Loss of gdnfa disrupts spermiogenesis and male courtship behavior in zebrafish

Spermatogenesis is essential for establishment and maintenance of reproduction in male vertebrates. Spermatogenesis, which is mainly regulated by the combined action of hormones, growth factors, and epigenetic factors, is highly conserved. Glial cell line-derived neurotrophic factor (GDNF) is a memb...

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Veröffentlicht in:Molecular and cellular endocrinology 2023-10, Vol.576, p.112010-112010, Article 112010
Hauptverfasser: Liao, Xianyao, Tao, Binbin, Zhang, Xiya, Chen, Lu, Chen, Ji, Song, Yanlong, Hu, Wei
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Sprache:eng
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Zusammenfassung:Spermatogenesis is essential for establishment and maintenance of reproduction in male vertebrates. Spermatogenesis, which is mainly regulated by the combined action of hormones, growth factors, and epigenetic factors, is highly conserved. Glial cell line-derived neurotrophic factor (GDNF) is a member of the transforming growth factor-β superfamily. In this study, global gdnfa knockout and Tg (gdnfa: mcherry) transgenic zebrafish lines were generated. Loss of gdnfa resulted in disorganized testes, decreased gonadosomatic index, and low percentage of mature spermatozoa. In the Tg (gdnfa: mcherry) zebrafish line, we found that gdnfa was expressed in Leydig cells. The mutation in gdnfa significantly decreased Leydig cell marker gene expression and androgen secretion in Leydig cells. In addition, courtship behavior was disrupted in the male mutants. We present in vivo data showing that global knockout of gdnfa disrupts spermiogenesis and male courtship behavior in zebrafish. The first viable vertebrate model with a global gdnfa knockout may be valuable for studying the role of GDNF in animal reproduction. •Generation of global gdnfa knockout and Tg (gdnfa: mcherry) transgenic zebrafish lines.•Loss of gdnfa disrupts spermiogenesis in zebrafish.•Loss of gdnfa disrupts male courtship behavior in zebrafish.•The development of Leydig cells and androgen synthesis were affected in gdnfa mutant males.
ISSN:0303-7207
1872-8057
DOI:10.1016/j.mce.2023.112010