Li Shaoqing, Wan Cuixiang, Kong Jin, Zhang Zaijun, Li Yangsheng, Zhu Yingguo
Key Laboratory of MOE for Plant Developmental Biology, College of Life Sciences, Wuhan University, Wuhan, Hubei 430072, China.
Key Laboratory of MOE for Plant Developmental Biology, College of Life Sciences, Wuhan University, Wuhan, Hubei 430072, China. Corresponding author; email:
Funct Plant Biol. 2004 May;31(4):369-376. doi: 10.1071/FP03224.
The key role of mitochondria in the integration of apoptosis and oxidative stress in mammals has been documented. In plants, mitochondria are implicated in cytoplasmic male sterility (CMS), programmed cell death (PCD), and oxidative stress. However, to date there has been no evidence presented of the interplay among CMS, PCD and oxidative stress. In this study, we demonstrate that the pollen abortion of Honglian CMS line of rice (Oryza sativa L.) displays a PCD phenotype. A premature loss of microspores was accompanied by several biochemical markers of apoptosis. Analysis of mitochondria revealed that during the PCD process there was disruption of the inner mitochondrial membrane potential in microspores. This disruption was correlated with excess production of reactive oxygen species and down-regulation of the activity of superoxide dismutase (SOD), ascorbate peroxidase (APX) and catalase in mitochondria. The excess accumulation of ROS spanned three stages from pollen mother cell to early-uninucleate stage, and was followed by the occurrence of PCD at meiosis. Our data suggest that the microspores suffered from severe oxidative stress during pollen development. It is likely the chronic oxidative stress triggered the tissue-specific PCD and consequently resulted in the abortion of microspores.
线粒体在哺乳动物细胞凋亡与氧化应激整合过程中的关键作用已有文献记载。在植物中，线粒体与细胞质雄性不育（CMS）、程序性细胞死亡（PCD）及氧化应激有关。然而，迄今为止，尚无证据表明CMS、PCD和氧化应激之间存在相互作用。在本研究中，我们证明水稻红莲CMS系的花粉败育表现出PCD表型。小孢子过早丧失伴随着细胞凋亡的几个生化标记。线粒体分析表明，在PCD过程中，小孢子线粒体内膜电位遭到破坏。这种破坏与活性氧的过量产生以及线粒体中超氧化物歧化酶（SOD）、抗坏血酸过氧化物酶（APX）和过氧化氢酶活性的下调相关。活性氧的过量积累从花粉母细胞到早期单核期跨越三个阶段，随后在减数分裂时发生PCD。我们的数据表明，小孢子在花粉发育过程中遭受了严重的氧化应激。很可能是慢性氧化应激引发了组织特异性PCD，从而导致小孢子败育。
