Abstract
BACKGROUND: As a member of the Ankyrin repeat and SOCS box (Asb) family, the Asb3 is enriched in the testes and highly conserved in multiple species. The knockout of the Asb12 gene not significantly affect spermatogenesis, but led to a compensatory increase in the mRNA expression level of the Asb3. Although it has been reported that the Asb12 is not required for spermatogenesis and male fertility in mice, the functional role of Asb3 remains not to be clearly elucidated. METHODS AND RESULTS: Asb3 was predominantly expressed in mouse testis and primarily localized to the elongated spermatids, as determined by real-time fluorescent quantitative PCR and fluorescence in situ hybridization. The Asb3-KO mice were successfully generated using CRISPR Cas9 technology. Sperm quantity and motility from the cauda epididymidis were assessed via the hemocytometer. Histological analysis and immunostaining confirmed that normal fertility, normal spermatozoa and normal spermatogenesis in Asb3-KO mice. Additionally, no significant differences were observed between Asb3-KO mice and heterozygous mice regarding seminiferous tubule apoptosis via the TUNEL analysis. CONCLUSIONS: There is no significant difference in fertility between Asb3-KO mice and heterozygous mice. Despite a significant increase in the relative mRNA expression level of the Asb3 gene due to the absence of the Asb12, the deficiency of ASB3 did not adversely affect fertility or spermatogenesis in males. Hence, we demonstrated that ASB3 ablation has no detectable effects on spermatogenesis and fertility in male mice.