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干旱胁迫通过引发12-氧植物二烯酸(12-OPDA)作为气孔孔径的有效调节剂来调节氧脂素特征。

Drought stress modulates oxylipin signature by eliciting 12-OPDA as a potent regulator of stomatal aperture.

作者信息

Savchenko Tatyana, Dehesh Katayoon

机构信息

Department of Plant Biology; University of California; Davis, CA USA.

出版信息

Plant Signal Behav. 2014;9(4):e28304. doi: 10.4161/psb.28304. Epub 2014 Mar 10.

Abstract

Through evolution, plants have developed a myriad of strategies to adapt to environmental perturbations. Using 3 Arabidopsis ecotypes in conjunction with various transgenic and mutant lines, we provide evidence that wounding and drought differentially alter the metabolic signatures derived from the 2 main competing oxylipin-pathway branches, namely the JA and its precursor 12-OPDA produced by Allene oxide synthase (AOS) branch, and aldehydes and corresponding alcohols generated by Hydroperoxide lyase (HPL) branch. Specifically, we show that wounding induces production of both HPL and AOS-derived metabolites whereas, drought stress only elicits production of hexenal but suppresses hexenol, and further uncouples the conversion of 12-OPDA to JA. This finding led to uncovering of 12-OPDA as a functional convergence point of oxylipin and ABA pathways to control stomatal aperture in plant adaptive responses to drought. In addition, using transgenic lines overexpressing plastidial and extraplastidial HPL enzyme establish the strong interdependence of AOS- and HPL-branch pathways, and the importance of this linkage in tailoring plant adaptive responses to the nature of perturbations.

摘要

通过进化,植物已经发展出无数策略来适应环境扰动。我们使用3种拟南芥生态型以及各种转基因和突变株系,证明了创伤和干旱会以不同方式改变源自两条主要相互竞争的氧化脂质途径分支的代谢特征,即茉莉酸(JA)及其由丙二烯氧化物合酶(AOS)分支产生的前体12-氧植物二烯酸(12-OPDA),以及由氢过氧化物裂解酶(HPL)分支产生的醛类和相应的醇类。具体而言,我们发现创伤会诱导HPL和AOS衍生代谢物的产生,而干旱胁迫仅引发己醛的产生但抑制己烯醇,并进一步解偶联12-OPDA向JA的转化。这一发现揭示了12-OPDA是氧化脂质和脱落酸(ABA)途径在植物对干旱的适应性反应中控制气孔开度的功能汇聚点。此外,使用过表达质体和质体外HPL酶的转基因株系,确立了AOS和HPL分支途径的强烈相互依赖性,以及这种联系在根据扰动性质调整植物适应性反应中的重要性。

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