Ozone-induced cell death occurs via two distinct mechanisms in Arabidopsis:: the role of salicylic acid
Ozone-induced cell death occurs via two distinct mechanisms in Arabidopsis:: the role of salicylic acid
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DOI：
10.1046/j.1365-313x.1999.00400.x
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发表时间：
1999-03-01
期刊：
影响因子：
7.2
通讯作者：
Davis, KR
中科院分区：
文献类型：
--
作者：
Rao, MV;Davis, KR
为了进一步明确水杨酸在O-3诱导的植物响应中的作用，我们比较了两个积累了不同量水杨酸的拟南芥基因型和一个表达水杨酸羟化酶（NahG）的SA缺陷型转基因Col-0系对O-3的响应。在O-3诱导的SA水平的变化，活性氧的积累，防御基因的表达，以及病变形成的动力学和严重程度的差异表明，SA通过两种不同的机制影响O-3耐受性。详细的分析表明，与过敏反应（HR）的功能显着更大的O-3暴露Cvi-0比Col-0，NahG植物未能表现出这些HR样的反应。此外，Os-induced抗氧化防御，包括谷胱甘肽的氧化还原状态，大大减少了NahG植物相比，Col-0和Cvi-0。这表明，O-3诱导的细胞死亡NahG植物是由于SA介导的增强抗氧化防御的损失，而OS诱导的细胞死亡Cvi-0是由于激活的HR。这一假设是支持的观察，抑制NADPH氧化酶减少O-3诱导的H2 O2水平和O-3诱导的细胞死亡Cvi-0，而没有观察到重大变化NahG植物。我们的结论是，虽然SA是需要维持细胞的氧化还原状态和增强防御反应在O-3暴露的植物，高水平的SA也增强激活的氧化爆发和细胞死亡途径，导致明显的O-3敏感性。
Previous studies suggest that salicylic acid (SA) plays an important role in influencing plant resistance to ozone (O-3) TO further define the role of SA in O-3-induced responses, we compared the responses of two Arabidopsis genotypes that accumulate different amounts of SA in response to O-3 and a SA-deficient transgenic Col-0 line expressing salicylate hydroxylase (NahG). The differences observed in O-3-induced changes in SA levels, the accumulation of active oxygen species, defense gene expression, and the kinetics and severity of lesion formation indicate that SA influences O-3 tolerance via two distinct mechanisms. Detailed analyses indicated that features associated with a hypersensitive response (HR) were significantly greater in O-3-exposed Cvi-0 than in Col-0, and that NahG plants failed to exhibit these HR-like responses. Furthermore, Os-induced antioxidant defenses, including the redox state of glutathione, were greatly reduced in NahG plants compared to Col-0 and Cvi-0. This suggests that O-3-induced cell death in NahG plants is due to the loss of SA-mediated potentiation of antioxidant defenses, while Os-induced cell death in Cvi-0 is due to activation of a HR. This hypothesis is supported by the observation that inhibition of NADPH-oxidases reduced O-3-induced H2O2 levels and the O-3-induced cell death in Cvi-0, while no major changes were observed in NahG plants. We conclude that although SA is required to maintain the cellular redox state and potentiate defense responses in O-3 exposed plants, high levels of SA also potentiate activation of an oxidative burst and a cell death pathway that results in apparent O-3 sensitivity.