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作 者:罗达[1] 吴正保[1] 宋锋惠[1] 史彦江[1] LUO Da;WU Zhengbao;SONG Fenghui;SHI Yanjiang(Institute of Economic Forests,Xinjiang Academy of Forestry Science,Urumqi 830063,China)
机构地区:[1]新疆林业科学院经济林研究所,乌鲁木齐830063
出 处:《植物生理学报》2023年第5期889-898,共10页Plant Physiology Journal
基 金:国家自然科学基金(31960324);新疆自然科学基金(2022D01A62);新疆“天山英才”计划(TSYC-343)。
摘 要:盐胁迫导致平欧杂种榛体内原有的K^(+)/Na^(+)失衡,但活体状态下的根系离子动态转运对盐胁迫的响应机制仍未明晰。以平欧杂种榛‘达维’苗木为材料,在水培条件下经0(对照)和200 mmol·L−1 NaCl处理,利用非损伤微测技术,研究盐胁迫下的根系离子流特征及其对抑制剂的响应。结果表明,分生区Na^(+)流速稳定,流向不变,为离子流的最佳扫描位置。根系离子流对盐胁迫与离子转运体抑制剂的响应具有高度特异性。盐胁迫下,分生区Na^(+)、K^(+)净外排量和H^(+)净内流量均显著增加,分别较对照提高287.8%、134.4%和188.7%。质膜Na^(+)/H^(+)逆向转运蛋白抑制剂阿米洛利和质膜H^(+)-ATP酶抑制剂钒酸钠显著限制了NaCl胁迫引起的Na^(+)外排和H^(+)内流,Na^(+)净外排量和H^(+)净内流量分别降低63.5%和138.1%。NaCl胁迫引起的K^(+)外排受到K^(+)通道抑制剂氯化四乙胺的明显抑制和钒酸钠的显著促进,K^(+)净外排量分别降低68.5%和提高69.0%。综合分析表明,NaCl胁迫通过上调根系质膜Na^(+)/H^(+)逆向转运体系(Na^(+)/H^(+)逆向转运体和H^(+)泵)活性,在促进Na^(+)和H^(+)逆向跨膜转运的同时,抑制去极化激活的K^(+)通道来减缓盐诱导的K^(+)外流。Salt stress leads to the original K^(+)/Na^(+)imbalance in the Corylus heterophylla×C.avellana,however,the response mechanism of root ion dynamic transport to salt stress remains unclear in the living state.In this study,the C.heterophylla×C.avellana‘Dawei’were selected as testing materials.The seedlings were treated with 0(control)and 200 mmol·L−1 NaCl under hydroponic conditions.Subsequently,the ion flux characteristics and their response to inhibitors of root under salt stress were studied using the non-invasive micro-test technique(NMT).The results showed that the net Na^(+)flux in the meristematic zone was stable and the direction was unchanged,which was the best scanning position for ion flow.There were mainly high ion-specific effects on NaCl and inhibitor-induced ion flux in roots.Under salt stress,the net Na^(+)and K^(+)efflux and H^(+)influx in the meristematic zone were significantly increased,which increased by 287.8%,134.4%and 188.7%compared with the control,respectively.Amiloride,an inhibitor of plasma membrane Na^(+)/H^(+)antiporter,and sodium vanadate,an inhibitor of plasma membrane H^(+)-ATPase,significantly restricted the NaCl-induced Na^(+)efflux and H^(+)influx.The net Na^(+)efflux and H^(+)influx decreased by 63.5%and 138.1%respectively.The NaCl-induced K^(+)efflux was significantly inhibited by the K^(+)channel inhibitor tetraethylammonium chloride,and significantly promoted by sodium vanadate,which decreased by 68.5%and increased by 69.0%,respectively.In conclusion,our data revealed that the NaCl stress upward regulated the plasma membrane Na^(+)/H^(+)antiport system(Na^(+)/H^(+)antiporter and H^(+)pump)activity,which promoted the reverse transmembrane transport of Na^(+)and H^(+),and slowed down the Na-Cl-induced K^(+)loss via restricting depolarization-activated K^(+)channels simultaneously.
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