FIGURE 3.

Schematic diagram of autophagy regulation by environmental stress through plant hormones. Under stress conditions, the concentration of ABA increases. ABA receptors, PYLs, bind to ABA and PP2C, resulting in the activation of SnRK2. SnRK2 phosphorylates RAPTOR and inactivates the TOR complex to induce autophagy. Under normal conditions, TOR kinase phosphorylates the PYL ABA receptors, preventing PYL from binding to ABA and PP2C. SnRK2 and PP2C form repressor complexes which interact with SnRK1 and prevent it from interacting with TOR. In response to biotic stress, ethylene signaling is activated by MAPK and CDPK. The ethylene signaling pathway may regulate autophagy through ROS signaling. Abiotic stresses also regulate autophagy through the JA pathway, in which the expression of ATGs can be induced by ERFs. Additionally, cold can enhance the stability of BZR1 to increase expression of ATGs, resulting in enhanced autophagy. The brassinosteroid-responsive transcription factor BES1 is selectively degraded by DSK2-mediated autophagy under starvation and drought stresses.