Autophagy as a conserved catabolic pathway can respond to reactive oxygen species (ROS)which are produced under various stress conditions and plays an important role in degrading oxidized proteins in plants.However, how ROS regulates autophagy in response to oxidative stresses is largely unknown.Here, we show that ATG3 interacts with the cytosolic glyceraldehyde-3-phosphate dehydrogenases (GAPCs) to regulate autophagy in plants.We found that oxidative stress inhibits the interaction of ATG3 with GAPCs.Silencing of GAPCs significantly activates ATG3-dependent autophagy whilst overexpression of GAPCs suppresses autophagy in plants.Moreover, silencing of GAPCs enhances N gene-mediated cell death and plant resistance against both incompatible pathogen Tobacco mosaic virus and compatible pathogen Pseudomonas syringae pv tabaci.These results indicate that GAPCs have multiple functions in the control of autophagy, hypersensitive response and plant innate immunity.