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2018年9月19日,北京林业大学陈少良、林善枝、赵楠、孙健利用NMT在Frontiers in Plant Science上发表了标题为Hydrogen Sulfide Mediates K+ and Na+ Homeostasis in the Roots of Salt-Resistant and Salt-Sensitive Poplar Species Subjected to NaCl Stress的研究成果。


  • 期刊:Frontiers in Plant Science
  • 主题:硫化氢介导盐胁迫和盐敏感杨树种根系中的K+和Na+稳态
  • 标题:Hydrogen Sulfide Mediates K+ and Na+ Homeostasis in the Roots of Salt-Resistant and Salt-Sensitive Poplar Species Subjected to NaCl Stress.
  • 影响因子:3.678
  • 检测指标:K+、Na+、H+流速
  • 检测部位:杨树根部(距离根尖300um)
  • K+、Na+、H+流实验处理方法:一年生的胡杨幼苗,在对照,对照加NaHS(50mM),NaCl(50mM)和NaCl(50mM)加上NaHS(50mM)这四种处理分别处理24小时和5天
  • K+、Na+、H+流实验测试液成份:0.1 mM KCl, 0.1 mM CaCl2, 0.1 mM MgCl2, 0.5 mM NaCl, 0.2 mM Na2SO4, and 0.3 mM MES, pH 4.0
  • 作者:北京林业大学陈少良、林善枝、赵楠、孙健


Non-invasive micro-test techniques (NMT) were used to analyze NaCl-altered flux profiles of K+, Na+, and H+ in roots and effects of NaHS (a H2S donor) on root ion fluxes in two contrasting poplar species, Populus euphratica (salt-resistant) and Populus popularis (salt-sensitive).

Both poplar species displayed a net K+ efflux after exposure to salt shock (100 mM NaCl), as well as after short-term (24 h), and long-term (LT) (5 days) saline treatment (50 mM NaCl, referred to as salt stress). NaHS (50 μM) restricted NaCl-induced K+ efflux in roots irrespective of the duration of salt exposure, but K+ efflux was not pronounced in data collected from the LT salt stress treatment of P. euphratica.

The NaCl-induced K+ efflux was inhibited by a K+ channel blocker, tetraethylammonium chloride (TEA) in P. popularis root samples, but K+ loss increased with a specific inhibitor of plasma membrane (PM) H+-ATPase, sodium orthovanadate, in both poplar species under LT salt stress and NaHS treatment. This indicates that NaCl-induced K+ loss was through depolarization-activated K+ channels. NaHS caused increased Na+ efflux and a corresponding increase in H+ influx for poplar roots subjected to both the short- and LT salt stress.

The NaHS-enhanced H+ influx was not significant in P. euphratica samples subjected to short term salt stress. Both sodium orthovanadate and amiloride (a Na+/H+ antiporter inhibitor) effectively inhibited the NaHS-augmented Na+ efflux, indicating that the H2S-enhanced Na+ efflux was due to active Na+ exclusion across the PM. We therefore conclude that the beneficial effects of H2S probably arise from upward regulation of the Na+/H+ antiport system (H+ pumps and Na+/H+ antiporters), which promote exchange of Na+ with H+ across the PM and simultaneously restricted the channel-mediated K+ loss that activated by membrane depolarization.



非侵入性微测试技术(NMT)用于分析NaCl中改变的根中K+,Na+和H+的通量分布以及NaHS(H2S供体)对两种对比杨树胡杨(Populus euphratica)根系离子通量的影响(耐盐)和Populus popularis(盐敏感)。

在暴露于盐休克(100mM NaCl)之后,以及在短期(24小时)和长期(LT)(5天)盐水处理(50mM NaCl,参考)之后,两种杨树物种都表现出净K+外排。作为盐胁迫)。无论盐暴露的持续时间如何,NaHS(50μM)都限制了NaCl诱导的根中的K+流出,但是从胡杨的LT盐胁迫处理收集的数据中K+流出不明显。

NaCl诱导的K+流出受到K+通道阻滞剂,四乙基氯化铵(TEA)在P.pularis根样品中的抑制,但K+损失随着特异性质膜抑制剂(PM)H+ -ATPase,原钒酸钠在杨树中的增加而增加。 LT盐胁迫和NaHS处理下的物种。这表明NaCl诱导的K+损失是通过去极化激活的K+通道。 NaHS导致Na+流出增加,并且受到短盐和LT盐胁迫的杨树根的H+流入相应增加。

经受短期盐胁迫的胡杨(P. euphratica)样品中NaHS增强的H+流入量不显着。原钒酸钠和阿米洛利(Na+ / H+逆向转运蛋白抑制剂)均有效抑制NaHS增强的Na+流出,表明H2S增强的Na+流出是由于PM中的活性Na+排斥。因此,我们得出结论,H2S的有益作用可能源于Na+ / H+反向运输系统(H+泵和Na+ / H+反向运输)的向上调节,其促进Na+与H+在PM上的交换并同时限制通道介导的K+损失。通过膜去极化激活。

FIGURE 1丨Effects of NaHS on NaCl shock-altered transient K+ kinetics within P. euphratica and P. popularis root samples. Young root samples of P. euphratica and P. popularis were equilibrated for 30 min in a basic solution [NaCl (0.1 mM), MgCl2 (0.1 mM), CaCl2 (0.1 mM), and KCl (0.5 mM)] supplemented with or without 25, 50, and 200 µM NaHS. Thereafter, K+ kinetics were recorded at meristems (300 µm from the root tip) for ca. 40 min after NaCl shock. The salt shock (100 mM NaCl) was given by adding acquired amount of NaCl stock (0.2 M, pH 6.0 adjusted with NaOH and HCl) to the measuring solution. Before the NaCl shock, steady-state K+ fluxes were recorded for 10 min. Each point is the mean of five individual plants and bars represent the standard error of the mean.