Fig. 3. Model for meiosis II exit after fertilization-induced destruction of XErp1. During CSF arrest, the APC/C is kept inactive by XErp1. Fertilization leads to the production of intracellular Ca²⁺ transients that activate CaMKII. CaMKII phosphorylation on Thr195 directs Plx1 to its substrate XErp1. Plx1 phosphorylation then triggers SCF^ß-TRCP-dependent degradation of XErp1 by the ubiquitin/proteasome system. As a result, the APC/C is liberated from its repression and triggers meiosis II exit.