Model for TgTEP-dependent vesicular transport. The schematic illustrates the role of TgTEP in coordinating vesicle transport from the TGN to the PLVAC. TgTEP, in complex with the AP4, binds to vesicles that bud from the TGN. These vesicles are transported along actin filaments in a MyoF-dependent manner (orange arrow). A subset of these TgTEP/AP4-positive vesicles may fuse with endocytic vesicles originating from the micropore, contributing to the delivery of internalized material to the PLVAC (red arrow). Upon TgTEP deletion, vesicle trafficking is disrupted, leading to the accumulation of vesicles at the TGN, fragmentation of the trans-Golgi, and impaired delivery of PLVAC cargo. As a result, the PLVAC fails to properly digest or recycle material, which may lead to secondary defects such as mitochondrial fragmentation. Other secretory pathways (e.g., to micronemes, rhoptries, or dense granules) remain functional and are shown as unaffected (gray arrows).