Salt-Stress-Induced Ion Transport Contributes to K+/Na+ Homeostasis in Roots of Ping’ou Hybrid Hazelnut
Salt-Stress-Induced Ion Transport Contributes to K+/Na+ Homeostasis in Roots of Ping’ou Hybrid Hazelnut
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DOI：
10.3390/f14081651
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发表时间：
2023-08
期刊：
影响因子：
2.9
通讯作者：
Da Luo;Fenghui Song;Ming-Rui Lu;Yan-Jiang Shi;Qinghua Ma
中科院分区：
文献类型：
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作者：
Da Luo;Fenghui Song;Ming-Rui Lu;Yan-Jiang Shi;Qinghua Ma
土壤盐渍化是一个世界性的问题，对植物的生长和发育产生不利影响。新疆土壤盐渍化十分严重。平欧杂交榛是新疆重要的生态经济树种，也是耐盐植物，在新疆已有20多年的种植历史。了解平欧杂交榛的耐盐机理，对于耐盐品种的选育和盐碱地的合理利用具有重要意义。以平欧杂交榛优良品种辽榛7号为试材，用0（对照）、50、100和200 mM NaCl溶液处理其幼苗。随后，利用非侵入性微测试技术（NMT）研究了NaCl诱导的根分生区Na+、K+和H+的通量及其对离子转运抑制剂的响应。不同浓度的NaCl胁迫均显著增加了根中Na+浓度，而K+浓度则随着NaCl浓度的增加先降低后升高。同时，NaCl胁迫导致K+/Na+比值显著下降。对照和200 mM NaCl诱导的Na+和K+通量在根表现出向外流出，而向内通量观察到H+。在200 mM NaCl胁迫下，根系Na+、K+净流出速率和H+内流速率均显著增加，分别是对照的11.6、6.7和2.3倍。此外，药理学实验表明，200 mM NaCl诱导的Na+外流; H+内流显着抑制阿米洛利，质膜（PM）Na+/H+逆向转运蛋白的抑制剂，钒酸钠，PM H+-ATP酶的抑制剂。NaCl诱导的Na+净流出和H+内流分别减少89.9%和135.0%。NaCl诱导的Na+外流是由Na+/H+逆向转运蛋白利用PM H+-ATP酶提供的能量介导的。钾通道抑制剂氯化四乙胺（tetraethylaminechloride）可显著抑制NaCl诱导的钾离子外排，钒酸钠（sodium vanadate）可显著促进NaCl诱导的钾离子外排，抑制率分别为111.2%和80.8%，表明钾离子外排受去极化激活的外向整流钾通道和非选择性阳离子通道（non-selective cationchannels，NSCCs）的调节。NMT结果表明，NaCl胁迫上调了“辽珍7号”根系Na+/H+逆向转运蛋白和质膜Na+/H+逆向转运系统中的H+泵活性，促使Na+/H+跨质膜交换，同时抑制K+通过去极化激活的K+通道和NSCC的损失，从而维持了K+/Na+的稳态，提高了耐盐性。
Soil salinity is a worldwide problem that adversely affects plant growth and development. Soil salinization in Xinjiang of China is very serious. Ping’ou hybrid hazelnut, as an important ecological and economic tree species, as well as a salt-tolerant plant, has been grown in Xinjiang for over 20 years. Understanding the salt-tolerance mechanism of Ping’ou hybrid hazelnut is of great significance for the breeding of salt-tolerant varieties and the rational utilization of salinized land. In this study, ‘Liaozhen 7’, a fine variety of Ping’ou hybrid hazelnut, was selected as test material, and seedlings were treated with 0 (control), 50, 100 and 200 mM NaCl. Subsequently, the pattern of NaCl-induced fluxes of Na+, K+ and H+ in the root meristematic zone and their response to ion transport inhibitors were studied using non-invasive micro-test technology (NMT). Different concentrations of NaCl stress significantly increased the Na+ concentration in roots, while K+ concentration decreased first and then increased with the increase of NaCl concentration. Meanwhile, NaCl stress induced a significant decline in K+/Na+ ratio. Control and 200 mM NaCl-induced Na+ and K+ fluxes in roots exhibited an outward efflux, whereas an inward flux was observed for H+. Under 200 mM NaCl stress, the average rates of net Na+ and K+ efflux, as well as H+ influx in roots were significantly increased, which were 11.6, 6.7 and 2.3 times higher than that of control, respectively. Furthermore, pharmacological experiments showed that 200 mM NaCl-induced Na+ efflux; H+ influx was significantly suppressed by amiloride, an inhibitor of plasma membrane (PM) Na+/H+ antiporter, and sodium vanadate, an inhibitor of PM H+-ATPase. Net Na+ efflux and H+ influx induced by NaCl decreased by 89.9% and 135.0%, respectively. The NaCl-induced Na+ efflux was mediated by a Na+/H+ antiporter using energy provided by PM H+-ATPase. The NaCl-induced K+ efflux was significantly restricted by tetraethylamine chloride, a K+ channel inhibitor, and promoted by sodium vanadate, which decreased by 111.2% and increased by 80.8%, respectively, indicating that K+ efflux was regulated by depolarization-activated outward-rectifying K+ channels and non-selective cation channels (NSCCs). In conclusion, NMT data revealed that NaCl stress up regulated the root Na+/H+ antiporter and H+ pump (an activity of PM Na+/H+ antiport system) of ‘Liaozhen 7’, which compelled the Na+/H+ exchange across the PM and restricted K+ loss via depolarization-activated K+ channels and NSCCs simultaneously, thereby maintaining the K+/Na+ homeostasis and higher salt tolerance.