Previous results have shown that Ivy1 localizes to the vacuole and is an effector of the small GTP-binding protein Ypt7. Ivy1 controls the function of TORC1 in combination with the V-ATPase, as the strain with a double deletion of IVY1 and one of the subunits of the V-ATPase VAM16 cannot grow in the presence of rapamycin (Numrich et al. 2015). This double mutant strain has an invaginated vacuolar surface phenotype, which suggests that Ivy1, together with the V-ATPase, functions to maintain vacuolar shape as well as regulate the function of TORC1 (Numrich et al. 2015). Ivy1 may function by increasing the fusion between the autophagosome and the vacuole as it is required for the integrity of the vacuole membrane. We observed that IVY1 is a weaker suppressor of the autophagy activity of ypt6Δ compared to ATG5 (see the Pho8Δ60 assay in Figure 3B). This result may due to the fact that Ivy1 is indirectly involved in autophagosome formation.