Phospholipid scramblase involved in autophagy by mediating autophagosomal membrane expansion (PubMed:23402761, PubMed:27587839). Cycles between the preautophagosomal structure/phagophore assembly site (PAS) and the cytoplasmic vesicle pool and supplies membrane for the growing autophagosome (By similarity). Lipid scramblase activity plays a key role in preautophagosomal structure/phagophore assembly by distributing the phospholipids that arrive through ATG2 (ATG2A or ATG2B) from the cytoplasmic to the luminal leaflet of the bilayer, thereby driving autophagosomal membrane expansion (By similarity). Also required to supply phosphatidylinositol 4-phosphate to the autophagosome initiation site by recruiting the phosphatidylinositol 4-kinase beta (PI4KB) in a process dependent on ARFIP2, but not ARFIP1 (By similarity). In addition to autophagy, also plays a role in necrotic cell death (PubMed:27811852). a 1,2-diacyl-sn-glycero-3-phosphocholine(in) = a 1,2-diacyl-sn-glycero-3-phosphocholine(out) a 1,2-diacyl-sn-glycero-3-phospho-L-serine(in) = a 1,2-diacyl-sn-glycero-3-phospho-L-serine(out) a 1,2-diacyl-sn-glycero-3-phosphoethanolamine(in) = a 1,2-diacyl-sn-glycero-3-phosphoethanolamine(out) Homotrimer; forms a homotrimer with a central pore that forms a path between the two membrane leaflets (By similarity). Interacts (via cytoplasmic its C-terminus) with ATG2A (By similarity). Interacts with SUPT20H (By similarity). Interacts (via the tyrosine-based sorting signal motif) with AP4M1; promoting association with the AP-4 complex (By similarity). Interacts with ARFIP1 and ARFIP2 (By similarity). Interacts with ATG4A; the interaction is direct and promotes ATG9A trafficking (By similarity). Mainly localizes to the trans-Golgi network (TGN) and the endosomal system; cycles between them though vesicle trafficking (PubMed:27587839). Export from the TGN to promote formation of autophagosomes is mediated by the AP-4 complex. Under amino acid starvation or rapamycin treatment, redistributes to preautophagosomal structure/phagophore assembly site (PAS). The starvation-induced redistribution depends on ULK1, ATG13, as well as SH3GLB1. Upon autophagy induction, a portion of transiently localizes to the autophagic membranes (By similarity). Recruited to damaged mitochondria during mitophagy in a RIMOC1-dependent manner (By similarity). Forms a homotrimer with a solvated central pore, which is connected laterally to the cytosol through the cavity within each protomer. Acts as a lipid scramblase that uses its central pore to function: the central pore opens laterally to accommodate lipid headgroups, thereby enabling lipid flipping and redistribution of lipids added to the outer leaflet of ATG9A-containing vesicles, thereby enabling growth into autophagosomes. The tyrosine-based sorting signal motif, also named YXX-psi motif, promotes interaction with the AP-4 complex. Lethality; mice die within one day after birth caused by impaired autophagy (PubMed:19926846). Mice also show aberrant activation of the innate immune response (PubMed:19926846). Fetal mice display significantly retarded growth (PubMed:26370455). Conditional deletion in brain causes axon-specific degeneration: mice were born normally, but half of them die within one week, and none live beyond 4 weeks of age (PubMed:28513333). Defects are caused by impaired autophagy in neurons, leading to progressive degeneration in the axons and their terminals, but not in neuronal cell bodies (PubMed:28513333). In addition to defects in autophagy, mice also display impaired necrotic cell death during bone morphogenesis: the bone surface is rougher and bones are more porous due to defects in necrotic cell death in bone surface formation (PubMed:27811852). Belongs to the ATG9 family.