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Methyl Jasmonate-Induced Lipidomic and Biochemical Alterations in the Intertidal Macroalga Gracilaria dura (Gracilariaceae Rhodophyta)

机译:茉莉酸甲酯诱导潮间带Macroalga Gracilaria dura(GracilariaceaeRhodophyta)的血脂和生化变化。

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摘要

The role of exogenously added methyl jasmonate (MeJA), a lipid-derived signaling compound, in inducing oxidative stress in the marine red macroalga Gracilaria dura was investigated. MeJA at a concentration of 1–100 µM was a strong stimulant of reactive oxygen species (H2O2, HO· and O2·−) (P < 0.05) causing considerable oxidative stress in G. dura. This further led to lipid peroxidation and degradation of the pigments Chl a and phycocyanin, with a concomitant increase in phycoerythrin. The MeJA-induced oxidative burst also led to the induction of a fatty acid oxidation cascade, resulting in the synthesis of hydroxy-oxylipins and the up-regulation of the 13-lipoxygenase pathway. Electrospray ionization-mass spectrometry-based shotgun lipidomic analysis revealed that monogalactosyldiacylglycerol (a chloroplastic glycerolipid) and phosphatidylcholine (extrachloroplastidic phopholipid) were the most affected lipid classes. The degradation of 18:3-fatty acid-containing monogalactosyldiacylglycerol inferred that it provided fatty acyl chains for the biosynthesis of 13-hydroperoxylinolenic acid, which was further directed towards either the jasmonate pathway or other alternative pathways of the fatty acid oxidation cascade, analogous to higher plants. Also, G. dura modulated the lipid acyl chains in such a way that no significant change was observed in the fatty acid profile of the treated thalli as compared with those of the control, except for C16:0, C16:1 (n-9), C20:3 (n-6) and C20:4 (n-6) (P < 0.05). Furthermore, MeJA caused the accumulation of phenolic compounds and the up-regulation of enzymes involved in secondary metabolism such as polyphenol oxidase, shikimate dehydrogenase and phenylalanine ammonia-lyase, indicating a shift towards secondary metabolism as a defense strategy to combat the induced oxidative stress.
机译:研究了外源添加的茉莉酸甲酯(MeJA),一种脂质衍生的信号化合物,在海洋红巨藻硬脑膜中诱导氧化应激的作用。浓度为1–100 µM的MeJA是一种强烈的活性氧(H2O2,HO·和O 2 ·-)刺激物(P <0.05),引起大量的氧化硬脑膜的压力。这进一步导致脂质Chl a和藻蓝蛋白的脂质过氧化作用和降解,并伴随藻红蛋白的增加。 MeJA诱导的氧化爆发也导致了脂肪酸氧化级联反应的诱导,导致了羟基-脂蛋白的合成和13-脂氧化酶途径的上调。基于电喷雾电离质谱的shot弹枪脂质组学分析显示,单半乳糖基二酰基甘油(一种氯塑性甘油脂)和磷脂酰胆碱(一种超氯塑性磷脂)是受影响最大的脂质类别。包含18:3-脂肪酸的单半乳糖基二酰基甘油的降解表明它为13-氢过氧亚麻酸的生物合成提供了脂肪酰基链,该脂肪酰基链进一步针对了茉莉酸酯途径或脂肪酸氧化级联反应的其他替代途径,类似于高等植物。另外,硬脑膜梭菌以这样的方式调节脂质酰基链:除了C16:0,C16:1(n-9)外,与对照相比,处理过的thalli的脂肪酸谱没有显着变化。 ),C20:3(n-6)和C20:4(n-6)(P <0.05)。此外,MeJA引起酚类化合物的积累和涉及次级代谢的酶(例如多酚氧化酶,sh草酸脱氢酶和苯丙氨酸氨裂合酶)的上调,表明向次级代谢的转变已成为对抗诱导的氧化应激的防御策略。

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