Loss of Adgra3 causes obstructive azoospermia with high penetrance in male mice

This article is currently being updated. View its version on PubMed.

https://pubmed.ncbi.nlm.nih.gov/36688818

Research summary

This study investigates the role of the adhesion G protein-coupled receptor A3 (Adgra3) in male fertility. Using a conditional Knockout mouse model, researchers found that 55% of male mice lacking Adgra3 were infertile from puberty despite normal spermatogenesis and epididymal sperm count. The infertility was attributed to obstructive azoospermia caused by a blockage between the ejaculatory duct and the urethra. Additionally, Adgra3-deficient mice exhibited decreased estrogen receptor alpha expression and transient dilation of the epididymis, indicating a post-pubertal hormonal imbalance and fluid retention.

Key outcome of the study

Loss of Adgra3 leads to obstructive azoospermia due to ejaculatory duct obstruction, mimicking certain forms of human male infertility. The study highlights the importance of Adgra3 in male reproductive tract development and its potential interaction with estrogen signaling pathways.

Mouse model

Adgra3 conditional Knockout mouse model developed by genOway, featuring loxP-flanked exons 5 and 6 of the Adgra3 gene. The model was generated via homologous recombination, and global excision was achieved by crossing with CMV-Cre transgenic mice.

TARGET:
Adgra3
GPR125, TEM5-like, 3830613O22Rik

Keywords

Male infertility, Obstructive azoospermia, Reproductive tract development, Estrogen signaling, G protein-coupled receptors

Technical specifications

Conditional Knockout model, LoxP-flanked exons, Homologous recombination, CMV-Cre driver, Global gene deletion

Related products

Catalogue product

No items found.

Customized product

Tissue-specific KO mouse

Use tissue- or cell-specific conditional Knockout mouse models to bypass embryonic lethality, compensatory mechanisms, complex phenotypes, etc.