Autophagy regulates the turnover of cytosolic components in order to increase the availability of nutrients during starvation or to remove damaged cellular material. More than 30 autophagy-related genes (Atgs), which encode the proteins that are required for the formation of the autophagosomal membranes, have been identified. But an important question remains: which cellular membrane are these structures derived from? The ER, the Golgi network and mitochondria have all been implicated as membrane sources for the autophagosome. On page , Wei Lu and colleagues now provide additional insight by showing that membranes from the trans-Golgi network (TGN) are involved in the formation of autophagosomal structures. They find that an increase in traffic from the TGN to the plasma membrane induces the formation of microtubule-associated protein light chain 3 (LC3)-positive structures, whereas blocking transport from the Golgi complex inhibits autophagosome biogenesis. Furthermore, LC3 binds directly to TGN membranes and, during starvation, LC3-positive vesicles bud from the TGN in a process that requires the clathrin adaptor protein AP1. Together, these results confirm a role for the TGN in autophagosome formation and highlight a role for AP1-mediated clathrin coating of TGN membranes in promoting starvation-induced autophagy.
