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| Autores principales: | , , , , , , , , |
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| Formato: | Artículo científico |
| Lenguaje: | en |
| Publicado: |
Zoological research
2026
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| Materias: | |
| Acceso en línea: | https://pubmed.ncbi.nlm.nih.gov/42237942/ |
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- Knockout of disrupts steroid hormone homeostasis and compromises gonadal development in zebrafish. He, Lijia Wang, Yaqing Ren, Zhiqin Wang, Chaofan Qu, Rui Wang, Houpeng Ye, Ding Chen, Zhengfang Sun, Yonghua Animals Zebrafish Female Progesterone Reductase Male Homeostasis Steroid Isomerases Gonads Gene Expression Regulation, Developmental Gene Knockout Techniques Multienzyme Complexes Steroids Gonadal Steroid Hormones Steroid hormones are central regulators of gonadal differentiation, endocrine homeostasis, and reproductive function, with impaired steroid biosynthesis leading to metabolic dysfunction and reproductive disease. 3β-Hydroxysteroid dehydrogenase (3β-HSD), encoded by , catalyzes the conversion of inactive Δ -3β-hydroxysteroid precursors into bioactive Δ -ketosteroids, representing a pivotal enzymatic step in steroidogenesis. In this study, CRISPR/Cas9-mediated disruption of in zebrafish produced pronounced endocrine and reproductive abnormalities, including aberrant gonadal development, interrenal hyperplasia, hyperpigmentation, and reduced fertility. Integrated RNA sequencing and targeted steroid hormone metabolomics further demonstrated extensive disruption of steroid hormone homeostasis in mutants, with attenuated sex-specific metabolic differences between males and females. These findings establish as an essential determinant of steroidogenic balance and gonadal development in zebrafish. The mutant line provides a robust and tractable vertebrate model for investigating how steroidogenic disruption reshapes reproductive development and endocrine physiology.