Does ozone increase ABA levels by non‐enzymatic synthesis causing stomata to close?

Reactive oxygen species (ROS) are widely recognized as important regulators of stomatal aperture and plant gas exchange. The pathways through which stomata perceive ROS share many common linkages with the well characterized signalling pathway for the hormone abscisic acid (ABA), a major driver of stomatal closure. Given reports that ABA receptor mutants have no stomatal response to ozone‐triggered ROS production, as well as evidence that all steps in the ABA biosynthetic pathway can be non‐enzymatically converted by ROS, here we investigated the possibility that ozone closes stomata by directly converting ABA precursors to ABA. In plants where stomata were responsive to ozone, we found that foliar ABA levels rapidly increased upon exposure to ozone. Recovery of gas exchange post‐exposure occurred only when ABA levels declined. Our data suggest that stomatal closure in response to ozone exposure occurs as a result of direct oxidation of ABA precursors leading to ABA production, but the importance of this ROS interaction remains uncertain under normal photosynthetic conditions. Here, we investigate the possibility that stomatal responses to reactive oxygen species (ROS), particularly ozone, are driven by rapid non‐enzymatic synthesis of abscisic acid (ABA). By measuring ABA levels and stomatal responses after a short pulse of ozone, we find that in species with stomata that are sensitive to ozone, foliar and guard cell ABA levels increase rapidly. This stomatal sensitivity to ozone, and increase in ABA level, also occurs in ABA biosynthetic mutants, suggesting that non‐enzymatic oxidation of ABA precursors drives the increase in ABA levels. Our results have important implications for guard cell ROS signalling.