801:Humans; D020409:Molecular Motor Proteins; D009154:Mutation; D009344:Neisseria gonorrhoeae / Q000235:genetics* / Q000648:ultrastructure; D018933:Pili, Sex / Q000235:genetics
D018829:Adhesins, Bacterial; D001426:Bacterial Proteins; D020409:Molecular Motor Proteins; C079208:pilC protein, Neisseria gonorrhoeae; D036781:Fimbriae Proteins; D000251:Adenosine Triphosphatases