Changes in hydrogen peroxide homeostasis trigger an active cell death process in tobacco
Changes in hydrogen peroxide homeostasis trigger an active cell death process in tobacco
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DOI：
10.1046/j.1365-313x.2003.01655.x
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发表时间：
2003-02-01
期刊：
影响因子：
7.2
通讯作者：
Van Breusegem, F
中科院分区：
文献类型：
--
作者：
Dat, JF;Pellinen, R;Van Breusegem, F
在过氧化氢酶活性降低的转基因烟草植株中，高水平的过氧化氢（H-2 O-2）可在光呼吸条件下积累。这种对H-2 O-2内稳态的扰动诱导了栅栏薄壁细胞群的细胞死亡，主要是沿着脉.超微结构的改变，如染色质凝聚和线粒体完整性的破坏，发生在细胞死亡之前。此外，增强的线粒体防御基因的转录水平伴随着这些线粒体的变化。药理学数据表明，细胞死亡的启动和执行需要从头蛋白质合成，并且导致细胞死亡的信号转导途径涉及离子稳态的变化、（去）磷酸化事件和氧化爆发，如在过敏反应期间所观察到的。这种氧化酶依赖的氧化爆发是细胞死亡所必需的，但它不是防御蛋白的积累所必需的，这表明氧化爆发在非生物胁迫诱导的细胞死亡中具有更突出的作用。
In transgenic tobacco plants with reduced catalase activity, high levels of hydrogen peroxide (H-2 O-2 ) can accumulate under photorespiratory conditions. Such a perturbation in H-2 O-2 homeostasis induced cell death in clusters of palisade parenchyma cells, primarily along the veins. Ultrastructural alterations, such as chromatin condensation and disruption of mitochondrial integrity, took place before cell death. Furthermore, enhanced transcript levels of mitochondrial defense genes accompanied these mitochondrial changes. Pharmacological data indicated that the initiation and execution of cell death require de novo protein synthesis and that the signal transduction pathway leading to cell death involved changes in ion homeostasis, (de)phosphorylation events and an oxidative burst, as observed during hypersensitive responses. This oxidase-dependent oxidative burst is essential for cell death, but it is not required for the accumulation of defense proteins, suggesting a more prominent role for the oxidative burst in abiotic stress-induced cell death.