Convergence of calcium signaling pathways of pathogenic elicitors and abscisic acid in Arabidopsis guard cells
Convergence of calcium signaling pathways of pathogenic elicitors and abscisic acid in Arabidopsis guard cells
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DOI：
10.1104/pp.012187
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发表时间：
2002-12-01
期刊：
影响因子：
7.4
通讯作者：
Schroeder, JI
中科院分区：
文献类型：
--
作者：
Klüsener, B;Young, JJ;Schroeder, JI
各种刺激，如脱落酸(ABA)、活性氧(ROS)和植物防御反应的激发子，都能诱导气孔关闭。我们的研究解决了这些刺激触发的信号通路中的共性。最近的一份报告表明，ABA和ROS都能在拟南芥保卫细胞中激活一种NADPH依赖的、超极化激活的钙内流电流，称为“I-Ca”(Z.M.Pei，Y.Murata，G.Benning，S.Thomine，B.Klusener，G.J.Allen，E.Grill，J.I.Schroeder，Nature[2002]406：731-734)。我们发现，酵母和壳聚糖都是植物防御反应的激发子，它们也激活这一电流，激活需要胞内NAD(P)H。这些激发子还诱导保卫细胞内游离钙浓度([Ca~(2+)](Cyt))的升高和气孔关闭。ABA和ROS只有在细胞外有钙离子存在的情况下才能引起保卫细胞的[Ca~(2+)]_(Cyt)振荡。在5 mM KCl胞外缓冲液中，45%的保卫细胞表现出自发的[Ca~(2+)](Cyt)振荡，其动力学特性与ABA诱导的Ca~(2+)升高不同。这些自发的[Ca~(2+)](Cyt)振荡也需要细胞外Ca~(2+)的有效性，并依赖于细胞外钾浓度。有趣的是，当ABA应用于自发振荡细胞时，ABA导致101个细胞中62个细胞的[Ca~(2+)](Cyt)升高，揭示了ABA信号的一种新模式。这些数据表明，真菌激发子在保卫细胞的胁迫信号转导通路中与ABA共同激活一个分支，激活质膜I-Ca通道，支持细胞外钙离子对激发子和ABA信号的需求，以及细胞内[Ca2+](Cyt)振荡的维持。
A variety of stimuli, such as abscisic acid (ABA), reactive oxygen species (ROS), and elicitors of plant defense reactions, have been shown to induce stomatal closure. Our study addresses commonalities in the signaling pathways that these stimuli trigger. A recent report showed that both ABA and ROS stimulate an NADPH-dependent, hyperpolarization-activated Ca2+ influx current in Arabidopsis guard cells termed "I-Ca" (Z.M. Pei, Y. Murata, G. Benning, S. Thomine, B. Klusener, G.J. Allen, E. Grill, J.I. Schroeder, Nature [2002] 406: 731-734). We found that yeast (Saccharomyces cerevisiae) elicitor and chitosan, both elicitors of plant defense responses, also activate this current and activation requires cytosolic NAD(P)H. These elicitors also induced elevations in the concentration of free cytosolic calcium ([Ca2+](cyt)) and stomatal closure in guard cells. ABA and ROS elicited [Ca2+](cyt), oscillations in guard cells only when extracellular Ca2+ was present. In a 5 mM KCl extracellular buffer, 45% of guard cells exhibited spontaneous [Ca2+](cyt) oscillations that differed in their kinetic properties from ABA-induced Ca2+ increases. These spontaneous [Ca2+](cyt) oscillations also required the availability of extracellular Ca2+ and depended on the extracellular potassium concentration. Interestingly, when ABA was applied to spontaneously oscillating cells, ABA caused cessation of [Ca2+](cyt), elevations in 62 of 101 cells, revealing a new mode of ABA signaling. These data show that fungal elicitors activate a shared branch with ABA in the stress signal transduction pathway in guard cells that activates plasma membrane I-Ca channels and support a requirement for extracellular Ca2+ for elicitor and ABA signaling, as well as for cellular [Ca2+](cyt) oscillation maintenance.