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脱落酸介导的PME12调控影响拟南芥的气孔密度、气孔孔径和热应激反应。

ABA-mediated regulation of PME12 influences stomatal density, pore aperture, and heat stress response in Arabidopsis thaliana.

作者信息

Wu Hui-Chen, Yu Shih-Yu, Vivek Sandeep, Wang Yin-Da, Jinn Tsung-Luo

机构信息

Department of Biological Sciences and Technology, National University of Tainan, Tainan, Taiwan.

Institute of Plant Biology, National Taiwan University, Taipei, Taiwan.

出版信息

Planta. 2025 Jan 9;261(2):29. doi: 10.1007/s00425-025-04606-3.

DOI:10.1007/s00425-025-04606-3
PMID:39786611
Abstract

PME12-mutated plants displayed altered stomatal characteristics and susceptibility to ABA-induced closure. Despite changes in PME activity, the mutant exhibited enhanced thermotolerance. These findings suggest a complex interplay between pectin methylesterification, ABA response, and stomatal function, contributing to plant adaptation to heat stress. Pectin, an essential component of plant cell walls, is synthesized in the Golgi apparatus and deposited into the cell wall in a highly methylesterified form. The degree and distribution of methylesterification within homogalacturonan (HGA) domains are crucial in determining its functional properties. Pectin methylesterase (PME) catalyzes the demethylesterification of HGA, which is pivotal for adjusting cell wall properties in response to environmental cues. Our investigation of PME12, a type-I pectin methylesterase in Arabidopsis, reveals its role in abscisic acid (ABA)-mediated stomatal regulation during heat stress, with the pme12 mutant showing increased stomatal density, reduced size, and heightened sensitivity to ABA-induced closure. Additionally, pme12 plants exhibited altered PME activities under heat stress but displayed enhanced thermotolerance. Moreover, our study identified SCRM as a transcriptional regulator positively influencing PME12 expression, linking stomatal development with PME12-mediated pectin methylesterification. These findings suggest that PME12-mediated pectin modification plays a role in coordinating ABA responses and influencing stomatal behavior under heat stress conditions.

摘要

PME12突变的植物表现出气孔特征的改变以及对脱落酸(ABA)诱导的关闭的敏感性。尽管果胶甲酯酶(PME)活性发生了变化,但突变体表现出增强的耐热性。这些发现表明果胶甲基酯化、ABA反应和气孔功能之间存在复杂的相互作用,有助于植物适应热胁迫。果胶是植物细胞壁的重要组成部分,在高尔基体中合成并以高度甲基酯化的形式沉积到细胞壁中。同型半乳糖醛酸聚糖(HGA)结构域内甲基酯化的程度和分布对于确定其功能特性至关重要。果胶甲酯酶(PME)催化HGA的去甲基酯化,这对于响应环境信号调节细胞壁特性至关重要。我们对拟南芥中的I型果胶甲酯酶PME12的研究揭示了其在热胁迫期间脱落酸(ABA)介导的气孔调节中的作用,pme12突变体表现出气孔密度增加、尺寸减小以及对ABA诱导的关闭的敏感性增强。此外,pme12植物在热胁迫下表现出PME活性的改变,但表现出增强的耐热性。此外,我们的研究确定SCRM是一种正向影响PME12表达的转录调节因子,将气孔发育与PME12介导的果胶甲基酯化联系起来。这些发现表明PME12介导的果胶修饰在热胁迫条件下协调ABA反应和影响气孔行为中发挥作用。

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