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高温下气孔的开放由OST1调控的TOT3-AHA1模块控制。

Stomatal opening under high temperatures is controlled by the OST1-regulated TOT3-AHA1 module.

作者信息

Xu Xiangyu, Liu Hongyan, Praat Myrthe, Pizzio Gaston A, Jiang Zhang, Driever Steven Michiel, Wang Ren, Van De Cotte Brigitte, Villers Selwyn L Y, Gevaert Kris, Leonhardt Nathalie, Nelissen Hilde, Kinoshita Toshinori, Vanneste Steffen, Rodriguez Pedro L, van Zanten Martijn, Vu Lam Dai, De Smet Ive

机构信息

Department of Plant Biotechnology and Bioinformatics, Ghent University, Ghent, Belgium.

VIB Center for Plant Systems Biology, Ghent, Belgium.

出版信息

Nat Plants. 2025 Jan;11(1):105-117. doi: 10.1038/s41477-024-01859-w. Epub 2024 Nov 29.

DOI:10.1038/s41477-024-01859-w
PMID:39613896
Abstract

Plants continuously respond to changing environmental conditions to prevent damage and maintain optimal performance. To regulate gas exchange with the environment and to control abiotic stress relief, plants have pores in their leaf epidermis, called stomata. Multiple environmental signals affect the opening and closing of these stomata. High temperatures promote stomatal opening (to cool down), and drought induces stomatal closing (to prevent water loss). Coinciding stress conditions may evoke conflicting stomatal responses, but the cellular mechanisms to resolve these conflicts are unknown. Here we demonstrate that the high-temperature-associated kinase TARGET OF TEMPERATURE 3 directly controls the activity of plasma membrane H-ATPases to induce stomatal opening. OPEN STOMATA 1, which regulates stomatal closure to prevent water loss during drought stress, directly inactivates TARGET OF TEMPERATURE 3 through phosphorylation. Taken together, this signalling axis harmonizes stomatal opening and closing under high temperatures and/or drought. In the context of global climate change, understanding how different stress signals converge on stomatal regulation allows the development of climate-change-ready crops.

摘要

植物不断响应变化的环境条件以防止受损并维持最佳性能。为了调节与环境的气体交换并控制非生物胁迫缓解,植物在其叶片表皮上有称为气孔的小孔。多种环境信号影响这些气孔的开闭。高温促进气孔开放(以降温),干旱诱导气孔关闭(以防止水分流失)。同时出现的胁迫条件可能引发相互冲突的气孔反应,但解决这些冲突的细胞机制尚不清楚。在这里,我们证明与高温相关的激酶温度靶点3直接控制质膜H-ATP酶的活性以诱导气孔开放。开放气孔1在干旱胁迫期间调节气孔关闭以防止水分流失,它通过磷酸化直接使温度靶点3失活。综上所述,该信号轴协调了高温和/或干旱条件下气孔的开闭。在全球气候变化的背景下,了解不同胁迫信号如何汇聚于气孔调节有助于培育适应气候变化的作物。

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本文引用的文献

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