Halitschke Rayko, Baldwin Ian T
Department of Molecular Ecology, Max Planck Institute for Chemical Ecology, Hans-Knöll-Str. 8, D-07745 Jena, Germany.
Plant J. 2003 Dec;36(6):794-807. doi: 10.1046/j.1365-313x.2003.01921.x.
Inhibition of jasmonic acid (JA) signaling has been shown to decrease herbivore resistance, but the responsible mechanisms are largely unknown because insect resistance is poorly understood in most model plant systems. We characterize three members of the lipoxygenase (LOX) gene family in the native tobacco plant Nicotiana attenuata and manipulate, by antisense expression, a specific, wound- and herbivory-induced isoform (LOX3) involved in JA biosynthesis. In three independent lines, antisense expression reduced wound-induced JA accumulation but not the release of green leaf volatiles (GLVs). The impaired JA signaling reduced two herbivore-induced direct defenses, nicotine and trypsin protease inhibitors (TPI), as well as the potent indirect defense, the release of volatile terpenes that attract generalist predators to feeding herbivores. All these defenses could be fully restored by methyl-JA (MeJA) treatment, with the exception of the increase in TPI activity, which was partially restored, suggesting the involvement of additional signals. The impaired ability to produce chemical defenses resulted in lower resistance to Manduca sexta attack, which could also be restored by MeJA treatment. Expression analysis using a cDNA microarray, specifically designed to analyze M. sexta-induced gene expression in N. attenuata, revealed a pivotal role for LOX3-produced oxylipins in upregulating defense genes (protease inhibitor, PI; xyloglucan endotransglucosylase/hydrolase, XTH; threonine deaminase, TD; hydroperoxide lyase, HPL), suppressing both downregulated growth genes (RUBISCO and photosystem II, PSII) and upregulated oxylipin genes (alpha-dioxygenase, alpha-DOX). By genetically manipulating signaling in a plant with a well-characterized ecology, we demonstrate that the complex phenotypic changes that mediate herbivore resistance are controlled by a specific part of the oxylipin cascade.
茉莉酸（JA）信号传导的抑制已被证明会降低植物对食草动物的抗性，但具体机制尚不清楚，因为在大多数模式植物系统中对昆虫抗性的了解较少。我们对野生烟草植物黄花烟草中的脂氧合酶（LOX）基因家族的三个成员进行了表征，并通过反义表达操作了一种参与JA生物合成的特定的、伤口和食草动物诱导的同工型（LOX3）。在三个独立的株系中，反义表达降低了伤口诱导的JA积累，但没有降低绿叶挥发物（GLV）的释放。受损的JA信号传导降低了两种食草动物诱导的直接防御物质，尼古丁和胰蛋白酶蛋白酶抑制剂（TPI），以及强效的间接防御物质，即挥发性萜类的释放，这些挥发性萜类会吸引多食性捕食者来捕食食草动物。除了TPI活性的增加部分恢复外，所有这些防御都可以通过甲基茉莉酸（MeJA）处理完全恢复，这表明还有其他信号参与其中。产生化学防御的能力受损导致对烟草天蛾攻击的抗性降低，这也可以通过MeJA处理恢复。使用专门设计用于分析烟草天蛾诱导的黄花烟草基因表达的cDNA微阵列进行的表达分析表明，LOX3产生的氧脂在上调防御基因（蛋白酶抑制剂，PI；木葡聚糖内转糖基酶/水解酶，XTH；苏氨酸脱氨酶，TD；氢过氧化物裂解酶，HPL）、抑制下调的生长基因（核酮糖-1,5-二磷酸羧化酶/加氧酶和光系统II，PSII）以及上调的氧脂基因（α-双加氧酶，α-DOX）方面起着关键作用。通过在具有特征明确的生态学的植物中进行遗传信号操作，我们证明介导食草动物抗性的复杂表型变化是由氧脂级联反应的特定部分控制的。
