Dual pathways mediated by Apc3-L and Apc8-L synergistically activate the APC/C. In interphase, the Cdc20 C-box binding site is blocked by Apc1-300L, preventing Cdc20 from associating with the APC/C and resulting in its inactivity. During mitosis, Apc8-L and Apc3-L work together to phosphorylate Apc1-300L, enabling APC/C activation upon Cdc20 association. If either Apc3-L or Apc8-L is restricted, Apc1-300L phosphorylation decreases due to one defective pathway, resulting in only partial activation. When both Apc8-L and Apc3-L are restricted, Apc1-300L phosphorylation is significantly impaired, leading to near-total APC/C inactivation.
