Many widely used autophagy-specific assays are challenging to adapt for high copy suppressor screening, due to the difficulty in manipulating large sample numbers for western blot analysis (GFP-Atg8 proteolysis), enzymatic activity (Pho8Δ60), or microscopy (GFP-Atg8 localization). Thus, we chose to use the rapamycin sensitivity assay as a preliminary screen, since we found that this phenotype correlated with phenotypes of the more specific assays. Rapamycin blocks the kinase function of TORC1, and in turn activates many TORC1-controlled pathways, including autophagy. However, because TORC1 regulates many pathways, such as the ribosome biogenesis pathway (Martin et al. 2004), cell cycle (Barbet et al. 1996), amino acid biosynthesis pathways (Komeili et al. 2000; Crespo et al. 2002), and the cell wall integrity pathway (Torres et al. 2002), the suppressors identified from this screen may not specifically suppress the autophagy defect of the arl1Δ and ypt6Δ strains. Therefore, we selected genes that express regulators for membrane traffic or autophagy, since the expectation would be that such genes could potentially be specific regulators of autophagy. Using this approach, we found that COG4, TAX4, and SNX4 suppressed the autophagy defect of the arl1Δ strain, while IVY1 and ATG5 suppressed the defect of the ypt6Δ strain.