Activates the ATG1 kinase in a nutritional condition dependent manner through the TOR pathway, leading to autophagy. Required for autophosphorylation of ATG1 at 'Thr-226' and its dimerization. May also be involved in the regulation of autophagy through SNF1. Involved in ATG9 and ATG23 cycling through the pre-autophagosomal structure. Also involved in cytoplasm to vacuole transport (Cvt) and more specifically in Cvt vesicle formation. Seems to play a role in the switching machinery regulating the conversion between the Cvt pathway and autophagy. Finally, ATG13 is also required for glycogen storage during stationary phase (By similarity). Hypophosphorylated form interacts with ATG1 to form the ATG1-ATG13 kinase complex. The ATG1-ATG13 complex interacts with the ATG17-ATG29-ATG31 complex through direct interaction with ATG17. Interacts with VAC8. Phosphorylated; hyperphosphorylated by the TORC1 kinase complex to repress the induction of autophagy. Starvation and TOR inactivation results in ATG13 partial dephosphorylation leading to ATG1-binding. Rephosphorylated by ATG1 during prolonged nitrogen starvation. Also phosphorylated by TPK1; TPK1 phosphorylation regulates the association of ATG13 with the PAS. Within this regulatory network, mitochondrial respiratory deficiency suppresses autophagic flux. Hyperphosphorylation in rich medium is impaired in the absence of VAC8. Belongs to the ATG13 family. Fungi subfamily.