Brassinosteroid and Hydrogen Peroxide Interdependently Induce Stomatal Opening by Promoting Guard Cell Starch Degradation.

Starch is the major storage carbohydrate in plants and functions in buffering carbon and energy availability for plant fitness with challenging environmental conditions. The timing and extent of starch degradation appear to be determined by diverse hormonal and environmental signals; however, our understanding of the regulation of starch metabolism is fragmentary. Here, we demonstrate that the phytohormone brassinosteroid (BR) and redox signal hydrogen peroxide (HO) induce the breakdown of starch in guard cells, which promotes stomatal opening. The BR-insensitive mutant accumulated high levels of starch in guard cells, impairing stomatal opening in response to light. The gain-of-function mutant suppressed the starch excess phenotype of , thereby promoting stomatal opening. BRASSINAZOLE-RESISTANT1 (BZR1) interacts with the basic leucine zipper transcription factor G-BOX BINDING FACTOR2 (GBF2) to promote the expression of (), which is responsible for starch degradation in guard cells. HO induces BZR1 oxidation, enhancing the interaction between BZR1 and GBF2 to increase transcription. Mutations in lead to starch accumulation and reduce the effects of BR and HO on stomatal opening. Overall, this study uncovers the critical roles of BR and HO in regulating guard cell starch metabolism and stomatal opening.