From the seven candidates, we found that COG4, TAX4, and SNX4 suppressed the autophagy defect of the arl1Δ strain, while IVY1 and ATG5 suppressed the defect in the ypt6Δ strain. Two genes identified in the primary screen, SLT2 and PEP3, selected from rapamycin sensitivity screens for the arl1Δ and ypt6Δ strains, respectively, did not suppress the defect in either strain as measured by the more specific assays. In order to confirm that these two genes were actually the relevant ones in the genomic fragments, we streaked the arl1Δ strain with a plasmid containing only the SLT2 gene and the ypt6Δ strain with a plasmid containing only the PEP3 gene onto medium containing 5 ng/ml rapamycin, and cultured them at 37°. These genes, SLT2 and PEP3, suppressed the high temperature rapamycin sensitivity of arl1Δ and ypt6Δ, respectively (Figure 5). These results indicate that genes that suppressed the rapamycin phenotype in these strains are not necessarily regulators of autophagy.