Abscisic acid-independent stomatal CO signal transduction pathway and convergence of CO and ABA signaling downstream of OST1 kinase.

Stomatal pore apertures are narrowing globally due to the continuing rise in atmospheric [CO]. CO elevation and the plant hormone abscisic acid (ABA) both induce rapid stomatal closure. However, the underlying signal transduction mechanisms for CO/ABA interaction remain unclear. Two models have been considered: () CO elevation enhances ABA concentrations and/or early ABA signaling in guard cells to induce stomatal closure and () CO signaling merges with ABA at OST1/SnRK2.6 protein kinase activation. Here we use genetics, ABA-reporter imaging, stomatal conductance, patch clamp, and biochemical analyses to investigate these models. The strong ABA biosynthesis mutants and remain responsive to CO elevation. Rapid CO-triggered stomatal closure in PYR/RCAR ABA receptor quadruple and hextuple mutants is not disrupted but delayed. Time-resolved ABA concentration monitoring in guard cells using a FRET-based ABA-reporter, ABAleon2.15, and ABA reporter gene assays suggest that CO elevation does not trigger [ABA] increases in guard cells, in contrast to control ABA exposures. Moreover, CO activates guard cell S-type anion channels in and ABA receptor hextuple mutants. Unexpectedly, in-gel protein kinase assays show that unlike ABA, elevated CO does not activate OST1/SnRK2 kinases in guard cells. The present study points to a model in which rapid CO signal transduction leading to stomatal closure occurs via an ABA-independent pathway downstream of OST1/SnRK2.6. Basal ABA signaling and OST1/SnRK2 activity are required to facilitate the stomatal response to elevated CO These findings provide insights into the interaction between CO/ABA signal transduction in light of the continuing rise in atmospheric [CO].