Mouse Emi2 is required to enter meiosis II by reestablishing cyclin B1 during interkinesis

During interkinesis, a metaphase II (Metil) spindle is built immediately after the completion of meiosis I. Oocytes then remain Metll arrested until fertilization. In mouse, we find that early mitotic inhibitor 2 (Emi2), which is an anaphase-promoting complex inhibitor, is involved in both the establishment and the maintenance of Metil arrest. In Metll oocytes, Emi2 needs to be degraded for oocytes to exit meiosis, and such degradation, as visualized by fluorescent protein tagging, occurred tens of minutes ahead of cyclin B1. Emi2 antisense morpholino knockdown during oocyte maturation did not affect polar body (PB) extrusion. However, in interkinesis the central spindle microtubules from meiosis I persisted for a short time, and a Metll spindle failed to assemble. The chromatin in the oocyte quickly decondensed and a nucleus formed. All of these effects were caused by the essential role of Emi2 in stabilizing cyclin B1 after the first PB extrusion because in Emi2 knockdown oocytes a Metll spindle was recovered by Emi2 rescue or by expression of nondegradable cyclin B1 after meiosis I.