Fig. 4. Emi2 links the Mos pathway and the APC/C to regulate CSF. The ability of Emi2 to bind and inhibit the APC/C is modulated by Cdc2–cyclin-B-mediated phosphorylation. Specifically, phosphorylation at the Emi2 C-terminus weakens the Emi2-APC/C interaction, promoting dissociation of the Emi2-APC/C complex and activation of APC/C. During CSF arrest, Cdc2–cyclin-B-mediated Emi2 phosphorylation is antagonized by the Mos-MAPK pathway. The Mos pathway promotes recruitment of PP2A to Emi2, keeping Emi2 dephosphorylated. This allows Emi2 activation and APC/C inhibition. Bound PP2A can also promote Emi2 stabilization by dephosphorylating Emi2 at its N-terminus – otherwise, Cdc2–cyclin-B-mediated phosphorylation at this terminus would trigger Emi2 ubiquitylation and degradation. The Mos pathway therefore works through Emi2 to modulate APC/C activity, providing a link between Mos and the APC/C to regulate CSF arrest.