Component of the autophagy machinery that controls the major intracellular degradation process by which cytoplasmic materials are packaged into autophagosomes and delivered to lysosomes for degradation (, ). Involved in an early step of the formation of preautophagosomal structures (, ). Binds and is activated by phosphatidylinositol 3-phosphate (PtdIns3P) forming on membranes of the endoplasmic reticulum upon activation of the upstream ULK1 and PI3 kinases . Mediates ER-isolation membranes contacts by interacting with the ULK1:RB1CC1 complex and PtdIns3P . Once activated, WIPI2 recruits at phagophore assembly sites the ATG12-ATG5-ATG16L1 complex that directly controls the elongation of the nascent autophagosomal membrane (, ).
Recruits the ATG12-ATG5-ATG16L1 complex to omegasomes and preautophagosomal structures, resulting in ATG8 family proteins lipidation and starvation-induced autophagy. Isoform 4 is also required for autophagic clearance of pathogenic bacteria. Isoform 4 binds the membrane surrounding Salmonella and recruits the ATG12-5-16L1 complex, initiating LC3 conjugation, autophagosomal membrane formation, and engulfment of Salmonella.
Subcellular locations: Preautophagosomal structure membrane
Localizes to omegasomes membranes which are endoplasmic reticulum connected structures at the origin of preautophagosomal structures. Enriched at preautophagosomal structure membranes in response to PtdIns3P.
Ubiquitously expressed (at protein level). Highly expressed in heart, skeletal muscle and pancreas. Expression is down-regulated in pancreatic and in kidney tumors.