Male germ cell-specific deletion of Eif5 causes the apoptosis of mouse progenitor spermatogonia by excessive endoplasmic reticulum stress and defective DNA repair - PubMed
4 hours ago
- #male infertility
- #eIF5
- #spermatogenesis
- Reduced expression of multiple eukaryotic translation initiation factors, including EIF5, is associated with idiopathic non-obstructive azoospermia (iNOA).
- Conditional knockout of Eif5 in male mouse germ cells leads to a decrease in SOX3+ progenitor spermatogonia and KIT+ differentiating spermatogonia, causing severe meiotic failure and complete male infertility.
- Eif5 deficiency impairs translation of genes involved in ubiquitination, autophagy, and DNA repair, resulting in excessive endoplasmic reticulum stress and compromised DNA repair.
- These defects promote DNA damage and apoptosis in SOX3+ progenitor spermatogonia, leading to progressive germ cell depletion and sterility.
- The findings highlight the essential role of eIF5 in spermatogenesis and suggest a potential therapeutic strategy for iNOA related to reduced translation initiation factor expression.