Here, we utilized a high copy genomic library (Nasmyth and Reed 1980) to perform a suppressor screen on arl1Δ and ypt6Δ strains. Since we found that neither deletion mutant strain can grow in the presence of rapamycin at 37°, we first used this assay to identify suppressors of the growth defects. Because we are interested in membrane traffic or autophagy regulators that have relationships with Arl1 or Ypt6 during autophagy, a total of seven genes (COG4, SNX4, TAX4, IVY1, PEP3, SLT2, and ATG5) were selected from the sequenced genomic fragments and were transformed into both the arl1Δ and ypt6Δ strains. Autophagy-specific assays were used to determine which genes suppressed the autophagy defects. As a result, we have identified novel partners of Arl1 or Ypt6 during autophagy.