Chloroplast K+/H+EXCHANGE ANTIPORTER 3 modulates abscisic acid‐induced reactive oxygen species generation in guard cells

Abstract

AbstractReactive oxygen species (ROS) are important signaling molecules in stomatal closure. In a previous report, we demonstrated that ROS generated through photosynthetic electron transport (PET) act as signaling molecules in abscisic acid (ABA)‐induced stomatal closure. However, the mechanism by which ABA induces ROS generation through PET remains unclear. Here, we assessed the possibility that chloroplast K+/H+ EXCHANGE ANTIPORTER 3 (KEA3) functions in ABA‐induced ROS generation in guard cells, resulting in stomatal closure. KEA3 localizes to a thylakoid membrane and allows proton efflux from the thylakoid lumen by K+/H+ antiport, regulating photosynthesis by proton motive force. KEA3 loss‐of‐function mutants (kea3‐1 and kea3‐2) were impaired in ABA‐induced ROS generation of guard cells and stomatal closure. The small molecule electroneutral K+/H+ antiporter nigericin induced ROS generation in guard cells and stomatal closures in the kea3 mutants. This study demonstrates that KEA3 is an important factor for ABA‐induced ROS generation in guard cells and stomatal closure.