Clathrin and post-Golgi trafficking: a very complicated issue

Clathrin-coated vesicles (CCVs) are formed at the plasma membrane and act as vectors for endocytosis. They also assemble at the trans-Golgi network (TGN), but their exact function at this organelle is unclear. Recent studies have examined the effects on vacuolar and secretory protein transport of knockout mutations of the adaptor protein 1 (AP1) μ-adaptin subunit AP1 M, but these investigations do not clarify the situation. These mutations lead to the abrogation of multiple trafficking pathways at the TGN and cannot be used as evidence in favour of CCVs being agents for receptor-mediated export of vacuolar proteins out of the TGN. This transport process could just as easily occur through the maturation of the TGN into intermediate compartments that subsequently fuse with the vacuole.