Dat James F, Pellinen Riikka, Beeckman Tom, Van De Cotte Brigitte, Langebartels Christian, Kangasjärvi Jaakko, Inzé Dirk, Van Breusegem Frank
Department of Plant Systems Biology, Flanders Interuniversity Institute for Biotechnology, Ghent University, K.L. Ledeganckstraat 35, B-9000 Gent, Belgium.
Plant J. 2003 Feb;33(4):621-32. doi: 10.1046/j.1365-313x.2003.01655.x.
In transgenic tobacco plants with reduced catalase activity, high levels of hydrogen peroxide (H2O2) can accumulate under photorespiratory conditions. Such a perturbation in H2O2 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.
在过氧化氢酶活性降低的转基因烟草植株中，在光呼吸条件下会积累高水平的过氧化氢（H2O2）。H2O2稳态的这种扰动导致栅栏薄壁组织细胞簇死亡，主要沿着叶脉。在细胞死亡之前发生了超微结构改变，如染色质浓缩和线粒体完整性破坏。此外，线粒体防御基因转录水平的提高伴随着这些线粒体变化。药理学数据表明，细胞死亡的起始和执行需要从头合成蛋白质，并且导致细胞死亡的信号转导途径涉及离子稳态变化、（去）磷酸化事件和氧化爆发，这与过敏反应中观察到的情况一样。这种依赖氧化酶的氧化爆发对于细胞死亡至关重要，但对于防御蛋白的积累并非必需，这表明氧化爆发在非生物胁迫诱导的细胞死亡中发挥着更突出的作用。
