果膠是植物初級細胞壁的主要成份之一,在高基氏體中形成,並以高度甲基酯化的形態被送至細胞壁中。在細胞壁中的果膠會受到甲基酯化酶 (PME) 的作用,去除所擁有的甲基酯結構。根據研究,甲基酯化酶在植物生長以及抗蟲害機制中扮演著重要的角色,但是在植物耐熱機制中所扮演的角色卻少有研究。我們以53個阿拉伯芥PME的T-DNA插入突變株進行耐熱性狀測試,發現二個PME34 (At3g49220) 相同基因座的突變株皆出現存活率下降的性狀。經過實驗後發現,PME34基因的受損並不會影響到熱休克蛋白基因的表現量,同時PME34的轉錄會受到ABA的誘導,並會在保衛細胞中會大量表現。所以我們推斷,PME34的突變會使得植株失去控制氣孔開關的能力,導致植株出現不耐熱的性狀。因此、在阿拉伯芥熱休克反應機制當中,PME34會藉由本身的酵素功能改變保衛細胞的細胞壁結構,影響細胞壁的彈性,從而改變氣孔的孔徑大小以調節蒸散作用的速率達到散熱的效果,增加植株對熱休克的耐受性。
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 de-methylesterified by pectin methylesterase (PME). The effect of PME on the pectin methylesterification status plays a key role in plant development and plant–pathogen interactions, but its role under heat stress (HS) was poorly studied. Thermotolerance assay of Arabidopsis 53 PME homologous-T-DNA insertion lines revealed 2 null-mutant alleles of PME34 (At3g49220) both consistently showed reduced thermotolerance; nevertheless their impairment was independently associated with the expression of HS-related genes. PME34 transcript induction depended on abscisic acid and was highly expressed in guard cells. We showed PME34 mutation has a defect in the control of stomatal movement resulted in a heat-sensitive phenotype. Hence, PME34 has a role in the regulation of transpiration by controlling the degree of stomatal aperture that was achieved by enzymatic actives during HS response. PME34 is required for regulating guard cell-wall flexibility to mediate HS tolerance in Arabidopsis.