| First Author | Liang QX | Year | 2020 |
| Journal | Cell Prolif | Volume | 53 |
| Issue | 1 | Pages | e12726 |
| PubMed ID | 31755150 | Mgi Jnum | J:289955 |
| Mgi Id | MGI:6435243 | Doi | 10.1111/cpr.12726 |
| Citation | Liang QX, et al. (2020) Deletion of Ck2beta gene causes germ cell development arrest and azoospermia in male mice. Cell Prolif 53(1):e12726 |
| abstractText | 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 CK2beta was abundantly and broadly expressed in spermatogenic cells. Here, we investigate whether protein CK2beta participates in spermatogenesis. MATERIALS AND METHODS: In this study, we separated spermatogenic cells using STA-PUT velocity sedimentation, analysed the expression pattern of protein CK2beta by immunoblotting, specifically deleted Ck2beta gene in early-stage spermatogenic cells by crossing Ck2beta(fl) mice with Stra8-Cre(+) mice and validated the knockout efficiency by quantitative RT-PCR and immunoblotting. The phenotypes of Ck2beta(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 Ck2beta gene triggered excessive germ cell apoptosis, germ cell development arrest, azoospermia and male infertility. Inactivation of Ck2beta gene caused distinctly reduced expression of Ck2alpha' gene and CK2alpha' protein. CONCLUSIONS: Ck2beta is a vital gene for germ cell survival and male fertility in mice. |
