Fig. P1.

Schematic diagram of autophagosomal growth in Drosophila fat body cells. In wild-type fat body cells, small autophagosomes form upon autophagy induction and grow into large autophagosomes. The transmembrane protein Ema and the peripheral membrane-associated protein Lva reside on the Golgi complex in the steady state and move onto these growing autophagosomes. In the ema-mutant cells, small autophagosomes form upon autophagy induction but fail to grow, and Lva is not recruited to autophagosomes. Autophagic turnover of the p62 protein and of mitochondria is impaired in the ema mutant. Thus, ema is required for both autophagosomal growth and autophagic function. These findings are consistent with a model in which ema promotes autophagosomal growth by promoting Golgi-to-autophagosomal membrane traffic.