Ubiquitin-like modifier involved in autophagosomes formation. With ATG4, mediates the delivery of the autophagosomes to the vacuole via the microtubule cytoskeleton. Participates also in membrane fusion events that take place in the early secretory pathway. Also involved in endoplasmic reticulum-specific autophagic process and is essential for the survival of cells subjected to severe ER stress. The ATG8-PE conjugate mediates tethering between adjacent membranes and stimulates membrane hemifusion, leading to expansion of the autophagosomal membrane during autophagy (By similarity). Required for selective autophagic degradation of the mitochondria (mitophagy) which contributes to regulate mitochondrial quantity and quality by eliminating the mitochondria to a basal level to fulfill cellular energy requirements and preventing excess ROS production. Required for wild-type budding of haploid sporidia and for complete symptom development during pathogenic growth such as gall formation and teliospore production in ears of mature maize (PubMed:20618705, PubMed:22843561). Conjugation to phosphatidylethanolamine (PE) leads to homodimerization. Interacts with ATG1, ATG3, ATG4, ATG7, ATG12, ATG32, ATG34 and the C-terminal 10 residues domain of ATG19. Interacts also with the endoplasmic reticulum to Golgi v-SNARE protein BET1 and the vacuolar v-SNARE protein NYV1. Interacts with the UBX domain-containing protein SHP1. Transcripts accumulate during carbon stress conditions. The C-terminal 2 residues are removed by ATG4 to expose Gly-116 at the C-terminus. The C-terminal Gly is then amidated with phosphatidylethanolamine by an activating system similar to that for ubiquitin. Prevents vacuolar accumulation of autophagosomes and affects survival during carbon starvation. Belongs to the ATG8 family.