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内源脱落酸参与茉莉酸甲酯诱导的拟南芥气孔关闭过程。

Involvement of endogenous abscisic acid in methyl jasmonate-induced stomatal closure in Arabidopsis.

作者信息

Hossain Mohammad Anowar, Munemasa Shintaro, Uraji Misugi, Nakamura Yoshimasa, Mori Izumi C, Murata Yoshiyuki

机构信息

Graduate School of Natural Science and Technology, Okayama University, Tsushima-Naka, Okayama 700-8530, Japan.

出版信息

Plant Physiol. 2011 May;156(1):430-8. doi: 10.1104/pp.111.172254. Epub 2011 Mar 14.

Abstract

In this study, we examined the involvement of endogenous abscisic acid (ABA) in methyl jasmonate (MeJA)-induced stomatal closure using an inhibitor of ABA biosynthesis, fluridon (FLU), and an ABA-deficient Arabidopsis (Arabidopsis thaliana) mutant, aba2-2. We found that pretreatment with FLU inhibited MeJA-induced stomatal closure but not ABA-induced stomatal closure in wild-type plants. The aba2-2 mutation impaired MeJA-induced stomatal closure but not ABA-induced stomatal closure. We also investigated the effects of FLU and the aba2-2 mutation on cytosolic free calcium concentration (Ca(2+)) in guard cells using a Ca(2+)-reporter fluorescent protein, Yellow Cameleon 3.6. In wild-type guard cells, FLU inhibited MeJA-induced Ca(2+) elevation but not ABA-induced Ca(2+) elevation. The aba2-2 mutation did not affect ABA-elicited Ca(2+) elevation but suppressed MeJA-induced Ca(2+) elevation. We also tested the effects of the aba2-2 mutation and FLU on the expression of MeJA-inducible VEGETATIVE STORAGE PROTEIN1 (VSP1). In the aba2-2 mutant, MeJA did not induce VSP1 expression. In wild-type leaves, FLU inhibited MeJA-induced VSP1 expression. Pretreatment with ABA at 0.1 μm, which is not enough concentration to evoke ABA responses in the wild type, rescued the observed phenotypes of the aba2-2 mutant. Finally, we found that in wild-type leaves, MeJA stimulates the expression of 9-CIS-EPOXYCAROTENOID DIOXYGENASE3, which encodes a crucial enzyme in ABA biosynthesis. These results suggest that endogenous ABA could be involved in MeJA signal transduction and lead to stomatal closure in Arabidopsis guard cells.

摘要

在本研究中,我们使用脱落酸(ABA)生物合成抑制剂氟啶酮(FLU)和ABA缺陷型拟南芥(Arabidopsis thaliana)突变体aba2-2,研究了内源性ABA在茉莉酸甲酯(MeJA)诱导的气孔关闭中的作用。我们发现,用FLU预处理可抑制野生型植物中MeJA诱导的气孔关闭,但不影响ABA诱导的气孔关闭。aba2-2突变损害了MeJA诱导的气孔关闭,但不影响ABA诱导的气孔关闭。我们还使用Ca(2+)报告荧光蛋白Yellow Cameleon 3.6研究了FLU和aba2-2突变对保卫细胞胞质游离钙浓度(Ca(2+))的影响。在野生型保卫细胞中,FLU抑制MeJA诱导的Ca(2+)升高,但不影响ABA诱导的Ca(2+)升高。aba2-2突变不影响ABA引发的Ca(2+)升高,但抑制MeJA诱导的Ca(2+)升高。我们还测试了aba2-2突变和FLU对MeJA诱导的营养贮藏蛋白1(VSP1)表达的影响。在aba2-2突变体中,MeJA不诱导VSP1表达。在野生型叶片中,FLU抑制MeJA诱导的VSP1表达。用0.1μm的ABA预处理,该浓度不足以在野生型中引发ABA反应,挽救了aba2-2突变体观察到的表型。最后,我们发现,在野生型叶片中,MeJA刺激9-顺式环氧类胡萝卜素双加氧酶3的表达,该酶编码ABA生物合成中的关键酶。这些结果表明,内源性ABA可能参与MeJA信号转导,并导致拟南芥保卫细胞气孔关闭。

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