Graduate School of Natural Science and Technology, Division of Bioscience, Okayama University, 1-1-1 Tsushima-Naka, Okayama, 700-8530 Japan.
Plant Cell Physiol. 2010 Nov;51(11):1915-21. doi: 10.1093/pcp/pcq145. Epub 2010 Sep 27.
Yeast elicitor (YEL) induces stomatal closure. We investigated reactive oxygen species (ROS) production, nitric oxide (NO) production and Ca(2+) oscillations to clarify YEL signaling in Arabidopsis guard cells. YEL induced ROS accumulation in guard cells. A peroxidase inhibitor [salicylhydroxamic acid (SHAM)] inhibited the stomatal closure and the ROS accumulation, but neither the atrbohD atrbohF mutation nor an NADPH oxidase inhibitor [diphenylene iodonium chloride (DPI)] had any effect. An NO scavenger [2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO)] inhibited the YEL-induced stomatal closure and SHAM abolished NO production. YEL-elicited Ca(2+) oscillations were inhibited by SHAM but not by the atrbohD atrbohF mutation. These results indicate that YEL induces stomatal closure accompanied by ROS production mediated by peroxidases and NO production.
酵母激发子（YEL）诱导气孔关闭。我们研究了活性氧（ROS）的产生、一氧化氮（NO）的产生和Ca(2+)的振荡，以阐明 YEL 在拟南芥保卫细胞中的信号转导。YEL 诱导保卫细胞中 ROS 的积累。过氧化物酶抑制剂[水杨羟肟酸（SHAM）]抑制气孔关闭和 ROS 的积累，但 atrbohD atrbohF 突变体或 NADPH 氧化酶抑制剂[二苯基碘（DPI）]均无作用。NO 清除剂[2-(4-羧基苯基）-4,4,5,5-四甲基咪唑啉-1-氧-3-氧化物（cPTIO）]抑制 YEL 诱导的气孔关闭和 SHAM 抑制 NO 的产生。YEL 诱导的Ca(2+)振荡被 SHAM 抑制，但 atrbohD atrbohF 突变体不抑制。这些结果表明，YEL 诱导气孔关闭，同时伴有过氧化物酶介导的 ROS 产生和 NO 的产生。
