Figure 2.

Schematic diagram of autophagy regulation under various stresses. KIN10, a catalytic subunit of SnRK1, is activated by stresses to phosphorylate TOR-interacting proteins, in turn inhibiting TOR kinase activity and activating ATG1. Additionally, active KIN10 can phosphorylate ATG6 and activate the PI3K complex to induce autophagy by an ATG1 kinase independent pathway. Under nutrient starvation stress, SnRK2 is activated by ABA to inhibit the activity of the TOR complex, and the expression of ATG genes are induced by the transcription factor ATAF1, resulting in the promotion of autophagy. Nutrient starvation stress can also cause the dissociation of GAPDH and ATG3, thus promoting the binding of ATG8 and ATG3. The expression of ATG genes are induced by WRKY33 and HsfA1a under heat stress to promote the degradation of protein aggregates through autophagy. Autophagy can also be induced by drought stress in an ethylene-dependent manner. Moreover, autophagy is also regulated by ROS levels during drought stress, in which AOX plays an important role.