Deletion of Ck2β gene causes germ cell development arrest and azoospermia in male mice.

Objectives In humans, non-obstructive azoospermia (NOA) is a major cause of male infertility. However, the aetiology of NOA is largely unknown. Previous studies reported that protein CK2 beta was abundantly and broadly expressed in spermatogenic cells. Here, we investigate whether protein CK2 beta participates in spermatogenesis. Materials and Methods In this study, we separated spermatogenic cells using STA-PUT velocity sedimentation, analysed the expression pattern of protein CK2 beta by immunoblotting, specifically deleted Ck2 beta gene in early-stage spermatogenic cells by crossing Ck2 beta(fl) mice with Stra8-Cre(+) mice and validated the knockout efficiency by quantitative RT-PCR and immunoblotting. The phenotypes of Ck2 beta(fl/Delta);SCre(+) mice were studied by immunohistochemistry and immunofluorescence. The molecular mechanisms of male germ cell development arrest were elucidated by immunoblotting and TUNEL assay. Results Ablation of Ck2 beta gene triggered excessive germ cell apoptosis, germ cell development arrest, azoospermia and male infertility. Inactivation of Ck2 beta gene caused distinctly reduced expression of Ck2 alpha ' gene and CK2 alpha ' protein. Conclusions Ck2 beta is a vital gene for germ cell survival and male fertility in mice.