Vacuolar CAX1 and CAX3 Influence Auxin Transport in Guard Cells via Regulation of Apoplastic pH
Vacuolar CAX1 and CAX3 Influence Auxin Transport in Guard Cells via Regulation of Apoplastic pH
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DOI：
10.1104/pp.112.201442
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发表时间：
2012-11-01
期刊：
影响因子：
7.4
通讯作者：
Kwak, June M.
中科院分区：
文献类型：
--
作者：
Cho, Daeshik;Villiers, Florent;Kwak, June M.
阳离子交换体CAX1和CAX3是参与植物离子稳态的液泡离子转运体。它们在植物中广泛表达，通过细胞质的质子梯度介导钙从细胞质转运到液泡腔。在这里，我们报告了CAX1和CAX3在调节外胞体pH中的意想不到的作用，并描述了它们如何通过保护细胞的激素信号传导和串音反应来促进生长素运输。我们发现吲哚-3-乙酸（IAA）对脱落酸（ABA）诱导的气孔关闭的抑制作用在cax1、cax3和cax1/cax3中受损。这些突变体表现出质膜的结构性低极化，膜电位的时间过程分析表明，iaa诱导的质膜超极化在这些突变体中也发生了改变。乙烯和1-萘乙酸都抑制了aba触发的cax1、cax3和cax1/cax3的气孔关闭，这表明生长素信号级联是功能性的，IAA运输的缺陷导致了cax突变体的表型。与这一发现一致，野生型植物中AUX1的化学抑制使cax突变体表型化。我们还发现cax1/cax3突变体比野生型具有更高的胞外pH值，进一步支持了cax突变体在IAA输入方面存在缺陷的假设。因此，当在较低的细胞外pH下进行气孔运动分析时，我们能够完全恢复IAA对aba诱导的cax1、cax3和cax1/cax3气孔关闭的抑制。我们的研究结果表明，液泡阳离子交换剂与胞外pH维持之间存在联系，在细胞过程中起着至关重要的作用。
CATION EXCHANGERs CAX1 and CAX3 are vacuolar ion transporters involved in ion homeostasis in plants. Widely expressed in the plant, they mediate calcium transport from the cytosol to the vacuole lumen using the proton gradient across the tonoplast. Here, we report an unexpected role of CAX1 and CAX3 in regulating apoplastic pH and describe how they contribute to auxin transport using the guard cell's response as readout of hormone signaling and cross talk. We show that indole-3-acetic acid (IAA) inhibition of abscisic acid (ABA)-induced stomatal closure is impaired in cax1, cax3, and cax1/cax3. These mutants exhibited constitutive hypopolarization of the plasma membrane, and time-course analyses of membrane potential revealed that IAA-induced hyperpolarization of the plasma membrane is also altered in these mutants. Both ethylene and 1-naphthalene acetic acid inhibited ABA-triggered stomatal closure in cax1, cax3, and cax1/cax3, suggesting that auxin signaling cascades were functional and that a defect in IAA transport caused the phenotype of the cax mutants. Consistent with this finding, chemical inhibition of AUX1 in wild-type plants phenocopied the cax mutants. We also found that cax1/cax3 mutants have a higher apoplastic pH than the wild type, further supporting the hypothesis that there is a defect in IAA import in the cax mutants. Accordingly, we were able to fully restore IAA inhibition of ABA-induced stomatal closure in cax1, cax3, and cax1/cax3 when stomatal movement assays were carried out at a lower extracellular pH. Our results suggest a network linking the vacuolar cation exchangers to apoplastic pH maintenance that plays a crucial role in cellular processes.