| First Author | Liang QX | Year | 2018 |
| Journal | Cell Death Dis | Volume | 9 |
| Issue | 5 | Pages | 508 |
| PubMed ID | 29725001 | Mgi Jnum | J:305036 |
| Mgi Id | MGI:6510122 | Doi | 10.1038/s41419-018-0505-1 |
| Citation | Liang QX, et al. (2018) Ablation of beta subunit of protein kinase CK2 in mouse oocytes causes follicle atresia and premature ovarian failure. Cell Death Dis 9(5):508 |
| abstractText | Premature ovarian failure (POF), a major cause of female infertility, is a complex disorder, but the molecular mechanisms underlying the disorder are only poorly understood. Here we report that protein kinase CK2 contributes to maintaining follicular survival through PI3K/AKT pathway and DNA damage response pathway. Targeted deletion of CK2beta in mouse oocytes from the primordial follicle stage resulted in female infertility, which was attributed to POF incurring by massive follicle atresia. Downregulated PI3K/AKT signaling was found after CK2beta deletion, indicated by reduced level of phosphorylated AKT (S473, T308, and S129) and altered AKT targets related to cell survival. Further studies discovered that CK2beta-deficient oocytes showed enhanced gammaH2AX signals, indicative of accumulative unrepaired DSBs, which activated CHK2-dependant p53 and p63 signaling. The suppressed PI3K/AKT signaling and failed DNA damage response signaling probably contribute to large-scale oocyte loss and eventually POF. Our findings provide important new clues for elucidating the mechanisms underlying follicle atresia and POF. |
