Polyamine Oxidase Triggers H(2)O(2)-Mediated Spermidine Improved Oxidative Stress Tolerance of Tomato Seedlings Subjected to Saline-Alkaline Stress.
Polyamine Oxidase Triggers H(2)O(2)-Mediated Spermidine Improved Oxidative Stress Tolerance of Tomato Seedlings Subjected to Saline-Alkaline Stress.
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多胺氧化酶触发 H2O2 介导的亚精胺提高了遭受盐碱胁迫的番茄幼苗的氧化应激耐受性
DOI：
10.3390/ijms23031625
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发表时间：
2022-01-30
影响因子：
5.6
通讯作者：
Hu X
中科院分区：
文献类型：
--
作者：
Yang J;Wang P;Li S;Liu T;Hu X
盐碱胁迫是作物生产中的主要非生物胁迫之一。外源亚精胺（Spd）可通过减轻膜脂过氧化损伤，有效提高番茄的抗盐碱能力。然而，外源亚精胺预处理触发番茄抗氧化系统抵抗盐碱胁迫的机制尚不清楚。H_2O_2和多胺氧化酶（PAO）是否参与了Spd诱导的番茄耐盐碱性的研究尚需进一步证实。本文研究了PAO和H2 O2在外源Spd诱导番茄耐盐碱胁迫中的作用。结果表明，在盐碱胁迫下，施亚精胺可提高超氧化物歧化酶（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）的表达和活性，以及还原型抗坏血酸（阿萨）和谷胱甘肽（GSH）的比值。外源亚精胺处理引发内源H2 O2水平，SlPAO 4基因表达，以及PAO活性在正常条件下。用1，8-二氨基辛烷（1，8-DO，一种多胺氧化酶抑制剂）抑制内源PAO活性，可显著降低后期H2 O2水平。此外，抑制内源PAO或沉默SlPAO 4基因均增加了盐碱胁迫下番茄叶片的过氧化损伤。这些结果表明，外源Spd处理刺激SlPAO 4基因表达和PAO活性增加，介导的H2 O2水平的升高在正常条件下。因此，下游的抗氧化系统被激活，以消除过量的ROS积累，缓解膜脂过氧化损伤和生长抑制盐碱胁迫。总之，PAO引发H2 O2介导的Spd诱导的番茄耐盐碱胁迫的增加。
Saline-alkaline stress is one of several major abiotic stresses in crop production. Exogenous spermidine (Spd) can effectively increase tomato saline-alkaline stress resistance by relieving membrane lipid peroxidation damage. However, the mechanism through which exogenous Spd pre-treatment triggers the tomato antioxidant system to resist saline-alkaline stress remains unclear. Whether H2O2 and polyamine oxidase (PAO) are involved in Spd-induced tomato saline-alkaline stress tolerance needs to be determined. Here, we investigated the role of PAO and H2O2 in exogenous Spd-induced tolerance of tomato to saline-alkaline stress. Results showed that Spd application increased the expression and activities of superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX), glutathione reductase (GR), and the ratio of reduced ascorbate (AsA) and glutathione (GSH) contents under saline-alkaline stress condition. Exogenous Spd treatment triggered endogenous H2O2 levels, SlPAO4 gene expression, as well as PAO activity under normal conditions. Inhibiting endogenous PAO activity by 1,8-diaminooctane (1,8-DO, an inhibitor of polyamine oxidase) significantly reduced H2O2 levels in the later stage. Moreover, inhibiting endogenous PAO or silencing the SlPAO4 gene increased the peroxidation damage of tomato leaves under saline-alkaline stress. These findings indicated that exogenous Spd treatment stimulated SlPAO4 gene expression and increased PAO activity, which mediated the elevation of H2O2 level under normal conditions. Consequently, the downstream antioxidant system was activated to eliminate excessive ROS accumulation and relieve membrane lipid peroxidation damage and growth inhibition under saline-alkaline stress. In conclusion, PAO triggered H2O2-mediated Spd-induced increase in the tolerance of tomato to saline-alkaline stress.
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