Autophagy is a cellular degradation process that sequesters organelles or proteins into a double-membrane structure called the autophagosome, which then fuses with the lysosome or vacuole for hydrolysis. Factors that control membrane traffic are also essential for each step of autophagy. Here we demonstrate that two small GTP-binding proteins in Saccharomyces cerevisiae, Arl1 and Ypt6, which belong to the Arf/Arl/Sar protein family and the Rab family, respectively, and control endosome – trans-Golgi traffic, are also necessary for starvation-induced autophagy under high temperature stress. Using established autophagy-specific assays we found cells lacking either ARL1 or YPT6, which exhibit synthetic lethality with one another, were unable to undergo autophagy at an elevated temperature, although autophagy proceeds normally at normal growth temperature; specifically strains lacking one or the other of these genes are unable to construct the autophagosome because these two proteins are required for proper traffic of Atg9 to the phagophore assembly site at the restrictive temperature. Using degron technology to construct an inducible arl1Δ ypt6Δ double mutant, we demonstrated that cells lacking both genes show defects in starvation-inducted autophagy at the permissive temperature. Our data show that these two membrane traffic regulators have novel roles in autophagy.