Deletion of Ck2? gene causes germ cell development arrest and azoospermia in male mice.

ABSTRACT:

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? was abundantly and broadly expressed in spermatogenic cells. Here, we investigate whether protein CK2? 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? by immunoblotting, specifically deleted Ck2? gene in early-stage spermatogenic cells by crossing Ck2?^fl mice with Stra8-Cre⁺ mice and validated the knockout efficiency by quantitative RT-PCR and immunoblotting. The phenotypes of Ck2?^fl/? ;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? gene triggered excessive germ cell apoptosis, germ cell development arrest, azoospermia and male infertility. Inactivation of Ck2? gene caused distinctly reduced expression of Ck2?' gene and CK2?' protein.

Conclusions

Ck2? is a vital gene for germ cell survival and male fertility in mice.

SUBMITTER: Liang QX 

PROVIDER: S-EPMC6985669 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature