Spermiogenesis is an indispensable process occurring during the later stages of spermatogenesis. Despite multiple proteins being associated with spermiogenesis, the molecular mechanisms that control spermiogenesis remain poorly characterized. In this study, we show that 1700030J22RIK is exclusively expressed in the testis of mice and investigate its roles in spermiogenesis using genetic and proteomic approaches. The deficiency in 1700030J22RIK in male mice results in severe subfertility, characterized by a substantial decrease in sperm concentration, motility, and abnormalities in the flagella. Furthermore, 1700030J22RIK interacts with the A-kinase-anchoring protein AKAP3, and 1700030J22RIK knockout decreases AKAP3 and AKAP4 protein levels. Additionally, the absence of 1700030J22RIK alters spermatozoal levels of the subunits of protein kinase A, leading to reduced protein phosphorylation and impaired sperm motility. This study reveals that 1700030J22RIK plays a crucial role in the organization of sperm morphology and function in mice.
Keywords: 1700030J22RIK; Asthenoteratozoospermia; Flagellum; Male infertility; Protein kinase A; Spermiogenesis.
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