Fig. S8.

Schematic model shows the cooperation between AP2 and TWD40-2/TPC during clathrin-mediated endocytosis and describes potential unique functions of TWD40-2. Our study suggests that faulty CSCs are likely targeted for endocytosis because defective CME leads to the accumulation of enzymatically inefficient CSCs at the plasma membrane. It is unknown whether CSCs disintegrate into smaller complexes before endocytosis. CSCs and CESAs are displayed as representative CME cargos, but many other CME cargo proteins also exist in Arabidopsis. Our study shows that both AP2M and TWD40-2 persist throughout CME initiation, maturation, and scission and that the behavior of each component is dependent on the other. Our study also shows that genetic disruptions in AP2M and TWD40-2 differentially affect the CME process, suggesting that TWD40-2 has certain functions that are distinct from AP2. The model proposes that TWD40-2 might play unique roles during maturation or scission. Future studies can focus on deciphering specific functions of TWD40-2 and whether TWD40-2 is a permanent or transient member of the TPC.