Testis-enriched Asb15 is not required for spermatogenesis and male fertility in mice

Background: The function of Asb15, which encodes an ASB protein with ankyrin (ANK) repeats and a C-terminal suppressor of cytokine signaling (SOCS) box motif, in male germ cells is poorly understood. Because expression of Asb15 is enriched in mouse testis, it may have a role in spermatogenesis. Methods and results: We used a computer-assisted sperm analysis (CASA) system to analyze sperm from Asb15 gene knockout (KO) mice that we generated using the clustered regularly interspaced short palindromic repeats (CRISPR)-associated protein 9 (Cas9) technique. Histological staining and immunostaining were used to evaluate spermatogenesis in Asb15- KO mice. Asb15-KO and wild-type mice showed no differences in histology or in semen quality, fertility, or sperm apoptosis. Asb15-and Asb17-double KO (dKO) mice were generated to determine whether Asb17 compensated for the loss of Asb15. However, Asb15/17-dKO mice also showed normal fertility, except for an increase in giant cells in testicular tubules, suggesting a minor functional compensation between the two genes during spermatogenesis. Conclusions: Our study suggests thatAsb15 was individually not required for spermatogenesis or for fertility in mice. However, further investigation might be needed to reach a firm conclusion. These findings can prevent redundant research by other scientists and provides new information for further studies on the genetics of fertility in humans.

Automated summary

This study suggests that the Asb15 gene is not essential for spermatogenesis or fertility in mice. These findings can prevent redundant research by other scientists and provide new information for further studies on the genetics of fertility in humans.