Brassinosteroid and Hydrogen Peroxide Interdependently Induce Stomatal Opening by Promoting Guard Cell Starch Degradation
Brassinosteroid and Hydrogen Peroxide Interdependently Induce Stomatal Opening by Promoting Guard Cell Starch Degradation
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油菜素类固醇和过氧化氢通过促进保卫细胞淀粉降解相互依赖地诱导气孔打开
DOI：
10.1105/tpc.19.00587
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发表时间：
2020-04-01
期刊：
影响因子：
11.6
通讯作者：
Bai, Ming-Yi
中科院分区：
文献类型：
--
作者：
Li, Jin-Ge;Fan, Min;Bai, Ming-Yi
保卫细胞中的淀粉降解是由植物激素油菜素类固醇和氧化还原信号过氧化氢诱导的，以促进气孔开放。淀粉是植物体内主要的贮藏碳水化合物，在植物适应复杂环境条件下起着缓冲碳和能量供应的作用。淀粉降解的时间和程度似乎是由不同的激素和环境信号决定的，然而，我们对淀粉代谢调节的理解是零碎的。在这里，我们证明了植物激素油菜素内酯（BR）和氧化还原信号过氧化氢（H2 O2）诱导保卫细胞中的淀粉分解，从而促进气孔开放。BR不敏感突变体bri 1 -116在保卫细胞中积累高水平的淀粉，损害气孔开放响应光。功能获得性突变体bzr 1 -1D抑制了bri 1 -116的淀粉过剩表型，从而促进气孔开放。油菜素耐药1（BZR 1）与碱性亮氨酸拉链转录因子G盒结合因子2（GBF 2）相互作用，促进β-淀粉酶1（BAM 1）的表达，后者负责保卫细胞中的淀粉降解。H2 O2诱导BZR 1氧化，增强BZR 1和GBF 2之间的相互作用，从而增加BAM 1的转录。BAM 1基因突变导致淀粉积累，降低BR和H2 O2对气孔开放的影响。总之，本研究揭示了BR和H2 O2在调节保卫细胞淀粉代谢和气孔开放中的关键作用。
Starch degradation in guard cells is induced by the phytohormone brassinosteroid and the redox signal hydrogen peroxide to promote stomatal opening. 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 (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-RESISTANT1 (BZR1) interacts with the basic leucine zipper 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 BZR1 oxidation, 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, this study uncovers the critical roles of BR and H2O2 in regulating guard cell starch metabolism and stomatal opening.