Kintake Sonoike

Reactive 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.

SUMMARY In the cyanobacterium Synechocystis sp. PCC 6803, translation factor EF‐Tu is inactivated by reactive oxygen species (ROS) via oxidation of Cys82 and the oxidation of EF‐Tu enhances the inhibition of the repair of photosystem II (PSII) by suppressing protein synthesis. In our present study, we generated transformants of Synechocystis that overexpressed a mutated form of EF‐Tu, designated EF‐Tu (C82S), in which Cys82 had been replaced by a Ser residue, and ROS‐scavenging enzymes individually or together. Expression of EF‐Tu (C82S) alone in Synechocystis enhanced the repair of PSII under strong light, with the resultant mitigation of PSII photoinhibition, but it stimulated the production of ROS. However, overexpression of superoxide dismutase and catalase, together with the expression of EF‐Tu (C82S), lowered intracellular levels of ROS and enhanced the repair of PSII more significantly under strong light, via facilitation of the synthesis de novo of the D1 protein. By contrast, the activity of photosystem I was hardly affected in wild‐type cells and in all the lines of transformed cells under the same strong‐light conditions. Furthermore, transformed cells that overexpressed EF‐Tu (C82S), superoxide dismutase, and catalase were able to survive longer under stronger light than wild‐type cells. Thus, the reinforced capacity for both protein synthesis and ROS scavenging allowed both photosynthesis and cell proliferation to tolerate strong light.