The role of clathrin in post-Golgi secretion in plant cells.

Within the plant endomembrane system, the vesicle coat protein clathrin localizes to the plasma membrane (PM) and the trans-Golgi Network/early endosome (TGN/EE). While the role of clathrin in endocytosis at the PM is well established, its function at TGN/EE, presumably in late secretion (trafficking from the TGN/EE to the cell surface) or en route to the vacuole, is debated. Similarly debated are potential homeostatic mechanisms balancing the trafficking routes, especially endocytosis and late secretion. We address these questions in Arabidopsis thaliana using conditional silencing of CLATHRIN HEAVY CHAIN (CHC), conditional overexpression of the clathrin uncoating factor AUXILIN-LIKE1, and secretory mutants. CHC silencing interferes with trafficking of cargoes destined for the apoplast and the PM, supporting a function of clathrin in late secretion. The secretory cargoes become abnormally rerouted from the TGN/EE to the vacuole. Unlike CHC silencing, overexpression of AUXILIN-LIKE1 selectively inhibits clathrin-mediated endocytosis while secretion continues normally at early points of induction. Conversely, secretory mutants exhibit a reduced PM recruitment of clathrin, and variably, of the TPLATE endocytic component. Together, our data show a role of clathrin in secretion and suggest secretion as a fundamental trafficking process to which endocytosis is adjusted by a weak homeostatic mechanism.