AUTHOR=Zhao Nan , Zhu Huipeng , Zhang Huilong , Sun Jian , Zhou Jinchi , Deng Chen , Zhang Yuhong , Zhao Rui , Zhou Xiaoyang , Lu Cunfu , Lin Shanzhi , Chen Shaoliang TITLE=Hydrogen Sulfide Mediates K+ and Na+ Homeostasis in the Roots of Salt-Resistant and Salt-Sensitive Poplar Species Subjected to NaCl Stress JOURNAL=Frontiers in Plant Science VOLUME=9 YEAR=2018 URL=https://www.frontiersin.org/journals/plant-science/articles/10.3389/fpls.2018.01366 DOI=10.3389/fpls.2018.01366 ISSN=1664-462X ABSTRACT=

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.