ArticleCommunications biology2025
Disruption of TEX38 impairs sperm morphogenesis and the migration of sperm into the oviduct.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Biogenesis and migration of the sperm cytoplasmic droplet require ARRDC5 and TEX38.Cell reports · 2026Article
- Let the female tract choose: finding the sperm to enhanceAnimal reproduction · 2026Article
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Authors and funding
14 authors.
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Abstract
In male reproduction, spermatogenesis and sperm maturation are critical for the production of normal sperm and offspring, yet the underlying molecular mechanisms remain largely elusive. Tex38 is a testis-enriched gene, and its deficiency results in oligoasthenoteratospermia (OAT) with aberrant epididymis, leading to male infertility in mice. Tex38 knockout (KO) sperm primarily exhibited neck bending deformities and functional abnormalities, including impaired fertilization. Proteomic analysis identified ADAM3 and its maturation-associated chaperones (CALR3, CLGN, and PDILT) as the most significantly altered proteins among the differentially expressed proteins (DEPs) in both sperm and epididymis of Tex38 knockout mice. GO analysis revealed that DEPs were primarily involved in sperm morphogenesis, motility, and fertilization. ARRDC5 was identified as a novel interacting protein of TEX38, and its deletion resulted in similar male infertility phenotypes as Tex38 deletion. Immunoprecipitation-mass spectrometry identified TEX38 and ARRDC5 interact with CLGN and PDILT. The interactions among TEX38, ARRDC5, PDILT, and CLGN were found to affect ADAM3 maturation, resulting in the failure of both Tex38
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