Component of the autophagy machinery that is recruited to phosphatidylinositols on preautophagosomal structures, which are early autophagic structures, to promote autophagosome formation, and the subsequent degradation and clearance of engulfed apoptotic cells and P-granules in somatic cells (PubMed:12958363, PubMed:19167332, PubMed:21183797, PubMed:21802374, PubMed:22451698, PubMed:25124690, PubMed:28557996). In particular, binds with high affinity to phosphatidylinositols including phosphatidylinositol 3-phosphate (PtdIns(3)P), phosphatidylinositol 4-phosphate (PtdIns(4)P), and phosphatidylinositol 5-phosphate (PtdIns(5)P), and more weakly to phosphatidylinositol 3,5-bisphosphate (PtdIns(3,5)P2) (PubMed:21802374, PubMed:22451698). Plays a role in mitophagy, which is the autophagic consumption of mitochondria, in response to dietary restriction (PubMed:30133321). Involved in xenophagy, the autophagy-mediated degradation of pathogens and pathogen products, such as toxins (PubMed:27875098). Also plays a role in membrane-pore repair (PubMed:27875098). In a daf-18/PTEN- and daf-16/FOXO-dependent manner, required for the proliferation of germ stem cell progenitors in the gonad during the late phases of larval development (PubMed:28285998). By regulating the release of neurotransmitters and neuropeptides, involved in the control of lifespan in response to dietary restriction and daf-2 signaling (PubMed:28557996). Probably through its involvement in autophagy, required for dauer formation (PubMed:12958363). Partially localizes to the phagosome membrane of engulfed apoptotic cells. Expressed in neurons and intestinal cells. The L/FRRG motif is required for recruitment to phosphatidylinositols including phosphatidylinositol 3-phosphate (PtdIns(3)P), phosphatidylinositol 4-phosphate (PtdIns(4)P), phosphatidylinositol 5-phosphate (PtdIns(5)P), and phosphatidylinositol 3,5-bisphosphate (PtdIns(3,5)P2). RNAi-mediated knockdown results in defective clearance of engulfed apoptotic cells (PubMed:21183797). RNAi-mediated knockdown reduces autophagic degradation of membrane pore-forming toxin Cry5B (PubMed:27875098). RNAi-mediated knockdown results in reduced germ stem cell proliferation during larval development (PubMed:28285998). RNAi-mediated knockdown causes abnormalities in constitutive dauer formation in daf-2 e1370 mutant including a lack of autophagosome formation (PubMed:12958363). Belongs to the WD repeat PROPPIN family.