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

 

英文摘要

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.

 

中文摘要（谷歌机翻）

非损伤微测技术（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。

 

文章链接： 

https://www.frontiersin.org/articles/10.3389/fpls.2018.01366/full

 

标签: H+, K+, Na+, 杨树, 盐敏感, 盐胁迫, 硫化氢