Arabidopsis HSFA1b functions as a heat sensor inhibiting OST1-mediated stomatal closure through its adenylate-cyclase activity.

Abstract

Global warming profoundly affects plant communities, but the mechanisms and the identity of sensors controlling plant thermosensing remain poorly understood. In this study, we identify the heat-shock factor A1b (HSFA1b) transcription factor as a heat sensor that regulates stomatal responses by inhibiting open stomata 1 (OST1) kinase activity in Arabidopsis. OST1 induces stomatal closure under heat stress independently of abscisic acid, and its activity is inhibited in the cytosol by the C-terminus of HSFA1b through intrinsic adenylate cyclase (AC) activity. Arabidopsis HSFA1b could complement an AC-deficient bacterium, and the cyclic AMP produced by HSFA1b could bind to and inhibit OST1 kinase activity. This inhibition is relieved under heat stress by HSFA1b translocation into the nucleus, coupling OST1 inhibition with the activation of heat-shock protein genes involved in the perception and signaling of high temperature. Collectively, our study demonstrates that HSFA1b functions as a heat sensor, inhibiting heat stress-induced and OST1-mediated stomatal closure through its AC activity.