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 that Asb15 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.