Liu Xuan-Shan, Liang Chao-Chao, Hou Shu-Guo, Wang Xin, Chen Dong-Hua, Shen Jian-Lin, Zhang Wei, Wang Mei
Key Laboratory of Plant Development and Environmental Adaption Biology, Ministry of Education, School of Life Sciences, Shandong University, Qingdao, China.
School of Municipal and Environmental Engineering, Shandong Jianzhu University, Jinan, China.
Front Plant Sci. 2020 Nov 27;11:548034. doi: 10.3389/fpls.2020.548034. eCollection 2020.
Guard cells shrink in response to drought stress and abscisic acid (ABA) signaling, thereby reducing stomatal aperture. Hydrogen peroxide (HO) is an important signaling molecule acting to induce stomatal closure. As yet, the molecular basis of control over the level of HO in the guard cells remains largely unknown. Here, the leucine-rich repeat (LRR)-receptor-like kinase (RLK) protein HSL3 has been shown to have the ability to negatively regulate stomatal closure by modulating the level of HO in the guard cells. was markedly up-regulated by treating plants with either ABA or HO, as well as by dehydration. In the loss-of-function mutant, both stomatal closure and the activation of anion currents proved to be hypersensitive to ABA treatment, and the mutant was more tolerant than the wild type to moisture deficit; the overexpression of had the opposite effect. In the mutant, the transcription of NADPH oxidase gene involved in HO production showed marked up-regulation, as well as the level of catalase activity was weakly inducible by ABA, allowing HO to accumulate in the guard cells. HSL3 was concluded to participate in the regulation of the response to moisture deficit through ABA-induced stomatal closure triggered by the accumulation of HO in the guard cells.
保卫细胞会因干旱胁迫和脱落酸（ABA）信号而收缩，从而减小气孔孔径。过氧化氢（H₂O₂）是一种诱导气孔关闭的重要信号分子。然而，保卫细胞中H₂O₂水平调控的分子基础仍 largely unknown。在这里，富含亮氨酸重复序列（LRR）的受体样激酶（RLK）蛋白HSL3已被证明能够通过调节保卫细胞中H₂O₂的水平来负向调控气孔关闭。用ABA或H₂O₂处理植物以及脱水处理后，HSL3显著上调。在功能缺失的HSL3突变体中，气孔关闭和阴离子电流的激活对ABA处理均表现出超敏反应，且该突变体比野生型更耐水分亏缺；HSL3过表达则产生相反的效果。在HSL3突变体中，参与H₂O₂产生的NADPH氧化酶基因RbohF的转录显著上调，过氧化氢酶活性水平对ABA的诱导较弱，使得H₂O₂在保卫细胞中积累。得出的结论是，HSL3通过保卫细胞中H₂O₂积累引发的ABA诱导气孔关闭参与水分亏缺响应的调控。
