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 CO(2) ([CO(2)]) [1]. Increased [CO(2)] 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 [CO(2)] controls stomatal development and function [7]. Here, we report that elevated [CO(2)]-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 [CO(2)]-induced stomatal density response. Taken together, our results suggest that stomatal responses to increased [CO(2)] operate through the intermediacy of ABA. In the case of [CO(2)]-induced reductions in stomatal aperture, this occurs by accessing the guard cell ABA signaling pathway. In both [CO(2)]-mediated responses, our data are consistent with a mechanism in which ABA increases the sensitivity of the system to [CO(2)] but could also be explained by requirement for a CO(2)-induced increase in ABA biosynthesis specifically in the guard cell lineage. Furthermore, the dependency of stomatal [CO(2)] signaling on ABA suggests that the ABA pathway is, in evolutionary terms, likely to be ancestral.