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两个偏爱保卫细胞的 MAPK,MPK9 和 MPK12,调控拟南芥保卫细胞中的 YEL 信号。

Two guard cell-preferential MAPKs, MPK9 and MPK12, regulate YEL signalling in Arabidopsis guard cells.

机构信息

Graduate School of Natural Science and Technology, Okayama University, Okayama, Japan.

出版信息

Plant Biol (Stuttg). 2013 May;15(3):436-42. doi: 10.1111/j.1438-8677.2012.00671.x. Epub 2012 Oct 8.

DOI:10.1111/j.1438-8677.2012.00671.x
PMID:23043299
Abstract

We report that two mitogen-activated protein kinases (MAPKs), MPK9 and MPK12, positively regulate abscisic acid (ABA)-induced stomatal closure in Arabidopsis thaliana. Yeast elicitor (YEL) induced stomatal closure accompanied by intracellular reactive oxygen species (ROS) accumulation and cytosolic free calcium concentration ([Ca(2+) ]cyt ) oscillation. In this study, we examined whether these two MAP kinases are involved in YEL-induced stomatal closure using MAPKK inhibitors, PD98059 and U0126, and MAPK mutants, mpk9, mpk12 and mpk9 mpk12. Both PD98059 and U0126 inhibited YEL-induced stomatal closure. YEL induced stomatal closure in the mpk9 and mpk12 mutants but not in the mpk9 mpk12 mutant, suggesting that a MAPK cascade involving MPK9 and MPK12 functions in guard cell YEL signalling. However, YEL induced extracellular ROS production, intracellular ROS accumulation and cytosolic alkalisation in the mpk9, mpk12 and mpk9 mpk12 mutants. YEL induced [Ca(2+) ]cyt oscillations in both wild type and mpk9 mpk12 mutant. These results suggest that MPK9 and MPK12 function redundantly downstream of extracellular ROS production, intracellular ROS accumulation, cytosolic alkalisation and [Ca(2+) ]cyt oscillation in YEL-induced stomatal closure in Arabidopsis guard cells and are shared with ABA signalling.

摘要

我们报告称,两种丝裂原活化蛋白激酶(MAPKs),MPK9 和 MPK12,正向调控拟南芥中脱落酸(ABA)诱导的气孔关闭。酵母诱导剂(YEL)诱导的气孔关闭伴随着细胞内活性氧(ROS)的积累和胞质游离钙浓度([Ca (2+) ] cyt )的振荡。在这项研究中,我们使用 MAPKK 抑制剂 PD98059 和 U0126 以及 MAPK 突变体 mpk9、mpk12 和 mpk9 mpk12 ,检查了这两种 MAPK 是否参与 YEL 诱导的气孔关闭。PD98059 和 U0126 均抑制了 YEL 诱导的气孔关闭。YEL 在 mpk9 和 mpk12 突变体中诱导气孔关闭,但在 mpk9 mpk12 突变体中没有诱导气孔关闭,这表明涉及 MPK9 和 MPK12 的 MAPK 级联在保卫细胞 YEL 信号转导中发挥作用。然而,YEL 在 mpk9、mpk12 和 mpk9 mpk12 突变体中诱导了细胞外 ROS 的产生、细胞内 ROS 的积累和胞质碱化。YEL 在野生型和 mpk9 mpk12 突变体中均诱导了[Ca (2+) ] cyt 振荡。这些结果表明,MPK9 和 MPK12 在 YEL 诱导的拟南芥保卫细胞气孔关闭中,在细胞外 ROS 产生、细胞内 ROS 积累、胞质碱化和[Ca (2+) ] cyt 振荡的下游功能上是冗余的,并且与 ABA 信号转导共享。

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