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Dissecting the role of IKK-epsilon in tick immunity and vector competence

Award Number: F32AI202938
ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 01/29/2027
PERIOD OF PERFORMANCE END DATE: 01/28/2028

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Dissecting the role of IKK-epsilon in tick immunity and vector competence - PROJECT SUMMARY Tick species such as Ixodes scapularis are major vectors of bacterial pathogens, including Lyme disease and granulocytic anaplasmosis. Nevertheless, strategies for controlling tick-borne disease are extremely limited and do not address vector competence, or the ability for ticks to harbor and transmit these pathogens. One major factor controlling vector competence is the tick immune response to infection, of which mechanistic knowledge is profoundly lacking. To develop effective, targeted methods to prevent tick-borne disease before patients become sick, a far greater understanding of tick immune pathways is necessary. We recently discovered that the non-canonical IκB kinase IKKε restricts tick bacterial burden by stimulating the IMD pathway, a vital arthropod innate immune response orthologous to mammalian TNFR-NF-κB signaling. Furthermore, phosphoproteomic analysis indicates that IKKε regulates numerous signaling pathways relevant to tick immunity. The central hypothesis of this study is that tick IKKε functions as a central point of immune regulation, interacting with multiple signaling networks, including the IMD pathway, which impact vector competence. Preliminary data indicate that IKKε phosphorylates the IMD pathway core regulator XIAP. In Aim 1, IMD-activating interactions between IKKε and XIAP will be characterized by performing molecular and biochemical interaction assays and by applying Cas9-mediated gene editing and targeted mutagenesis techniques. In Aim 2, the tick IKKε signaling network will be mapped through complementary unbiased methods including proximity-based protein labeling, proteomics, and transcriptomics. Many tick orthologs of canonical phosphorylation targets of IKKε are lacking conserved motifs, rendering the mechanisms of IKKε immune induction unclear. These screens will reveal molecular targets which IKKε signals through to restrict tick pathogen burden. The results of this study will lead to new avenues of investigation for targeted control of tick-borne disease at the vector level. This project is conducted at Washington State University, which has long-standing prominence in the field of tick-borne disease and whose investigators foster a highly collaborative research community. The training plan associated with this project is facilitated by the joint mentorship of Dr. Dana Shaw (primary sponsor) and Dr. Erol Fikrig (co-sponsor). At the conclusion of this fellowship, Dr. Osbron will transition into a position as an independent investigator.


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 = $76,780 )
2026	2026	WASHINGTON STATE UNIVERSITY	240 FRENCH ADMINISTRATION BLDG	PULLMAN	WA	99164	WHITMAN	USA	Allergy and Infectious Diseases Research	000	1	7/29/2026	NEW	$76,780
														Subtotal = $76,780

Grand Total All Awards = $76,780

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Dissecting the role of IKK-epsilon in tick immunity and vector competence

Award Number: F32AI202938

ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 01/29/2027

PERIOD OF PERFORMANCE END DATE: 01/28/2028

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