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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Cytosolic abscisic acid activates guard cell anion channels without preceding Ca~(2+) signals
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Cytosolic abscisic acid activates guard cell anion channels without preceding Ca~(2+) signals

机译：胞质脱落酸可激活保卫细胞阴离子通道而无先前的Ca〜（2+）信号

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摘要

The phytohormone abscisic acid (ABA) reports on the water status of the plant and induces stomatal closure. Guard cell anion channels play a central role in this response, because they mediate anion efflux, and in turn, cause a depolarization-induced K~+ release. We recorded early steps in ABA signaling, introducing multibarreled microelectrodes in guard cells of intact plants. Upon external ABA treatment, anion channels transiently activated after a lag phase of ≈2 min. As expected for a cytosolic ABA receptor, iontophoretic ABA loading into the cytoplasm initiated a rise in anion current without delay. These ABA responses could be elicited repetitively at resting and at largely depolarized potentials (e.g., 0 mV), ruling out signal transduction by means of hyperpolarization-activated calcium channels. Likewise, ABA stimulation did not induce a rise in the cytosolic free-calcium concentration. However, the presence of ≈100 nM background Ca~(2+) was required for anion channel function, because the action of ABA on anion channels was repressed after loading of the Ca~(2+) chelator 1,2-bis(2-aminophe-noxy)ethane-N,N,N′,N′-tetraacetate. The chain of events appears very direct, because none of the tested putative ABA-signaling intermediates (inositol 1,4,5 trisphosphate, inositol hexakisphos-phate, nicotinic acid adenine dinucleotide phosphate, and cyclic ADP-ribose), could mimic ABA as anion channel activator. In patch-clamp experiments, cytosolic ABA also evoked anion current transients carried by R- and S-type anion channels. The response was dose-dependent with half-maximum activation at 2.6 μM ABA. Our studies point to an ABA pathway initiated by ABA binding to a cytosolic receptor that within seconds activates anion channels, and in turn, leads to depolarization of the plasma membrane.
机译：植物激素脱落酸（ABA）报告了植物的水分状况，并导致气孔关闭。保卫细胞阴离子通道在该反应中起着核心作用，因为它们介导阴离子外排，进而引起去极化诱导的K +释放。我们记录了ABA信号转导的早期步骤，在完整植物的保卫细胞中引入了多管微电极。在进行外部ABA处理后，在约2分钟的滞后阶段后，阴离子通道会暂时激活。正如对胞质ABA受体的预期，离子电渗ABA载入细胞质中会立即引起阴离子电流的增加。这些ABA反应可以在静止和很大程度上去极化电位（例如0 mV）下反复引发，排除了通过超极化激活的钙通道进行的信号转导。同样，ABA刺激也不会引起胞浆游离钙浓度的升高。然而，阴离子通道功能需要存在约100 nM的本底Ca〜（2+），因为加载Ca〜（2+）螯合剂1,2-bis（2）后，ABA对阴离子通道的作用受到抑制。 -氨基苯氧基）乙烷-N，N，N'，N'-四乙酸酯事件链看起来非常直接，因为测试的推定的ABA信号传导中间体（肌醇1,4,5三磷酸，肌醇六磷酸盐，烟酸腺嘌呤二核苷酸磷酸酯和环状ADP-核糖）都不能模仿ABA作为阴离子。通道激活剂。在膜片钳实验中，胞质ABA还引起R型和S型阴离子通道携带的阴离子电流瞬变。响应是剂量依赖性的，在2.6μMABA下具有最大激活的一半。我们的研究指向由ABA结合至胞质受体而引发的ABA途径，该途径可在数秒内激活阴离子通道，进而导致质膜去极化。

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