Figure 8. Hypothetical model of ethylene and H₂O₂-induced stomatal closure responses via AHK5. The H₂O₂ branch of the pathway (red arrows) occurs via AHK5- or ETR1-activated AHP2/AHP5 signaling which leads to the activation and phosphorylation of ARR4, and thus resulting in stomatal closure. The stimulus which generates H₂O₂ in guard cells and functions via ARR4 phosphorylation remains to be determined. Ethylene stimulates H₂O₂ production via ETR1/AHK5. Ethylene response occurs via AHK5-AHP1/AHP2-ARR4 pathway (blue arrows), independent of ARR4 phosphorylation or via ARR7. In the H₂O₂-independent branch (dashed lines), AHP1 or AHP3 might act via ARR2 which induces ARR4 transcription, followed by protein accumulation; ethylene signaling therefore requires ARR4 function for stomatal closure. Black arrow represents transcriptional control.