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Exploring Tr1-regulated transcription networks underpinning adaptation of pathogenic Anaplasma to the tick host

Award Number: R21AI178392
ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 07/01/2023
PERIOD OF PERFORMANCE END DATE: 06/30/2025

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Exploring Tr1-regulated transcription networks underpinning adaptation of pathogenic Anaplasma to the tick host - Project Summary Tick-borne diseases are on the increase and are responsible for nearly all of the vector-transmitted disease in the US. Vector-borne pathogens face the dual challenge of adaptation to two very different host environments: the arthropod vector and the mammalian host. Ticks contain distinct physiological cues including disparities in body temperature, nutrient availability, physiological architecture, and unique immunological pressures. Once in the tick, A. phagocytophilum must further adapt to construct a replicative niche within the arthropod’s cells. In response to the tick environment, A. phagocytophilum differentially transcribes 41% of its genes when infecting tick cells in comparison to mammalian cell culture. It is not known what controls this extensive reprogramming or how it facilitates A. phagocytophilum adaptation to the tick. One predicted transcription factor, tr1, displays the highest tick-specific expression of all A. phagocytophilum genes. Our structural modeling identifies Tr1 as a homo-dimeric helix-turn-helix DNA binding protein in the xenobiotic response element family of transcription factors. Disruption of tr1 by transposon insertion had no impact on bacterial burden in mice or growth in human cell lines. However, A. phagocytophilum lacking tr1 was greatly attenuated for acquisition by ticks and is unable to survival in tick cells. Given the importance of Tr1 for survival in the arthropod vector and its predicted role as a transcriptional switch, we hypothesize that: Tr1 operates as a master regulator for tick adaptation by orchestrating the expression of tick-specific gene networks. In this study we will identify the DNA sequences bound by Tr1 and its mode of transcription regulation. Further, we will identify how Tr1 contributes to completion of the tick cell infection cycle and measure how Tr1 remodels the A. phagocytophilum transcriptome during tick cell infection. Revealing how A. phagocytophilum adapts to infect tick cells will open the door to development of vector targeted interventions to reduce transmissibility of the pathogen.


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 = -$277 )
2026	2024	WASHINGTON STATE UNIVERSITY	240 FRENCH ADMINISTRATION BLDG	PULLMAN	WA	99164	WHITMAN	USA	Allergy and Infectious Diseases Research	000	2	12/18/2025	NON-COMPETING CONTINUATION	-$277
														Subtotal = -$277

Issue Date FY: 2024 ( Subtotal = $163,213 )
2024	2024	WASHINGTON STATE UNIVERSITY	240 FRENCH ADMINISTRATION BLDG	PULLMAN	WA	99164	WHITMAN	USA	Allergy and Infectious Diseases Research	000	2	5/30/2024	NON-COMPETING CONTINUATION	$163,213
														Subtotal = $163,213

Issue Date FY: 2023 ( Subtotal = $215,355 )
2023	2023	WASHINGTON STATE UNIVERSITY	240 FRENCH ADMINISTRATION BLDG	PULLMAN	WA	99164	WHITMAN	USA	Allergy and Infectious Diseases Research	000	1	6/23/2023	NEW	$215,355
														Subtotal = $215,355

Grand Total All Awards = $378,291

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Exploring Tr1-regulated transcription networks underpinning adaptation of pathogenic Anaplasma to the tick host

Award Number: R21AI178392

ORGANIZATION: NATIONAL INSTITUTE OF ALLERGY & INFECTIOUS DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 07/01/2023

PERIOD OF PERFORMANCE END DATE: 06/30/2025

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