Huang Ya-Chen, Wu Hui-Chen, Wang Yin-Da, Liu Chia-Hung, Lin Ching-Chih, Luo Dan-Li, Jinn Tsung-Luo
Institute of Plant Biology, National Taiwan University, Taipei 10617, Taiwan (Y.C.H., H.C.W., Y.D.W., C.H.L., C.C.L., D.L.L., T.L.J.); and.
Department of Biological Sciences and Technology, National University of Tainan, Tainan 70005, Taiwan (H.C.W.).
Plant Physiol. 2017 Jun;174(2):748-763. doi: 10.1104/pp.17.00335. Epub 2017 Apr 5.
Pectin, a major component of the primary cell wall, is synthesized in the Golgi apparatus and exported to the cell wall in a highly methylesterified form, then is partially demethylesterified by pectin methylesterases (PMEs; EC 3.1.1.11). PME activity on the status of pectin methylesterification profoundly affects the properties of pectin and, thereby, is critical for plant development and the plant defense response, although the roles of PMEs under heat stress (HS) are poorly understood. Functional genome annotation predicts that at least 66 potential genes are contained in Arabidopsis (). Thermotolerance assays of gene T-DNA insertion lines revealed two null mutant alleles of (At3g49220) that both consistently showed reduced thermotolerance. Nevertheless, their impairment was independently associated with the expression of HS-responsive genes. It was also observed that transcription was induced by abscisic acid and highly expressed in guard cells. We showed that the mutation has a defect in the control of stomatal movement and greatly altered PME and polygalacturonase (EC 3.2.1.15) activity, resulting in a heat-sensitive phenotype. has a role in the regulation of transpiration through the control of the stomatal aperture due to its cell wall-modifying enzyme activity during the HS response. Hence, PME34 is required for regulating guard cell wall flexibility to mediate the heat response in Arabidopsis.
果胶是植物初生细胞壁的主要成分，在高尔基体中合成，并以高度甲酯化的形式输出到细胞壁，然后被果胶甲酯酶（PMEs；EC 3.1.1.11）部分去甲酯化。PME对果胶甲酯化状态的作用深刻影响果胶的特性，因此对植物发育和植物防御反应至关重要，尽管人们对热胁迫（HS）下PME的作用了解甚少。功能基因组注释预测拟南芥中至少包含66个潜在基因（）。对基因T-DNA插入系的耐热性分析揭示了（At3g49220）的两个无效突变等位基因，它们均一致表现出耐热性降低。然而，它们的损伤与热应激反应基因的表达独立相关。还观察到该基因的转录受脱落酸诱导并在保卫细胞中高表达。我们表明，该基因突变在气孔运动控制方面存在缺陷，并极大地改变了PME和多聚半乳糖醛酸酶（EC 3.2.1.15）的活性，从而导致热敏感表型。由于其在热应激反应期间具有细胞壁修饰酶活性，该基因在通过控制气孔孔径调节蒸腾作用中发挥作用。因此，PME34是调节保卫细胞壁柔韧性以介导拟南芥热反应所必需的。
