| First Author | Feng T | Year | 2021 |
| Journal | Transl Androl Urol | Volume | 10 |
| Issue | 5 | Pages | 1988-1999 |
| PubMed ID | 34159079 | Mgi Jnum | J:307623 |
| Mgi Id | MGI:6721235 | Doi | 10.21037/tau-21-18 |
| Citation | Feng T, et al. (2021) Eef2k is not required for fertility in male mice. Transl Androl Urol 10(5):1988-1999 |
| abstractText | Background: Eukaryotic elongation factor-2 kinase (Eef2k) is a protein kinase associated with the calmodulin-induced signaling pathway and an atypical alpha-kinase family member. Eef2k-mediated phosphorylation of eukaryotic translation elongation factor 2 (Eef2) can inhibit the functionality of this protein, altering protein translation. Prior work suggests Eef2k to be overexpressed in breast, pancreatic, brain, and lung cancers wherein it may control key processes associated with apoptosis, autophagy, and cell cycle progression. The functional importance of Eef2k in the testes of male mice, however, has yet to be clarified. Methods: A CRISPR/Cas9 approach was used to generate male Eef2k-knockout mice, which were evaluated for phenotypic changes in epididymal or testicular tissues through histological and immunofluorescent staining assays. In addition, TUNEL staining was conducted to assess the apoptotic death of cells in the testis. Fertility, sperm counts, and sperm motility were further assessed. Results: Male Eef2k-knockout mice were successfully generated, and exhibited normal fertility and development. No apparent differences were observed with respect to spermatogenesis, sperm counts, or germ cell apoptosis when comparing male Eef2k (-/-) and Eef2k (+/+) mice. Conclusions: Male Eef2k-knockout mice remained fertile and were free of any evident developmental or spermatogenic abnormalities, suggesting Eef2k to be dispensable in the context of male fertility. |
