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Molecular and Developmental Mechanisms of Phosducin-like Protein 3 Function in Spermatogenesis

Award Number: R15HD122211
ORGANIZATION: NATIONAL INSTITUTE OF CHILD HEALTH AND HUMAN DEVELOPMENT
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 07/01/2026
PERIOD OF PERFORMANCE END DATE: 06/30/2029

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Molecular and Developmental Mechanisms of Phosducin-like Protein 3 Function in Spermatogenesis - Project Summary Approximately 10-15% of couples in the United States experience infertility. In one-third of these cases, infertility is linked to male factors, primarily due to abnormal sperm production and function. Addressing this issue requires identifying and characterizing the genetic mechanisms that control sperm production. Recently, we identified the Drosophila Phosducin-like Protein 3 (PhLP3) as essential for male fertility. PhLP3 mutant males are sterile and cannot produce mature sperm. Spermatid nuclei fail to cluster, complete nuclear elongation, and individualize, resulting in seminal vesicles without sperm and sterility. To understand how PhLP3 functions in vivo, it’s important to consider its molecular role. PhLP3 belongs to a family of small thioredoxin- domain-containing proteins that are highly conserved among all eukaryotes. Members of the PhLP3 family exhibit cysteine-dependent redox activity, and their functions are linked to the regulation of microtubules and actin filaments. Recent studies have shown conservation of this redox activity across species, from the protozoan parasite Plasmodium berghei to humans and Drosophila, although the cysteine dependence of Drosophila PhLP3’s redox activity has not yet been confirmed. Given the proposed role for PhLP3 as a regulator of cytoskeletal proteins and the critical importance of cytoskeletal remodeling during spermatid maturation, we hypothesize that PhLP3 is necessary for the cytoskeletal changes that promote nuclear elongation and sperm individualization. We also hypothesize that the conserved redox activity of PhLP3 is essential for its biological function. This project aims to elucidate the molecular and developmental mechanisms of PhLP3 function during spermatogenesis through a multi-faceted approach: (1) understanding the biochemical function of PhLP3 by identifying the key cysteine(s) involved in redox activity and its in vivo binding partners, and (2) characterizing the tissue and subcellular localization of PhLP3 and examining how PhLP3 mutations affect critical stages of late spermatogenesis. These studies will shed light on the biochemical and genetic mechanisms by which PhLP3 regulates spermatogenesis. Considering the high level of sequence conservation across species, we propose that PhLP3 performs similar functions related to spermatogenesis across different organisms.


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 = $545,625 )
2026	2026	LOYOLA UNIVERSITY OF CHICAGO	820 N MICHIGAN AVE	CHICAGO	IL	60611	COOK	USA	Child Health and Human Development Extramural Research	000	1	6/19/2026	NEW	$545,625
														Subtotal = $545,625

Grand Total All Awards = $545,625

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Molecular and Developmental Mechanisms of Phosducin-like Protein 3 Function in Spermatogenesis

Award Number: R15HD122211

ORGANIZATION: NATIONAL INSTITUTE OF CHILD HEALTH AND HUMAN DEVELOPMENT

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

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

PERIOD OF PERFORMANCE START DATE: 07/01/2026

PERIOD OF PERFORMANCE END DATE: 06/30/2029

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