Kadota Yasuhiro, Fujii Shinsuke, Ogasawara Yoko, Maeda Yutaka, Higashi Katsumi, Kuchitsu Kazuyuki
Department of Applied Biological Science, Tokyo University of Science, 2641 Yamazaki, Noda, Chiba, 278-8510 Japan.
Plant Cell Physiol. 2006 Sep;47(9):1337-42. doi: 10.1093/pcp/pcj098. Epub 2006 Aug 8.
To provide insights into the mechanisms by which receptors for pathogenic elicitors activate defense signaling, we investigated the duration of cryptogein treatment required for induction of various defense responses including programmed cell death in synchronized tobacco BY-2 cells. Transient cryptogein treatment induced only a rapid and transient phase of oxidative burst and mitogen-activated protein kinase (MAPK) activation. Prolonged production of *O(2)(-) and prolonged activation of MAPKs, as well as accumulation of transcripts of defense-related genes and cell death, required continuous recognition of cryptogein for several hours. In contrast, desensitization was gradually induced in the absence of the elicitor.
为深入了解病原激发子受体激活防御信号的机制,我们研究了在同步化的烟草BY-2细胞中诱导包括程序性细胞死亡在内的各种防御反应所需的隐地蛋白处理时间。短暂的隐地蛋白处理仅诱导了氧化爆发和丝裂原活化蛋白激酶(MAPK)激活的快速且短暂阶段。持续数小时的隐地蛋白识别是产生延长的超氧阴离子(*O(2)(-))、持续激活MAPK以及积累防御相关基因转录本和细胞死亡所必需的。相反,在没有激发子的情况下会逐渐诱导脱敏。