Figure 8. A hypothetical model of Atg13 function during basal and induced autophagy. Based on correlation of overall Atg13 phosphorylation level with autophagic status, Atg13 is likely activated at least in part by Atg1-mediated phosphorylation on multiple residues. Question marks near phosphogroups of Atg13 highlight the fact that the number and exact sites of these phosphorylation events is currently unknown. The ratio of this active Atg13 appears to be lower during nutrient-replete conditions relative to the inactive form, which is potentially phosphorylated by TOR or other kinases, or not phosphorylated at all. The presence of the active form at a lower level under basal conditions may be necessary to support low-level autophagic activity. Starvation, genetic inactivation of TOR, and overexpression of Atg1 or Atg17 appear to increase the ratio of active Atg13, which may contribute to increased autophagosome formation observed in response to these autophagy-inducing treatments.