Division of Agricultural and Life Science, Graduate School of Environmental and Life Science, Okayama University Okayama, Japan.
Front Plant Sci. 2013 Nov 20;4:472. doi: 10.3389/fpls.2013.00472. eCollection 2013.
The phytohormone abscisic acid (ABA) induces stomatal closure in response to drought stress, leading to reduction of transpirational water loss. A thiol tripeptide glutathione (GSH) is an important regulator of cellular redox homeostasis in plants. Although it has been shown that cellular redox state of guard cells controls ABA-mediated stomatal closure, roles of GSH in guard cell ABA signaling were largely unknown. Recently we demonstrated that GSH functions as a negative regulator of ABA signaling in guard cells. In this study we performed more detailed analyses to reveal how GSH regulates guard cell ABA signaling using the GSH-deficient Arabidopsis mutant cad2-1. The cad2-1 mutant exhibited reduced water loss from rosette leaves. Whole-cell current recording using patch clamp technique revealed that the cad2-1 mutation did not affect ABA regulation of S-type anion channels. We found enhanced activation of Ca(2+) permeable channels by hydrogen peroxide (H2O2) in cad2-1 guard cells. The cad2-1 mutant showed enhanced H2O2-induced stomatal closure and significant increase of ROS accumulation in whole leaves in response to ABA. Our findings provide a new understanding of guard cell ABA signaling and a new strategy to improve plant drought tolerance.
植物激素脱落酸(ABA)响应干旱胁迫诱导气孔关闭,从而减少蒸腾失水。硫醇三肽谷胱甘肽(GSH)是植物细胞氧化还原稳态的重要调节剂。尽管已经表明保卫细胞的细胞氧化还原状态控制着 ABA 介导的气孔关闭,但 GSH 在保卫细胞 ABA 信号转导中的作用在很大程度上尚不清楚。最近我们证明 GSH 作为保卫细胞 ABA 信号转导的负调节剂发挥作用。在这项研究中,我们使用 GSH 缺陷型拟南芥突变体 cad2-1 进行了更详细的分析,以揭示 GSH 如何调节保卫细胞 ABA 信号转导。cad2-1 突变体表现出从莲座叶中减少的水分损失。使用膜片钳技术进行全细胞电流记录表明,cad2-1 突变不影响 ABA 对 S 型阴离子通道的调节。我们发现 cad2-1 保卫细胞中过氧化氢(H2O2)诱导的 Ca2+渗透性通道的激活增强。cad2-1 突变体在响应 ABA 时表现出增强的 H2O2 诱导的气孔关闭和整个叶片中 ROS 积累的显著增加。我们的发现为保卫细胞 ABA 信号转导提供了新的认识,并为提高植物耐旱性提供了新的策略。