Testis-enriched Asb12 is not required for spermatogenesis and fertility in mice.

Abstract

BackgroundMembers of the ankyrin repeat and SOCS box (Asb) family are expressed abundantly in testes. Some Asb genes/proteins are required for spermatogenesis, but the function of Asb12 during spermatogenesis is not clear. We investigated the physiological role of Asb12 in murine testes.MethodsThe clustered regularly interspaced short palindromic repeats/CRISPR-associated protein 9 system was used to generate Asb12-knockout (KO) mice. Histology and immunostaining were done to assess the effects of Asb12 KO on mouse testes and epididymides. Semen quality was analyzed using a computer-assisted sperm analyzer. The terminal deoxynucleotidyl transferase-dUTP nick-end labeling assay was employed to examine testicular apoptosis. Real-time reverse transcription-quantitative polymerase chain reaction (PCR) was conducted to calculate gene transcription levels.ResultsAsb12 was expressed predominantly in murine testes. Immunostaining of Asb12 protein revealed that Asb12 was located specifically in the acrosome of elongated spermatids, which suggested a potential role of Asb12 during spermatogenesis. However, Asb12-KO mice had normal fertility, and no overt difference was detected in testicular morphology, semen quality, or apoptosis when comparing Asb12-KO and Asb12-wild type (WT) mice. Gene expression of several Asb family members was increased significantly in the testes of Asb12-KO mice when compared with that in Asb12-WT mice, which suggested functional compensation from paralogs for Asb12 loss.ConclusionsWe demonstrated that Asb12 is not essential for the spermatogenesis and fertility of mice. Our findings will assist researchers in avoiding redundant efforts, and provide a baseline resource for genetic studies on human fertility.