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阿司匹林和水杨酸对亚麻叶片伤口诱导的丙二烯氧化物合酶转录本积累的抑制作用。

Inhibition of wound-induced accumulation of allene oxide synthase transcripts in flax leaves by aspirin and salicylic acid.

作者信息

Harms K, Ramirez I, Pena-Cortes H

机构信息

Max-Planck-Institut for Molecular Plant Physiology, Karl-Liebknecht-Strasse 25, Haus 20, D-14476 Golm, Germany (K.H.).

出版信息

Plant Physiol. 1998 Nov;118(3):1057-65. doi: 10.1104/pp.118.3.1057.

DOI:10.1104/pp.118.3.1057
PMID:9808751
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC34779/
Abstract

Allene oxide synthase (AOS) mediates the conversion of lipoxygenase-derived fatty acid hydroperoxides to unstable allene epoxides, which supply the precursors for the synthesis of the phytohormone jasmonic acid (JA). In this study the characterization of AOS gene expression in flax (Linum usitatissimum) is reported. AOS was constitutively expressed in different organs of flax plants. Additionally, AOS gene expression was enhanced after mechanical wounding in both the directly damaged leaves and in the systemic tissue located distal to the treated leaves. This wound-induced accumulation of AOS required the de novo biosynthesis of other unknown proteins involved in the signaling pathway modulating wound-induced AOS gene expression. Furthermore, the wound-induced AOS mRNA accumulation was correlated with the increase in the levels of JA. Both JA and its precursor, 12-oxo-phytodienoic acid, activated AOS gene expression in a dose-dependent manner. Thus, JA could activate its own biosynthetic pathway in flax leaves. Moreover, neither salicylic acid (SA) nor aspirin influenced AOS enzymatic activity. It is interesting that pretreatment with SA or aspirin inhibited wound-induced accumulation of AOS transcripts. These results suggest that a potent inhibition of JA biosynthetic capacity in leaves can be affected by SA or aspirin at the level of AOS gene expression.

摘要

丙二烯氧化物合酶(AOS)介导脂氧合酶衍生的脂肪酸氢过氧化物向不稳定的丙二烯环氧化物的转化,这些丙二烯环氧化物为植物激素茉莉酸(JA)的合成提供前体。在本研究中,报道了亚麻(Linum usitatissimum)中AOS基因表达的特征。AOS在亚麻植株的不同器官中组成性表达。此外,在直接受损叶片以及处理叶片远端的系统组织中,机械损伤后AOS基因表达增强。这种伤口诱导的AOS积累需要从头合成参与调节伤口诱导的AOS基因表达信号通路的其他未知蛋白质。此外,伤口诱导的AOS mRNA积累与JA水平的增加相关。JA及其前体12-氧代-植物二烯酸均以剂量依赖性方式激活AOS基因表达。因此,JA可以激活亚麻叶片中其自身的生物合成途径。此外,水杨酸(SA)和阿司匹林均不影响AOS酶活性。有趣的是,用SA或阿司匹林预处理可抑制伤口诱导的AOS转录本积累。这些结果表明,SA或阿司匹林可在AOS基因表达水平上有效抑制叶片中JA的生物合成能力。

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