PUBLICATION

Loss of gdnfa disrupts spermiogenesis and male courtship behavior in zebrafish

Authors
Liao, X., Tao, B., Zhang, X., Chen, L., Chen, J., Song, Y., Hu, W.
ID
ZDB-PUB-230709-37
Date
2023
Source
Molecular and Cellular Endocrinology   576: 112010 (Journal)
Registered Authors
Hu, Wei
Keywords
Courtship behavior, Leydig cells, Spermiogenesis, Zebrafish, gdnfa
MeSH Terms
  • Animals
  • Courtship
  • Glial Cell Line-Derived Neurotrophic Factor*/genetics
  • Glial Cell Line-Derived Neurotrophic Factor*/metabolism
  • Male
  • Spermatogenesis/genetics
  • Testis/metabolism
  • Zebrafish*/genetics
  • Zebrafish*/metabolism
PubMed
37419437 Full text @ Mol. Cell. Endocrinol.
Abstract
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.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping