Abscisic acid-independent stomatal CO ₂ signal transduction pathway and convergence of CO ₂ and ABA signaling downstream of OST1 kinase

Abstract

Significance Elevated CO 2 and abscisic acid (ABA) induce rapid stomatal closure, but the underlying signal transduction mechanisms of CO 2 /ABA interaction remain unclear. Here we show that elevated CO 2 -induced stomatal closure is not abolished but is slowed in higher-order ABA biosynthesis and receptor mutants. Physiological CO 2 elevations activate anion channels in these mutants. In vivo time-resolved ABA nanoreporter imaging indicates that CO 2 elevation does not change ABA concentrations in guard cells. Unexpectedly, CO 2 signaling proceeds without direct OST1/SnRK2 kinase activation in guard cells. This study points to a model that elevated CO 2 triggers stomatal closure through an ABA-independent pathway downstream of OST1/SnRK2 kinases and that basal ABA signaling and OST1/SnRK2 activity enhance stomatal closure in response to CO 2 elevation.