Abstract
BACKGROUND: DCUN1D3, a member of the DCNL (defective in cullin neddylation-like) protein family, has been implicated in ultraviolet (UV) radiation-induced cell cycle checkpoints, cell growth, survival, and neddylation. However, its specific function in male germ cells and potential involvement in spermatogenesis remain poorly understood. METHODS: To investigate the role of Dcun1d3 in male reproduction, we generated Dcun1d3 knockout (KO) mice. Sperm parameters were evaluated using computer-assisted sperm analysis (CASA), while histological and immunohistochemical analyses were performed to assess spermatogenesis. RESULTS: Dcun1d3-KO mice exhibited no significant differences in testicular histology, sperm quality, levels of germ cell apoptosis, or fertility outcomes compared to wild-type controls. CONCLUSIONS: These findings indicate that Dcun1d3 is not essential for spermatogenesis or male fertility in mice. This study provides evidence to streamline future investigations by excluding Dcun1d3 as a critical regulator of male germ cell development and offers useful insights for human fertility gene research.