| First Author | Gui L | Year | 2013 |
| Journal | Dev Cell | Volume | 25 |
| Issue | 1 | Pages | 43-54 |
| PubMed ID | 23541922 | Mgi Jnum | J:196442 |
| Mgi Id | MGI:5488524 | Doi | 10.1016/j.devcel.2013.02.008 |
| Citation | Gui L, et al. (2013) Hec1-dependent cyclin B2 stabilization regulates the G2-M transition and early prometaphase in mouse oocytes. Dev Cell 25(1):43-54 |
| abstractText | The functions of the Ndc80/Hec1 subunit of the highly conserved Ndc80 kinetochore complex are normally restricted to M phase when it exerts a pivotal kinetochore-based role. Here, we find that in mouse oocytes, depletion of Hec1 severely compromises the G2-M transition because of impaired activation of cyclin-dependent kinase 1 (Cdk1). Unexpectedly, impaired M phase entry is due to instability of the Cdk1-activating subunit, cyclin B2, which cannot be covered by cyclin B1. Hec1 protects cyclin B2 from destruction by the Cdh1-activated anaphase-promoting complex (APC(Cdh1)) and remains important for cyclin B2 stabilization during early M phase, required for the initial stages of acentrosomal spindle assembly. By late M phase, however, Hec1 and cyclin B2 become uncoupled, and although Hec1 remains stable, APC(Cdc20) triggers cyclin B2 destruction. These data identify another dimension to Hec1 function centered on M phase entry and early prometaphase progression and challenge the view that cyclin B2 is completely dispensable in mammals. |
