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 1706, 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.