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乙烯和过氧化氢参与盐处理拟南芥愈伤组织中替代呼吸途径的诱导。

Involvement of ethylene and hydrogen peroxide in induction of alternative respiratory pathway in salt-treated Arabidopsis calluses.

机构信息

Key Laboratory of Arid and Grassland Agroecology (Ministry of Education), School of Life Sciences, Lanzhou University, Lanzhou 730000, PR China.

出版信息

Plant Cell Physiol. 2010 Oct;51(10):1754-65. doi: 10.1093/pcp/pcq134. Epub 2010 Aug 27.

Abstract

The role of ethylene and hydrogen peroxide (H₂O₂) in the induction of the alternative respiratory pathway (AP) in calluses from wild-type (WT) Arabidopsis and ethylene-insensitive mutant etr1-3 under salt stress was investigated. The capacity and the contribution of the AP to the total respiration were significantly induced by 100 mM sodium chloride (NaCl) in WT calluses but only slightly induced in etr1-3 calluses. Ethylene emission was enhanced in WT calluses under salt stress. Application of 1-aminocyclopropane-1-carboxylic acid (an ethylene precursor) further increased the AP capacity in WT calluses but not in etr1-3 calluses under salt stress. Reduction of ethylene production by aminooxyacetic acid (AOA, an ethylene biosynthesis inhibitor) in WT calluses eliminated the NaCl-induced increase of ethylene emission and inhibited AP induction under salt stress, suggesting that ethylene is required for AP induction. H₂O₂ enhanced ethylene production while ethylene reduced H₂O₂ generation in WT calluses under salt stress. In addition, ethylene and H₂O₂ modulated NaCl-induced alternative oxidase gene (AOX1a) expression and the increase in pyruvate content in WT calluses. Inhibition of the AP by salicylhydroxamic acid in WT calluses under salt stress resulted in severe cellular damage as indicated by the high content of H₂O₂, malondialdehyde and more electrolyte leakage. Taken together, ethylene and H₂O₂ are involved in the salt-induced increase of the AP, which plays an important role in salt tolerance in WT calluses, and ethylene may be acting downstream of H₂O₂.

摘要

在盐胁迫下,研究了乙烯和过氧化氢(H₂O₂)在野生型(WT)拟南芥和乙烯不敏感突变体 etr1-3 愈伤组织中诱导替代呼吸途径(AP)中的作用。100mM 氯化钠(NaCl)显著诱导 WT 愈伤组织中 AP 的容量和对总呼吸的贡献,但仅轻度诱导 etr1-3 愈伤组织中 AP 的容量。盐胁迫下,WT 愈伤组织中乙烯的排放增强。在盐胁迫下,1-氨基环丙烷-1-羧酸(乙烯前体)的应用进一步增加了 WT 愈伤组织中 AP 的容量,但在 etr1-3 愈伤组织中没有增加。WT 愈伤组织中氨基酸氧乙酸(AOA,乙烯生物合成抑制剂)对乙烯产生的还原消除了 NaCl 诱导的乙烯排放增加,并抑制了盐胁迫下 AP 的诱导,表明乙烯是 AP 诱导所必需的。在盐胁迫下,H₂O₂增强了乙烯的产生,而乙烯减少了 WT 愈伤组织中 H₂O₂的产生。此外,乙烯和 H₂O₂调节盐胁迫下 WT 愈伤组织中替代氧化酶基因(AOX1a)的表达和丙酮酸含量的增加。在盐胁迫下,WT 愈伤组织中 AP 的水杨羟肟酸抑制导致细胞严重损伤,表现为 H₂O₂、丙二醛含量较高和电解质泄漏增加。总之,乙烯和 H₂O₂参与了盐诱导的 AP 增加,AP 在 WT 愈伤组织的耐盐性中起重要作用,并且乙烯可能在 H₂O₂的下游起作用。

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