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Updated: Feb 15, 2026

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Published on: July 6, 2009
TEX30 safeguards sperm morphogenesis and quality consistency required for male fertility
Koji Kikuchi1,2,3, Sakie Iisaka1,2, Reika Uriu4,5
1Department of Chromosome Biology, Institute of Molecular Embryology and Genetics (IMEG), Kumamoto University, 2-2-1 Honjo, Chuo-ku, Kumamoto 860-0811, Japan.
Abstract:
Spermatogenesis, essential for male fertility, requires precise temporal and spatial regulation of gene expression to generate sperm that function robustly in vivo. Here, we show that testis-expressed 30 (Tex30) mRNA expression is induced by the germ-cell-specific transcription factors MEIOSIN and stimulated by retinoic acid 8 during meiotic prophase and is further upregulated in round spermatids. Despite this transcriptional activation, TEX30 protein is detected predominantly in the cytoplasm of step 16 spermatids, where it is highly enriched in the cytoplasmic lobe that is normally discarded as the residual body during spermiation. This strikingly restricted localization suggests that TEX30 safeguards sperm maturation during the final stages of spermiogenesis. Although overall testis morphology and gross spermatogenic progression are largely preserved in Tex30 knockout (KO) mice, epididymal sperm exhibit mild but reproducible abnormalities, including globozoospermia-like head defects and occasional tail deformities, together with variability in acrosome integrity. Importantly, Tex30 KO males display pronounced inter-individual variability in cauda epididymal sperm abundance-a feature not observed in wild-type controls-suggesting that TEX30 contributes to the robustness and consistency of late spermatogenesis rather than to its absolute production. Consistent with this, sperm number and distribution within the uterus are frequently reduced in Tex30 KO males, resulting in inefficient migration into the oviduct during natural mating. Together, these findings demonstrate that TEX30 is dispensable for early spermatogenic progression but is required to maintain the structural integrity, functional competence, and inter-individual robustness of sperm produced during late spermiogenesis, thereby supporting efficient in vivo fertilization.
Insights
Tex30 protein is crucial for sperm maturation, safeguarding structural integrity and fertilization efficiency. Its absence causes sperm defects and variable abundance, impacting male fertility.
Area of Science:
- Reproductive Biology
- Molecular Endocrinology
- Spermatogenesis Research
Background:
- Spermatogenesis requires precise gene regulation for functional sperm.
- The role of TEX30 in male fertility and sperm development is not fully understood.
Purpose of the Study:
- To investigate the function of TEX30 during spermatogenesis.
- To determine the impact of TEX30 deficiency on sperm quality and male fertility.
Main Methods:
- Analysis of Tex30 mRNA and protein expression during spermatogenesis.
- Phenotypic characterization of Tex30 knockout mice.
- Assessment of sperm morphology, abundance, and in vivo fertilization efficiency.
Main Results:
- Tex30 expression is regulated by MEIOSIN and STRA8, peaking in round spermatids, with protein localized to the cytoplasmic lobe of late spermatids.
- Tex30 knockout mice exhibit sperm head and tail deformities, variable acrosome integrity, and inconsistent sperm counts.
- Tex30 deficiency leads to reduced sperm in the uterus and inefficient fertilization during natural mating.
Conclusions:
- TEX30 is essential for maintaining sperm structural integrity and functional competence during late spermiogenesis.
- TEX30 contributes to the robustness and consistency of sperm production, impacting male fertility.
- Targeting TEX30 may offer strategies for improving male reproductive health and addressing infertility.
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