The PI(3,5)P2 regulatory complex regulates both the synthesis and turnover of phosphatidylinositol 3,5-bisphosphate (PtdIns(3,5)P2). Required for autophagy by autophagosome formation during nutrient deprivation, senescence and under abiotic stresses, including oxidative, high salt and osmotic stress conditions. Cooperates with jasmonate- and WRKY33-mediated signaling pathways in the regulation of plant defense responses to necrotrophic pathogens. Component of the PI(3,5)P2 regulatory complex at least composed of ATG18, SAC/FIG4, FAB1 and VAC14 (By similarity). Interacts with WRKY33. Peripheral membrane protein of pre-autophagosomal structure (PAS) and vacuole. A number of isoforms are produced. According to EST sequences. Expressed in roots, stems, flowers and leaves. By sucrose and nitrogen starvation and during senescence. By methyl viologen. By salt and osmotic stress. By necrotrophic fungal pathogen B.cinerea. Up-regulated in response to both water stress and hydrotropic stimulation. The first protein part may form a beta-propeller domain involved in specific binding to phosphatidylinositol 3,5-bisphosphate (PIP2), leading to the association of the protein to the membrane. Mutant is more sensitive to nutrient deprivation conditions and exhibits an early senescence phenotype. Prevents autophagosome formation during starvation. More sensitive to methyl viologen (oxidative stress) treatment and accumulates a higher level of oxidized proteins compared to wild type. High sensitivity to salt and osmotic/drought stresses. Displays an enhanced resistance to the powdery mildew pathogen G.cichoracearum with mildew-induced cell death and an enhanced resistance to P.syringae DC3000 but shows an enhanced susceptibility to infection with necrotrophic A.brassicicola and B.cinerea pathogens. Belongs to the WD repeat PROPPIN family.