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Examining the role of immune activation in transposon-triggered sterility.

Award Number: F31HD113207
ORGANIZATION: NATIONAL INSTITUTE OF CHILD HEALTH AND HUMAN DEVELOPMENT
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 09/01/2023
PERIOD OF PERFORMANCE END DATE: 08/31/2026

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Examining the role of immune activation in transposon-triggered sterility. - ABSTRACT. Infertility is a problem that affects one out of five couples, yet the cause of sterility is unknown in 30% of cases. One threat to viable gamete development is activity of a subset of transposons known as endogenous retroviruses (ERVs). ERVs have the ability to self-replicate and sometimes mobilize, creating new genomic insertions within the same cell or even neighboring cells. Previous studies have demonstrated that, in Drosophila, ERV activation within the follicle cells of developing eggs causes sterility. The current explanation for ERV-triggered sterility postulates that ERVs migrate from the follicle cells into the oocyte and insert themselves into new genomic loci, damaging DNA integrity. However, our lab has found no evidence of novel ERV insertions being made into the oocyte genome, suggesting sterility may arise from uncharacterized mechanism(s). Here, we propose an alternative explanation for transposon-triggered sterility: we hypothesize that ERV derepression induces sterility through activation of an aberrant immune response. We found that depletion of key immune pathway components rescued fertility despite ERV hyperactivity. These data provide evidence that transposon-triggered sterility may be due to immune activation rather than DNA damage within the oocyte. This proposal seeks to investigate how the immune system recognizes ERVs and whether that immune response can cause sterility. Ultimately, these findings may provide an alternative explanation for ERV-triggered sterility as well as advance our understanding of how ERVs impact human health.


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: 2025 ( Subtotal = $43,065 )
2025	2025	DUKE UNIVERSITY	2200 W MAIN ST	DURHAM	NC	27705	DURHAM	USA	Child Health and Human Development Extramural Research	000	3	8/1/2025	NON-COMPETING CONTINUATION	$43,065
														Subtotal = $43,065

Issue Date FY: 2024 ( Subtotal = $41,910 )
2024	2024	DUKE UNIVERSITY	2200 W MAIN ST	DURHAM	NC	27705	DURHAM	USA	Child Health and Human Development Extramural Research	001	2	8/5/2024	NON-COMPETING CONTINUATION	$41,910
2024	2023	DUKE UNIVERSITY	2200 W MAIN ST	DURHAM	NC	27705	DURHAM	USA	Child Health and Human Development Extramural Research	000	1	3/7/2024	NEW	$0
														Subtotal = $41,910

Issue Date FY: 2023 ( Subtotal = $40,287 )
2023	2023	DUKE UNIVERSITY	2200 W MAIN ST	DURHAM	NC	27705	DURHAM	USA	Child Health and Human Development Extramural Research	000	1	7/17/2023	NEW	$40,287
2023	2023	DUKE UNIVERSITY	2200 W MAIN ST	DURHAM	NC	27705	DURHAM	USA	Child Health and Human Development Extramural Research	001	1	7/17/2023	NEW	$0
														Subtotal = $40,287

Grand Total All Awards = $125,262

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Examining the role of immune activation in transposon-triggered sterility.

Award Number: F31HD113207

ORGANIZATION: NATIONAL INSTITUTE OF CHILD HEALTH AND HUMAN DEVELOPMENT

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 09/01/2023

PERIOD OF PERFORMANCE END DATE: 08/31/2026

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