Required for mitophagy, autophagy and endosome maturation, possibly by acting in multiple membrane trafficking pathways (PubMed:20194640, PubMed:22493244). Required for endosome trafficking and maturation (PubMed:20194640). Functions with the class C Vps-HOPS complex member Vps16a to promote endosomal maturation into degradative late endosomes and lysosomes (PubMed:20194640). In response to starvation, functions at an early stage of autophagy to promote autophagosome growth and efficient autophagy (PubMed:22493244). Essential for the recruitment of lva-positive Golgi elements to autophagosomes (PubMed:22493244). Likely to function by promoting membrane traffic from the Golgi complex to the developing autophagosomes (PubMed:22493244). Also regulates synaptic growth at the neuromuscular junctions (NMJ) by down-regulating BMP signaling (PubMed:20194640). Interacts with the class C Vps-HOPS complex components; Car, Dor and Vps16a. Under normal conditions detected in small punctate structures throughout the cytosol of fat body cells, upon induction of autophagy by starvation becomes localized to the outer membrane surface of autophagosomes. Not detected in the Golgi of Garland cells. Pupal lethal (PubMed:20194640). Larval neuromuscular junctions (NMJ) display an increase in synaptic bouton number and synaptic area (PubMed:20194640). In Garland cells endosome trafficking is impaired (PubMed:20194640). Early and late endosomes are unable to progress into mature degradative endosomes and lysosomes resulting in enlarged endosomal compartments (PubMed:20194640). In larvae, starvation-induced autophagosomes are significantly decreased in size (PubMed:22493244). However, autophagosomes are able to form and can mature via fusion with endosomes and lysosomes (PubMed:22493244). Belongs to the CLEC16A/gop-1 family.