Yoshinaga Keiko, Arimura Shin-ichi, Niwa Yasuo, Tsutsumi Nobuhiro, Uchimiya Hirofumi, Kawai-Yamada Maki
Institute of Molecular and Cellular Biosciences, University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-0032, Japan.
Ann Bot. 2005 Aug;96(2):337-42. doi: 10.1093/aob/mci181. Epub 2005 Jun 8.
Reactive oxygen species (ROS) are involved in triggering cell death. To visualize mitochondrial behaviour under ROS stress, transgenic arabidopsis plants possessing mitochondrial-targeted GFP (S65T) were studied.
Arabidopsis leaves were treated with ROS and ROS-inducing chemicals such as hydrogen peroxide, paraquat and menadione. Microscopic observations were carried out using a confocal laser scanning microscope system, and electrolyte leakage was also monitored.
After treatment, mitochondria showed morphological changes from a bacillus-like to a round shape. The size of mitochondria treated with H(2)O(2) decreased by half compared with controls. Concurrently, cytoplasmic streaming was blocked and mitochondria eventually swelled. Treatment of leaves with butanedione monoxime, an inhibitor of myosin ATPase, resulted in similar behaviour of mitochondria to that under ROS stress.
The results indicate that morphological changes of mitochondria and cessation of cytoplasmic streaming may interact, and this phenomenon is one of the features of ROS stress-induced cell death.
活性氧（ROS）参与触发细胞死亡。为了观察ROS应激下线粒体的行为，对具有线粒体靶向绿色荧光蛋白（S65T）的转基因拟南芥植株进行了研究。
用ROS及ROS诱导化学物质如过氧化氢、百草枯和甲萘醌处理拟南芥叶片。使用共聚焦激光扫描显微镜系统进行显微镜观察，并监测电解质渗漏情况。
处理后，线粒体呈现出从杆菌状到圆形的形态变化。与对照相比，用H₂O₂处理的线粒体大小减半。同时，细胞质流动受阻，线粒体最终肿胀。用肌球蛋白ATP酶抑制剂丁二酮肟处理叶片，导致线粒体出现与ROS应激下相似的行为。
结果表明，线粒体的形态变化与细胞质流动的停止可能相互作用，并且这种现象是ROS应激诱导细胞死亡的特征之一。
