Lipid Profiling of the Arabidopsis Hypersensitive Response Reveals Specific Lipid Peroxidation and Fragmentation Processes: Biogenesis of Pimelic and Azelaic Acid1[C][W]
Lipid Profiling of the Arabidopsis Hypersensitive Response Reveals Specific Lipid Peroxidation and Fragmentation Processes: Biogenesis of Pimelic and Azelaic Acid1[C][W]
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DOI：
10.1104/pp.112.202846
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发表时间：
2012-07
期刊：
影响因子：
7.4
通讯作者：
M. Zoeller;Nadja E. Stingl;Markus Krischke;Á. Fekete;F. Waller;S. Berger;Martin J. Mueller
中科院分区：
文献类型：
--
作者：
M. Zoeller;Nadja E. Stingl;Markus Krischke;Á. Fekete;F. Waller;S. Berger;Martin J. Mueller
脂质过氧化（LPO）是由多种非生物和生物胁迫引起的。虽然LPO参与多种信号传导过程，但对其氧化机制和主要脂质靶点知之甚少。对拟南芥（拟南芥）与丁香假单胞菌相互作用中LPO的系统脂质组学分析表明，LPO主要局限于含有半乳糖脂和甘油三酯的质体脂质，并在程序性细胞死亡之前发生。在基础条件下，单线态氧被确定为脂质氧化的主要原因，而13-脂氧合酶（LOX2）和自由基催化的脂质氧化在病原体感染后显著增加。对lox2突变体的分析表明，lox2是酶促膜过氧化所必需的，而不是病原体诱导的游离茉莉酸的产生。尽管质体脂质有大量氧化修饰，但感染后非氧化脂质水平显著增加。病原体感染也会引起碎片性脂质的积累。对9-脂氧合酶和LOX2缺陷突变体的分析表明，半乳糖脂质断裂与LOXs无关。我们提供了强有力的体内证据，证明自由基催化的半乳糖脂断裂机制负责形成必需生物素前体戊二酸和壬二酸，这是先前假设的启动拟南芥的免疫反应。我们的研究结果表明，壬二酸是LPO的一般标记物，而不是一般的免疫信号。提出的断裂机制使病原体诱导的自由基扩增和亲电信号（如植物蛋白酶、丙二醛和己烯醛）在质体中的形成合理化。
Lipid peroxidation (LPO) is induced by a variety of abiotic and biotic stresses. Although LPO is involved in diverse signaling processes, little is known about the oxidation mechanisms and major lipid targets. A systematic lipidomics analysis of LPO in the interaction of Arabidopsis (Arabidopsis thaliana) with Pseudomonas syringae revealed that LPO is predominantly confined to plastid lipids comprising galactolipid and triacylglyceride species and precedes programmed cell death. Singlet oxygen was identified as the major cause of lipid oxidation under basal conditions, while a 13-lipoxygenase (LOX2) and free radical-catalyzed lipid oxidation substantially contribute to the increase upon pathogen infection. Analysis of lox2 mutants revealed that LOX2 is essential for enzymatic membrane peroxidation but not for the pathogen-induced free jasmonate production. Despite massive oxidative modification of plastid lipids, levels of nonoxidized lipids dramatically increased after infection. Pathogen infection also induced an accumulation of fragmented lipids. Analysis of mutants defective in 9-lipoxygenases and LOX2 showed that galactolipid fragmentation is independent of LOXs. We provide strong in vivo evidence for a free radical-catalyzed galactolipid fragmentation mechanism responsible for the formation of the essential biotin precursor pimelic acid as well as of azelaic acid, which was previously postulated to prime the immune response of Arabidopsis. Our results suggest that azelaic acid is a general marker for LPO rather than a general immune signal. The proposed fragmentation mechanism rationalizes the pathogen-induced radical amplification and formation of electrophile signals such as phytoprostanes, malondialdehyde, and hexenal in plastids.