Molecular events coordinating Xenopus laevis oocyte meiotic divisions. From top to bottom: The prophase arrest is maintained by high PKA activity due to the constitutively expressed GPR185 receptor. The exocytic pathway is active while the endocytic pathway is downregulated. Cdk1-Cyclin B2 complexes are present under an inactive state due to Cdk1 phosphorylation. Progesterone activates the mPRb receptor, GPR185 is inactivated, the exocytosis and endocytosis pathways are inverted. PKA is inactivated and promotes translation and/or accumulation of new proteins, among them Mos (that does not accumulate due to its instability) and Cyclin B1 (due to its stabilization). New Cyclin B1 proteins associate with Cdk1 and form a starter amount of Cdk1 activity. This Cdk1 starter stabilizes Mos and promotes Cdk1-Cyclin B2 activation through the regulation of Myt1, Cdc25, Gwl and PP2A. The autoamplification loop is launched, whereby more Cdk1 is activated, more it activates kinases as Mos-MAPK, Aurora-A and Plk1, all of them contributing with Cdk1 to regulate Myt1 and Cdc25, hence accelerating Cdk1 activation. Phosphorylated substrates trigger NEBD and the MI spindle assembly as well as protein translation. APC is activated under the control of Cdk1 and leads to Cyclin B degradation. The Cdk1 activity decreases and allows anaphase I and expulsion of the 1st polar body. Under the Mos/MAPK control, Emi2/Erp1 inactivates APC, halting Cyclin B degradation. The re-accumulation of Cyclin B increases Cdk1 activity that triggers the formation of the MII spindle, avoiding the assembly of a nucleus and DNA replication. APC remains inhibited by Emi2/Erp1, what ensures the oocyte arrest in MII. Color code: red: inactivated proteins; green: activated proteins; red arrow: inhibition; green arrow: activation; yellow highlight: accumulated protein; blue highlight: protein synthesized but not accumulated.