Elevated CO 2 -Induced Responses in Stomata Require ABA and ABA Signaling

An integral part of global environment change is an increase in the atmospheric concentration of CO2 (CO2) 1. Increased CO2 reduces leaf stomatal apertures and density of stomata that plays out as reductions in evapotranspiration 2-4. Surprisingly, given the importance of transpiration to the control of terrestrial water fluxes 5 and plant nutrient acquisition 6, we know comparatively little about the molecular components involved in the intracellular signaling pathways by which CO2 controls stomatal development and function 7. Here, we report that elevated CO2-induced closure and reductions in stomatal density require the generation of reactive oxygen species (ROS), thereby adding a new common element to these signaling pathways. We also show that the PYR/RCAR family of ABA receptors 8, 9 and ABA itself are required in both responses. Using genetic approaches, we show that ABA in guard cells or their precursors is sufficient to mediate the CO2-induced stomatal density response. Taken together, our results suggest that stomatal responses to increased CO2 operate through the intermediacy of ABA. In the case of CO2-induced reductions in stomatal aperture, this occurs by accessing the guard cell ABA signaling pathway. In both CO2-mediated responses, our data are consistent with a mechanism in which ABA increases the sensitivity of the system to CO2 but could also be explained by requirement for a CO2-induced increase in ABA biosynthesis specifically in the guard cell lineage. Furthermore, the dependency of stomatal CO2 signaling on ABA suggests that the ABA pathway is, in evolutionary terms, likely to be ancestral.