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首页> 外文期刊>Journal of Experimental Botany >Novel roles of ascorbate in plants: induction of cytosolic Ca2+ signals and efflux from cells via anion channels
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Novel roles of ascorbate in plants: induction of cytosolic Ca2+ signals and efflux from cells via anion channels

机译：抗坏血酸在植物中的新作用：通过阴离子通道诱导细胞溶胶CA2 +信号和来自细胞的流出

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摘要

Ascorbate is not often considered as a signalling molecule in plants. This study demonstrates that, in Arabidopsis roots, exogenous L-ascorbic acid triggers a transient increase of the cytosolic free calcium activity ([Ca2+](cyt).) that is central to plant signalling. Exogenous copper and iron stimulate the ascorbate-induced [Ca2+](cyt). elevation, while cation channel blockers, free radical scavengers, low extracellular [Ca2+], transition metal chelators, and removal of the cell wall inhibit this reaction. These data show that apoplastic redox-active transition metals are involved in the ascorbate-induced [Ca2+] cyt. elevation. Exogenous ascorbate also induces a moderate increase in programmed cell death symptoms in intact roots, but it does not activate Ca2+ influx currents in patch-clamped root protoplasts. Intriguingly, the replacement of gluconate with ascorbate in the patch-clamp pipette reveals a large ascorbate efflux current, which shows sensitivity to the anion channel blocker, anthracene-9-carboxylic acid (A9C), indicative of the ascorbate release via anion channels. EPR spectroscopy measurements demonstrate that salinity (NaCl) triggers the accumulation of root apoplastic ascorbyl radicals in an A9C-dependent manner, confirming that l-ascorbate leaks through anion channels under depolarization. This mechanism may underlie ascorbate release, signalling phenomena, apoplastic redox reactions, iron acquisition, and control the ionic and electrical equilibrium (together with K+ efflux via GORK channels).
机译：抗坏血酸通常不被认为是植物中的信号分子。本研究表明，在拟南芥根系中，外源性L-抗坏血酸触发了胞质游离钙活性的瞬时增加（[Ca2 +]（cyt）。外源铜和铁刺激抗坏血酸诱导的[CA2 +]（CYT）。升高，而阳离子通道阻滞剂，自由基清除剂，低细胞外[Ca2 +]，过渡金属螯合剂和除去细胞壁的去除抑制了该反应。这些数据表明，妊娠氧化还原活性过渡金属涉及抗坏血酸诱导的[Ca2 +] cyt。海拔。外源性抗坏血酸在完整根部的编程细胞死亡症状中也诱导中等增加，但它不会在贴片根原生质体中激活CA2 +流入电流。有趣的是，用斑块夹液移液管替代葡萄糖酸盐露出抗坏血酸的抗坏血酸型流出电流，其显示对阴离子通道阻断剂，蒽-9-羧酸（A9C）的敏感性，指示抗坏血液通过阴离子通道释放。 EPR光谱测量结果表明，盐度（NaCl）触发了根部旋塞抗坏血酸的累积以A9C依赖性方式，证实L-抗坏血液在去极化下通过阴离子通道泄漏。该机制可以利于抗坏血酸释放，信号传导现象，妊娠氧化还原反应，铁采集和控制离子和电气平衡（通过Gork通道与K + Efflux一起）。

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