Figure 4.

Under normal conditions, ABA receptors (PYR/PYL/RCAR) bind to the PP2Cs and inhibit the activity of SnRK2.6, which deactivates NADPH oxidase, SALC1, and other ion channels to reinforce the normal functioning of stomata. Under water-stressed conditions, ABA signaling stimulates ABA receptors (PYR/PYL/RCAR) that lead to the activation of SnRK2.6, which triggers SLAC1 and NADPH oxidase to produce H₂O₂ and regulate stomatal movements. During drought stress, ABA signaling increases the biosynthesis of H₂S via persulfidation of ABI4-mediated activation of DES1 transcription. The burst of H₂S in guard cells activates the S-type anion and spikes the Ca²⁺ wave alongside strong persulfidation of SnRK2.6. The persulfidated SnRK2.6 robustly phosphorylates SALAC1 and NADPH oxidase to produce a long-lasting burst of ROS to modulate water efflux in guard cells to close stomata, similarly to the way that ABA induces stomatal closure.