New insights into the early biochemical activation of jasmonic acid biosynthesis in leaves
New insights into the early biochemical activation of jasmonic acid biosynthesis in leaves
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DOI：
10.4161/psb.5.3.10713
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发表时间：
2010-01-01
影响因子：
2.9
通讯作者：
Baldwin, Ian T.
中科院分区：
文献类型：
--
作者：
Bonaventure, Gustavo;Baldwin, Ian T.
在植物中，植食动物的攻击促进了茉莉酸（JA）的快速积累，这是由组成型表达的生物合成酶激活的结果。控制JA生物合成激活的分子机制在很大程度上仍然未知，但新的研究已经阐明了参与这一过程的一些早期调控成分。衰减烟草（Nicotiana attenuata）是一种野生烟草，其天然食草动物烟草天蛾（Manduca sexta）的口腔分泌物中含有脂肪酸氨基酸结合物（FAC）诱导子，烟草植物对FAC诱导子的应答是通过引发针对FAC诱导子的特异性防御和耐受性反应来实现的;迄今为止已知的所有防御反应都需要创伤诱导JA增加的放大。我们最近证明，这种FAC引起的JA爆发需要增加的游离亚麻酸（18：3）的流量，可能源于质体甘油脂酶（GLA 1）的激活，该酶被昆虫口腔分泌物中发现的丰富的FAC，N-亚麻酰谷氨酸（18：3-Glu）激活。诱导后游离18：3的缺乏表明，在N. attenuata叶子此外，水杨酸诱导的蛋白激酶（SIPK）和PR-1的非表达子（NPR 1）参与了这种控制18：3供应的激活机制。相比之下，创伤诱导蛋白激酶（WIPK）不调节13（S）-氢过氧-18：3转化为12-氧代-植物二烯酸（OPDA）。这些结果打开了新的视角的信号和调控成分诱导JA生物合成途径的复杂网络。
In plants, herbivore attack elicits the rapid accumulation of jasmonic acid (JA) which results from the activation of constitutively expressed biosynthetic enzymes. The molecular mechanisms controlling the activation of JA biosynthesis remain largely unknown however new research has elucidated some of the early regulatory components involved in this process. Nicotiana attenuata plants, a wild tobacco species, responds to fatty acid amino acid conjuguates (FAC) elicitors in the oral secretion of its natural herbivore, Manduca sexta, by triggering specific defense and tolerance responses against it; all of the defense responses known to date require the amplification of the wound-induced JA increase. We recently demonstrated that this FAC-elicited JA burst requires an increased flux of free linolenic acid (18: 3) likely originating from the activation of a plastidial glycerolipase (GLA1) which is activated by an abundant FAC found in insect oral secretions, N-linolenoyl-glutamate (18:3-Glu). The lack of accumulation of free 18: 3 after elicitation suggests a tight physical association between GLA1 and LOX3 in N. attenuata leaves. In addition, the salicylate-induced protein kinase (SIPK) and the nonexpressor of PR-1 (NPR1) participate in this activation mechanism that controls the supply of 18:3. In contrast, the wound-induced protein kinase (WIPK) does not but instead regulates the conversion of 13(S)-hydroperoxy-18: 3 into 12-oxo-phytodienoic acid (OPDA). These results open new perspectives on the complex network of signals and regulatory components inducing the JA biosynthetic pathway.