Extracellular ATP mediates cellular K+/Na+ homeostasis in two contrasting poplar species under NaCl stress
Extracellular ATP mediates cellular K+/Na+ homeostasis in two contrasting poplar species under NaCl stress
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细胞外 ATP 介导 NaCl 胁迫下两种对比杨树的细胞 K / Na 稳态
DOI：
10.1007/s00468-015-1324-y
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发表时间：
2016-06
期刊：
影响因子：
--
通讯作者：
Chen Shaoliang
中科院分区：
文献类型：
--
作者：
Li Nianfei;Zhao Chenjing;Zhao Rui;Chen Shaoliang
关键信息 eATP 介导两种不同耐盐性的杨树种的细胞 K+ 和 Na+ 稳态。 摘要：利用非侵入性微测试技术 (NMT)，研究了细胞外 ATP (eATP) 对耐盐杨树种、胡杨和盐敏感的白杨中 K+、Na+ 和 H+ 盐变化通量谱的影响。短期 NaCl（100 mM NaCl，12 小时）会导致胡杨细胞中 Na+ 外流和相应增加的 H+ 内流，但在普通胡杨中没有看到这种效果。 ATP (50 μM) 增强了两个物种（6、12 h）盐胁迫细胞中 Na+ 与 H+ 的交换，特别是在 P. popalis 中。然而，ATP 刺激的 Na+ 流出和 H+ 流入被阿米洛利（一种 Na+/H+ 逆向转运蛋白抑制剂）或原钒酸钠（一种质膜 H+-ATP 酶抑制剂）显着抑制，表明 ATP 诱导 Na+ 挤出是由于跨质膜 (PM) 的活性 Na+/H+ 逆向转运所致。氯化钠加速了这两个物种的钾离子外流，对盐敏感的杨树的影响更为明显。盐诱导的 K+ 外流明显受到 K+ 通道阻滞剂氯化四乙铵的限制，表明 K+ 外流是由去极化激活的外向整流 K+ 通道和非选择性阳离子通道介导的。 ATP 有利于杨树细胞，尤其是对盐敏感的大众杨细胞，有利于在外部盐度下维持 K+ 稳态。这可能是 PM 中激活的 H+ 泵的结果，它通过抑制两个物种中去极化激活的 K+ 通道来限制 K+ 外流。 Na+ 和 K+ 通量记录显示，ATP、αβ-meATP (50 μM) 和 ATPγS (50 μM) 的非水解类似物产生与可水解形式类似的效果，但效果更明显。然而，ADP 和 AMP 刺激的细胞 (50 μM) 表现出与 ATP、αβ-meATP 和 ATPγS 处理所引起的行为不同的行为。 K+ 和 Na+ 稳态中的 eATP 信号传导被动物 P2 受体拮抗剂、PPADS 和苏拉明阻断。此外，在 NaCl 胁迫细胞中 ATP 刺激的 Na+ 排出和 K+ 损失的减少被 LaCl3（Ca2+ 通透通道抑制剂）和 DPI（PM NADPH 氧化酶抑制剂）抑制，表明在耐盐性不同的两种杨树中，ATP 信号是通过第二信使 H2O2 和 Ca2+ 介导的。
Key messageeATP mediates cellular K+and Na+homeostasis in two contrasting poplar species differing in salt tolerance.AbstractUsing the non-invasive micro-test technology (NMT), the effects of extracellular ATP (eATP) on salt-altered flux profiles of K+, Na+, and H+ were investigated in salt-tolerant poplar species, Populus euphratica and salt-sensitive P. popularis. A short-term NaCl (100 mM NaCl, 12 h) resulted in a Na+ efflux and a correspondingly increased H+ influx in P. euphratica cells, but the effect was not seen in P. popularis. ATP (50 μM) enhanced exchange of Na+ with H+ in salt-stressed cells of two species (6, 12 h), especially in P. popularis. However, the ATP-stimulated Na+ efflux and H+ influx were significantly inhibited by amiloride (a Na+/H+ antiporter inhibitor) or sodium orthovanadate (a plasma membrane H+-ATPase inhibitor), indicating that the ATP induction of Na+ extrusion resulted from an active Na+/H+ antiport across the plasma membrane (PM). NaCl accelerated K+ efflux in the two species, with a more pronounced effect in the salt-sensitive poplar. The salt-induced K+ efflux was markedly restricted by the K+ channel blocker, tetraethylammonium chloride, indicating that the K+ efflux is mediated by depolarization-activated outward rectifying K+ channels and non-selective cation channels. ATP benifited poplar cells, especially the salt-sensitive P. popularis, in maintaining K+ homeostasis under external salinity. This was likely the result of activated H+ pump in the PM, which restricted the K+ efflux through the inhibition of depolarization-activated K+ channels in both species. Na+ and K+ flux recordings revealed that non-hydrolysing analogues of ATP, αβ-meATP (50 μM), and ATPγS (50 μM) produced an effect similar to that of the hydrolysable form but with a more pronounced effect. However, ADP- and AMP-stimulated cells (50 μM) exhibited behaviors different from those invoked by ATP, αβ-meATP, and ATPγS treatments. eATP signalling in K+ and Na+ homeostasis was blocked by the antagonists of animal P2 receptors, PPADS, and suramin. Moreover, ATP-stimulated Na+ extrusion and reduction of K+ loss in NaCl-stressed cells were inhibited by LaCl3 (an inhibitor of Ca2+-permeable channels) and DPI (an inhibitor of PM NADPH oxidase), indicating that ATP signalling was mediated via second messengers, H2O2 and Ca2+, in the two poplars differing in salt tolerance.
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影响因子：
3.7
作者：
Sun J;Zhang X;Deng S;Zhang C;Wang M;Ding M;Zhao R;Shen X;Zhou X;Lu C;Chen S
通讯作者：
Chen S
两种杨树叶片光合作用、对盐度的荧光响应以及与叶绿体盐区室和抗氧化应激的相关性
影响因子：
2.3
作者：
邓林;EBERHARD FRITZ;ALOYS HÜTTERMANN;王瑞刚;陈少良;ANDREA POLLE
通讯作者：
ANDREA POLLE
DOI：
10.1111/j.1365-3040.2007.01667.x
发表时间：
2007-07
期刊：
Plant, cell & environment
影响因子：
--
作者：
Feng Zhang;Yuping Wang;Yingli Yang;Hao Wu;Di Wang;Jianquan Liu
通讯作者：
Feng Zhang;Yuping Wang;Yingli Yang;Hao Wu;Di Wang;Jianquan Liu
影响因子：
7.4
作者：
Clark, Greg;Fraley, Devin;Roux, Stanley J.
通讯作者：
Roux, Stanley J.
影响因子：
12.6
作者：
D. Vanegas;G. Clark;A. Cannon;S. Roux;P. Chaturvedi;E. McLamore
通讯作者：
D. Vanegas;G. Clark;A. Cannon;S. Roux;P. Chaturvedi;E. McLamore