Hydrogen Sulfide Mediates K(+) and Na(+) Homeostasis in the Roots of Salt-Resistant and Salt-Sensitive Poplar Species Subjected to NaCl Stress.

Hydrogen Sulfide Mediates K(+) and Na(+) Homeostasis in the Roots of Salt-Resistant and Salt-Sensitive Poplar Species Subjected to NaCl Stress.
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硫化氢介导遭受 NaCl 胁迫的抗盐和盐敏感杨树根部 K 和 Na 稳态

DOI:
10.3389/fpls.2018.01366
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发表时间:
2018
影响因子:
5.6
通讯作者:
Chen S
Chen S
中科院分区:
生物学2区
文献类型:
--
作者:
Zhao N;Zhu H;Zhang H;Sun J;Zhou J;Deng C;Zhang Y;Zhao R;Zhou X;Lu C;Lin S;Chen S

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采用无创微测试技术(NMT)分析了nacl对两种杨树(耐盐杨树(Populus euphratica)和盐敏感杨树(popularis popularis)根系K+、Na+和H+通量的影响,以及NaHS (H2S供体)对根系离子通量的影响。两种杨树在盐胁迫(100 mM NaCl)、短期(24 h)和长期(LT) (5 d)盐胁迫(50 mM NaCl,称为盐胁迫)处理后均表现出净K+流出。NaHS (50 μM)抑制nacl诱导的根内K+外排,与盐暴露时间无关,但在低盐胁迫下胡杨的根内K+外排不明显。在低盐胁迫和NaHS处理下,两种杨根样品中,K+通道阻滞剂四乙基氯化铵(TEA)均能抑制nacl诱导的K+外排,但在质膜(PM) H+- atp酶特异性抑制剂正钒酸钠(sodium orthovanadate)的作用下,K+损失增加。这表明nacl诱导的K+损失是通过去极化激活的K+通道进行的。在短盐胁迫和低盐胁迫下,NaHS使杨树根系的Na+外排增加,H+内流相应增加。nahs增强的H+内流在短期盐胁迫下的胡杨样品中不显著。正钒酸钠和amiloride(一种Na+/H+反向转运抑制剂)均能有效抑制nahs增强的Na+外排,表明h2s增强的Na+外排是由于PM中Na+的活性排除。因此,我们得出结论,H2S的有益作用可能来自于Na+/H+反转运体系统(H+泵和Na+/H+反转运体)的向上调节,该系统促进了Na+与H+在PM上的交换,同时限制了由膜去极化激活的通道介导的K+损失。
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.
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