| First Author | Zhou C | Year | 2019 |
| Journal | J Cell Sci | Volume | 132 |
| Issue | 18 | PubMed ID | 31427428 |
| Mgi Jnum | J:287822 | Mgi Id | MGI:6363903 |
| Doi | 10.1242/jcs.233379 | Citation | Zhou C, et al. (2019) First meiotic anaphase requires Cep55-dependent inhibitory cyclin-dependent kinase 1 phosphorylation. J Cell Sci 132(18):jcs233379 |
| abstractText | During mitosis, anaphase is triggered by anaphase-promoting complex (APC)-mediated destruction of securin and cyclin B1, which leads to inactivation of cyclin-dependent kinase 1 (Cdk1). By regulating APC activity, the mitotic spindle assembly checkpoint (SAC) therefore has robust control over anaphase timing to prevent chromosome mis-segregation. Mammalian oocytes are prone to aneuploidy, the reasons for which remain obscure. In mitosis, Cep55 is required post-anaphase for the final steps of cytokinesis. We found that Cep55-depleted mouse oocytes progress normally through early meiosis I, but that anaphase I fails as a result of persistent Cdk1 activity. Unexpectedly, Cdk1 inactivation was compromised following Cep55 depletion, despite on-time SAC silencing and intact APC-mediated proteolysis. We found that impaired Cdk1 inactivation was caused by inadequate inhibitory Cdk1 phosphorylation consequent upon failure to suppress Cdc25 phosphatase, identifying a proteolysis-independent step necessary for anaphase I. Thus, the SAC in oocytes does not exert exclusive control over anaphase I initiation, providing new insight into vulnerability to error. |
