NO is involved in JA- and H2O2-mediated ALA-induced oxidative stress tolerance at low temperatures in tomato
NO is involved in JA- and H2O2-mediated ALA-induced oxidative stress tolerance at low temperatures in tomato
复制标题
NO 参与 JA 和 H2O2 介导的 ALA 诱导的番茄低温氧化应激耐受性
DOI：
10.1016/j.envexpbot.2018.10.020
复制
发表时间：
2019-05-01
影响因子：
5.7
通讯作者：
Hu, Xiaohui
中科院分区：
文献类型：
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作者：
Liu, Tao;Xu, Jiaojiao;Hu, Xiaohui
低温是华北地区早春和冬季番茄生产的限制因子。植物通过激活冷敏感信号通路感知低温，从而上调冷应答基因的表达，提高植物的耐冷性。许多研究报道，5-氨基乙酰丙酸（ALA）保护植物免受环境胁迫。我们发现ALA预处理通过过氧化氢（H2 O2）信号和随后的氧化还原信号的串扰增强番茄低温引发的氧化应激耐受性。本研究以番茄为材料，研究了ALA是否诱导茉莉酸（JA）和一氧化氮（NO）信号通路，并探讨了JA、NO和H2 O2之间的关系。用JA合成抑制剂[水杨基异羟肟酸（SHAM）和二乙基二硫代氨基甲酸（DIECA）]或NO合成抑制剂[钨酸盐和NG-硝基-L-精氨酸甲酯（L-NAME）]以及NO清除剂[2-（4-羧基苯基）-4，4，5，5-四甲基咪唑啉-1-氧基-3-氧化物（cPTIO）]或H2 O2 [二甲基硫脲（DMTU）]预处理番茄植株。然后，用外源ALA、JA或H2 O2处理这些植株。结果表明，ALA显著提高了正常和低温条件下的JA水平。外源JA和H_2O_2显著提高了超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、抗坏血酸过氧化物酶（APX）和谷胱甘肽还原酶（GR）的活性，降低了膜脂过氧化作用。JA合成抑制剂SHAM和DIECA没有显着影响膜脂损伤和SOD，CAT和GR活性，与单独冷处理的植物相比。而ALA则显著减弱SHAM和DIECA的抑制作用。相反，JA和H2 O2减轻了DMTU-，SHAM-和DIECA-介导的抗氧化降低。ALA、JA和H2 O2上调硝酸还原酶（NR）和一氧化氮合酶（NOS）的转录水平以及NR和NOS活性，从而触发NO爆发。cPTIO、钨酸盐和L-NAME均能减弱JA介导的抗氧化酶活性，并基本消除H_2O_2介导的抗氧化酶活性，减轻膜脂损伤。这些结果表明，ALA诱导的H_2O_2和JA在调节番茄抗氧化中表现出独立但协同的作用。NO可能与JA一起沿着作用于H2 O2的下游，调节抗氧化酶基因的表达，提高番茄的耐冷性。NO是H2 O2的下游信号，与JA协同作用，介导ALA调节番茄低温氧化胁迫耐受性。
Low temperature is a limiting factor in tomato production during early spring and winter in North China. Plants perceive low temperature through activation of cold-sensitive signaling pathways, which up-regulate cold-responsive gene expression and increase plant cold tolerance. Many studies reported that 5-aminolevulinic acid (ALA) protect plants against environmental stresses. We showed that ALA pretreatment enhanced cold-triggered oxidative stress tolerance in tomato via hydrogen peroxide (H2O2) signaling and subsequent cross-talk with redox signals. Here, we investigated whether ALA induced the jasmonic acid (JA) and nitric oxide (NO) signaling in response to cold stress in tomato, and evaluated the relationships between JA, NO, and H2O2. Tomato plants were pretreated with inhibitors of JA synthesis [salicylhydroxamic acid (SHAM) and diethyldithiocarbamic acid (DIECA)] or NO synthesis [tungstate and NG-nitro-L-arginine methyl ester (L-NAME)] as well as scavengers of NO [2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO)] or H2O2 [dimethylthiourea (DMTU)]. Then, these plants were treated with exogenous ALA, JA, or H2O2. Finally, plants were grown under normal or low temperature conditions, The results showed that ALA dramatically elevated JA levels under normal-and low-temperature conditions. Exogenous JA and H2O2 dramatically increased superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX), and glutathione reductase (GR) activities and reduced membrane lipid peroxidation. The JA synthesis inhibitors SHAM and DIECA did not significantly affect membrane lipid damage and SOD, CAT, and GR activities, compared with cold-treated plants alone. Whereas ALA significantly attenuated the inhibition effects of SHAM and DIECA. In contrast, JA and H2O2 mitigated the DMTU-, SHAM-, and DIECA-mediated reduction in antioxidation. ALA, JA, and H2O2 up-regulated nitrate reductase (NR) and nitric oxide synthase (NOS) transcript levels and NR and NOS activities, thereby triggering the NO bust. cPTIO, tungstate and L-NAME weakened JA-mediated, and essentially abolished H2O2-mediated antioxidase activity and mitigated membrane lipid damage. These results indicate that ALA induced H2O2 and JA displayed independent but synergistic roles in regulating tomato antioxidation. NO may act downstream of H2O2 along with JA to regulate antioxidant enzyme gene expression and increase tomato cold tolerance. In conclusion, NO is a downstream signal of H2O2 which cooperated with JA, mediated ALA-regulated oxidative stress tolerance under low temperatures in tomato.