胞外ATP、H_2O_2、Ca~(2+)与NO调控木榄根系离子平衡机理研究

• 作 者: 郎涛 李妮亚 鲁彦君 孙会敏 申泽丹 荆晓姝 赵瑞 沈昕 陈少良
• 机 构: 北京林业大学生物科学与技术学院,海南师范大学生命科学学院,
• 出 处: 北京林业大学学报
• 发表日期: 2014年04期
• 关键词: ATP Ca H_2O_2 NO 木榄 根系 Na+离子流 K+离子流 非损伤微测技术 盐胁迫

运用非损伤微测技术(NMT),研究了短期盐胁迫下胞外ATP(eATP)、H2O2、Ca2+与NO对非泌盐红树木榄根系K+Na+平衡的调控作用。NaCl(100 mmolL,24 h)与等渗甘露醇处理的实验表明,木榄根尖对盐胁迫的响应具有高度的离子特异性。盐胁迫增强了木榄根尖的Na+外流,但Na+外流被Na+H+逆向转运蛋白抑制剂Amiloride和质膜H+-ATPase抑制剂Vanadate抑制,表明Na+外流源于根尖表皮细胞质膜Na+H+逆向转运系统驱动的Na+外排。短期盐胁迫处理能诱导木榄根尖K+外流,但被氯化四乙胺(TEA,外向K+通道抑制剂)明显抑制,证明K+外流是由激活的去极化外向型离子通道KORCs介导。胞外ATP(300μmolL)、H2O2(10 mmolL)、Ca2+(10 mmolL)与SNP(NO供体,100μmolL)均能增加短期盐胁迫下的Na+外流,同时抑制K+外流。其中,促进Na+外流效果较强的是H2O2和Ca2+,而Ca2+和NO抑制K+外流的效果突出。这些实验结果表明,胞外ATP、H2O2、Ca2+与NO这4种盐胁迫信使是通过上调木榄根系细胞质膜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+离子通道来减少盐诱导的K+外流。

The effects of extracellular ATP (eATP), H2O2, Ca2 + and NO on the balance of K + Na + balance in root of Brassica juncea under short-term salt stress were studied using non-invasive micro-measurement technique (NMT). Experiments with NaCl (100 mmol  L, 24 h) and isotonic mannitol showed that the response of Salvia miltiorrhiza to salt stress was highly ion-specific. Salt stress increased Na + outflow from the root tips of M. gramineus, but Na + efflux was inhibited by Na + H + antiporter inhibitor Amiloride and plasma membrane H + -ATPase inhibitor Vanadate, indicating that Na + efflux originates from the reverse of Na + H + in the apical plasma membrane Transport system driven Na + efflux. Short-term salt stress induced K + outflow from root tips of M. gramineus, but was significantly inhibited by tetraethylammonium chloride (TEA, outward K + channel inhibitor), indicating that K + efflux was mediated by activated depolarizing extrinsic ion channel KORCs. Extracellular ATP (300μmol·L), H2O2 (10mmolL), Ca2 + (10mmolL) and SNP (NO donors, 100μmolL) all increased Na + efflux under short-term salt stress and inhibited K + efflux . Among them, H2O2 and Ca2 + were the most effective promoters to promote Na + outflow, while Ca2 + and NO inhibited K + outflow significantly. These experimental results showed that extracellular ATP, H2O2, Ca2 + and NO were the four kinds of salt stress messenger by up-regulating the activity of Na + H + antiporter (Na + H + antiporter and H + pump) And H + reverse transmembrane transport, while inhibiting the depolarization-activated K + ion channels to reduce salt-induced K + efflux.