Yoda Hiroshi, Yamaguchi Yube, Sano Hiroshi
Research and Education Center for Genetic Information, Nara Institute of Science and Technology, Nara 630-0192, Japan.
Plant Physiol. 2003 Aug;132(4):1973-81. doi: 10.1104/pp.103.024737.
Screening immediate-early responding genes during the hypersensitive response (HR) against tobacco mosaic virus infection in tobacco (Nicotiana tabacum) plants, we identified a gene encoding ornithine decarboxylase. Subsequent analyses showed that other genes involved in polyamine biosynthesis were also up-regulated, resulting in the accumulation of polyamines in apoplasts of tobacco mosaic virus-infected leaves. Inhibitors of polyamine biosynthesis, alpha-difluoromethyl-ornithine, however, suppressed accumulation of polyamines, and the rate of HR was reduced. In contrast, polyamine infiltration into a healthy leaf induced the generation of hydrogen peroxide and simultaneously caused HR-like cell death. Polyamine oxidase activity in the apoplast increased up to 3-fold that of the basal level during the HR, and its suppression with a specific inhibitor, guazatine, resulted in reduced HR. Because it is established that hydrogen peroxide is one of the degradation products of polyamines, these results indicate that one of the biochemical events in the HR is production of polyamines, whose degradation induces hydrogen peroxide, eventually resulting in hypersensitive cell death.
在烟草（Nicotiana tabacum）植株对烟草花叶病毒感染的过敏反应（HR）过程中筛选即时早期响应基因时，我们鉴定出一个编码鸟氨酸脱羧酶的基因。随后的分析表明，其他参与多胺生物合成的基因也上调，导致烟草花叶病毒感染叶片的质外体中多胺积累。然而，多胺生物合成抑制剂α-二氟甲基鸟氨酸抑制了多胺的积累，且过敏反应速率降低。相反，将多胺渗入健康叶片会诱导过氧化氢的产生，并同时导致类似过敏反应的细胞死亡。在过敏反应期间，质外体中的多胺氧化酶活性增加至基础水平的3倍，用特异性抑制剂胍嗪抑制该酶会导致过敏反应减弱。由于已经确定过氧化氢是多胺的降解产物之一，这些结果表明过敏反应中的生化事件之一是多胺的产生，其降解诱导过氧化氢，最终导致过敏细胞死亡。
