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首页> 外文期刊>Chinese science bulletin >Nitric oxide mediates the fungal elicitor-induced Taxol biosynthesis of Taxus chinensis suspension cells through the reactive oxygen species-dependent and -independent signal pathways
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Nitric oxide mediates the fungal elicitor-induced Taxol biosynthesis of Taxus chinensis suspension cells through the reactive oxygen species-dependent and -independent signal pathways

机译：一氧化氮通过依赖于活性氧和不依赖于活性氧的信号途径介导真菌激发子诱导的红豆杉悬浮细胞生物合成

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摘要

Nitric oxide and reactive oxygen species are two important signal molecules that play key roles in plant defense responses. Nitric oxide generation and oxidative burst and accumulation of reactive oxygen species are the early reactions of Taxus chinensis suspension cells to fungal elicitor prepared from the cell walls of Penicillium citrinum. In order to investigate the relationship and/or interactions of nitric oxide and reactive oxygen species in the eliei-tor-induced Taxol biosynthesis of T. chinensis suspension cells, we treated the cells with nitric oxide specific scavenger 2-4-carboxyphenyl-4,4,5,5-tetra-methylimidazoline-1-oxyl-3-oxide (cPITO), nitric oxide synthase inhibitor S,S'-1,3-phenylene-bis(1,2-eth-anediyl)-bis-isothiourea (PBITU), membrane NAD(P) H oxidase inhibitor diphenylene iodonium (DPI), su-peroxide dismutases (SOD) and catalase. The results show that pretreatment of T. chinensis cells with cPITO and DPI inhibited not only the elicitor-induced nitric oxide biosynthesis and oxidative burst, but also the elicitor-induced Taxol production, suggesting that both nitric oxide and reactive oxygen species are involved in elicitor-induced Taxol biosynthesis. Furthermore, pretreatment of the cells with cPITO and PBITU suppressed the elicitor-induced oxidative burst, indicating that the oxidative burst might be dependent on NO. Application of nitric oxide via its donor sodium nitroprusside (SNP) triggered Taxol biosynthesis of T. chinensis cells. The nitric ox-ide-induced Taxol production was suppressed by DPI, showing that the -oxidative burst is involved in' NO-triggered Taxoi biosynthesis. However, nitric oxide and the fungal eiicitor induced Taxol biosynthesis even though the accumulation of reactive oxygen species wass completely abolished in T, chinensis cells. Our data show that nitric oxide may mediate the elicitor-induced Taxol biosynthesis of T. chinensis suspension ceils through both reactive oxygen species-dependent and -independent signal pathways. Moreover, the results of our work show that the elicitor- and nitric oxide-induced Taxol biosynthesis is inhibited by catalase, indicating that H_2O_2 from the oxidative burst might be the signal molecule involved in induced Taxol production of T. chinensis cells.
机译：一氧化氮和活性氧是在植物防御反应中起关键作用的两个重要信号分子。一氧化氮的产生，氧化性爆发和活性氧的积累是红豆杉悬浮细胞对由柠檬青霉细胞壁制备的真菌激发子的早期反应。为了研究一氧化氮诱导的紫杉悬浮细胞的紫杉醇生物合成中一氧化氮与活性氧之间的关系和/或相互作用，我们用一氧化氮特异性清除剂2-4-羧苯基-4处理了这些细胞， 4,5,5-四甲基咪唑啉-1-氧基-3-氧化物（cPITO），一氧化氮合酶抑制剂S，S'-1,3-亚苯基-双（1,2-乙基-乙二基）-双-异硫脲（PBITU），膜NAD（P）H氧化酶抑制剂二亚苯基碘鎓（DPI），超氧化物歧化酶（SOD）和过氧化氢酶。结果表明，用cPITO和DPI预处理中华绒螯蟹细胞不仅抑制了诱导子诱导的一氧化氮的生物合成和氧化爆发，而且还抑制了诱导子诱导的紫杉醇的产生，表明一氧化氮和活性氧都参与了诱导子。诱导的紫杉醇的生物合成。此外，用cPITO和PBITU对细胞进行预处理可抑制激发子诱导的氧化爆发，表明氧化爆发可能取决于NO。一氧化氮通过其供体硝普钠（SNP）的应用触发了紫杉醇的紫杉醇生物合成。 DPI抑制了一氧化氮诱导的紫杉醇的产生，表明-氧化爆发与NO触发的紫杉生物合成有关。然而，即使完全消除了中华绒螯蟹细胞中活性氧的积累，一氧化氮和真菌激发剂仍能诱导紫杉醇的生物合成。我们的数据表明，一氧化氮可能通过反应性氧物种依赖性和非依赖性氧信号通路介导激发子诱导的紫杉悬浮细胞的生物合成。此外，我们的工作结果表明，过氧化氢酶抑制了引发剂和一氧化氮诱导的紫杉醇的生物合成，表明来自氧化爆发的H_2O_2可能是诱导中华induced紫杉醇产生的信号分子。

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