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Investingating the mechanisms controlling Neisseria gonorrhoeae Type IV pilus dynamics

Award Number: F32AI186488
ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 01/01/2026
PERIOD OF PERFORMANCE END DATE: 12/31/2027

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Investingating the mechanisms controlling Neisseria gonorrhoeae Type IV pilus dynamics - PROJECT SUMMARY The Neisseria gonorrhoeae (the gonococcus or Gc) Type IV pilus (T4p) is a critical colonization and virulence factor during pathogenesis. T4p are used to adhere to host cells and promote colonization. T4p are dynamic structures made of pilin fibers that extend and retract from the bacterial cell. Beyond host cell adhesion, T4p are involved in a variety of cellular processes including DNA uptake, twitching motility, and resistance to antimicrobial agents. We previously identified a novel component of the Gc T4p, TfpC. Our published data illustrated that TfpC is required for full piliation, and piliation is restored in tfpC mutants lacking the PilT retraction ATPase. There are eleven other such mutants in the Gc T4p. Here, we use genetic, biochemical, and biophysical techniques to define how TfpC contributes to T4p dynamics and architecture. We show that while TfpC is required for complete piliation of Gc, remaining pilus structures undergo extension at rates similar to parental strains. However, retraction is slower in strains lacking tfpC. Furthermore, we demonstrate that TfpC stability is dependent upon the PilQ secretin. We also identify an important motif within the flexible, disordered, proline-rich region of TfpC that is important for function or stability of TfpC. I hypothesize that TfpC interacts with the PilQ secretin or other components of the T4p to support a subset of T4p. To test this hypothesis, I will 1) determine if TfpC interacts with the PilQ secretin, 2) perform structure-function analyses of TfpC, and 3) interrogating the mechanism underlying reduced piliation in twelve pilus mutants. The proposed research is significant because it will define the previously uncharacterized TfpC protein required for piliation and link its activity to other pilus components. It will also provide important information for other species T4p systems and possibly some Type II secretion systems. These studies expand our current understanding of T4p architecture as well as the components governing mechanisms of extension and retraction, providing a foundation for future studies on the T4p dynamics essential for colonization and virulence. Long-term, the proposed research could provide new targets for treating gonorrhea infections.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2026 ( Subtotal = $0 )
2026	2025	NORTHWESTERN UNIVERSITY	633 CLARK ST	EVANSTON	IL	60208	COOK	USA	Allergy and Infectious Diseases Research	000	1	1/6/2026	NEW	$0
														Subtotal = $0

Issue Date FY: 2025 ( Subtotal = $75,520 )
2025	2025	NORTHWESTERN UNIVERSITY	633 CLARK ST	EVANSTON	IL	60208	COOK	USA	Allergy and Infectious Diseases Research	000	1	9/1/2025	NEW	$75,520
2025	2025	NORTHWESTERN UNIVERSITY	633 CLARK ST	EVANSTON	IL	60208	COOK	USA	Allergy and Infectious Diseases Research	001	1	9/1/2025	NEW	$0
														Subtotal = $75,520

Grand Total All Awards = $75,520

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Investingating the mechanisms controlling Neisseria gonorrhoeae Type IV pilus dynamics

Award Number: F32AI186488

ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 01/01/2026

PERIOD OF PERFORMANCE END DATE: 12/31/2027

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