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 appears to be determined by diverse hormonal and environmental signals. However, our understanding of the regulation of starch metabolism is fragmentary. Here, we demonstrate that phytohormone brassinosteroid (BR) and redox signal hydrogen peroxide (H2O2) induce the breakdown of starch in guard cells, which promotes stomatal opening. The BR-insensitive mutant bri1-116 accumulated high levels of starch in guard cells, impairing stomatal opening in response to light. The gain-of-function mutant bzr1-1D suppressed the starch excess phenotype of bri1-116, thereby promoting stomatal opening. BRASSINAZOLE-RESISTANT 1 (BZR1) interacts with the bZIP transcription factor G-BOX BINDING FACTOR2 (GBF2) to promote the expression of β-AMYLASE1 (BAM1), which is responsible for starch degradation in guard cells. H2O2 induces the oxidation of BZR1, enhancing the interaction between BZR1 and GBF2 to increase BAM1 transcription. Mutations in BAM1 lead to starch accumulation and reduce the effects of BR and H2O2 on stomatal opening. Overall, the present study uncovers the critical roles of BR and H2O2 in the regulation of guard cell starch metabolism and stomatal opening.

淀粉是植物中的主要储存碳水化合物，在具有挑战性的环境条件下，可以缓冲碳和能量的可用性，从而使植物适应健康。淀粉降解的时机和程度似乎由多种激素和环境信号决定。但是，我们对淀粉代谢调控的理解是零碎的。在这里，我们证明了植物激素油菜素类固醇（BR）和氧化还原信号过氧化氢（H2O2）诱导了保卫细胞中淀粉的分解，从而促进了气孔的开放。对BR不敏感的突变体bri1-116在保卫细胞中积聚了高水平的淀粉，从而损害了光对气孔的开放。功能获得突变体bzr1-1D抑制了bri1-116的淀粉过量表型，从而促进了气孔的开放。耐巴西环唑1（BZR1）与bZIP转录因子G-BOX BINDING FACTOR2（GBF2）相互作用，促进β-淀粉酶1（BAM1）的表达，后者负责保护细胞中的淀粉降解。H2O2诱导BZR1氧化，增强BZR1与GBF2之间的相互作用，从而增加BAM1转录。BAM1中的突变导致淀粉积累，并降低BR和H2O2对气孔开放的影响。总体而言，本研究揭示了BR和H2O2在调节保卫细胞淀粉代谢和气孔开放中的关键作用。BAM1中的突变导致淀粉积累，并降低BR和H2O2对气孔开放的影响。总体而言，本研究揭示了BR和H2O2在调节保卫细胞淀粉代谢和气孔开放中的关键作用。BAM1中的突变导致淀粉积累，并降低BR和H2O2对气孔开放的影响。总体而言，本研究揭示了BR和H2O2在调节保卫细胞淀粉代谢和气孔开放中的关键作用。