Li Jisheng, Jia Honglei, Wang Jue, Cao Qianhua, Wen Zichao
College of Life Sciences, Northwest A&F University, Yangling, Shaanxi, 712100, China,
Protoplasma. 2014 Jul;251(4):899-912. doi: 10.1007/s00709-013-0592-x. Epub 2013 Dec 7.
Hydrogen sulfide (H2S) and hydrogen peroxide (H2O2) function as the signaling molecules in plants responding to salt stresses. The present study presents a signaling network involving H2S and H2O2 in salt resistance pathway of the Arabidopsis root. Arabidopsis roots were sensitive to 100 mM NaCl treatment, which displayed a great increase in electrolyte leakage (EL) and Na(+)/K(+) ratio under salt stress. The treatment of H2S donors sodium hydrosulfide (NaHS) enhanced the salt tolerance by maintaining a lower Na(+)/K(+) ratio. In addition, the inhibition of root growth under salt stress was removed by H2S. Further studies indicated that H2O2 was involved in H2S-induced salt tolerance pathway. H2S induced the production of the endogenous H2O2 via regulating the activities of glucose-6-phosphate dehydrogenase (G6PDH) and plasma membrane (PM) NADPH oxidase, with the treatment with dimethylthiourea (DMTU, an ROS scavenger), diphenylene iodonium (DPI, a PM NADPH oxidase inhibitor), or glycerol (G6PDH inhibitor) removing the effect of H2S. Treatment with amiloride (an inhibitor of PM Na(+)/H(+) antiporter) and vanadate (an inhibitor of PM H(+)-ATPase) also inhibited the activity of H2S on Na(+)/K(+) ratio. Through an analysis of quantitative real-time polymerase chain reaction and Western blot, we found that H2S promoted the genes expression and the phosphorylation level of PM H(+)-ATPase and Na(+)/H(+) antiporter protein level. However, when the endogenous H2O2 level was inhibited by DPI or DMTU, the effect of H2S on the PM Na(+)/H(+) antiporter system was removed. Taken together, H2S maintains ion homeostasis in the H2O2-dependent manner in salt-stress Arabidopsis root.
硫化氢（H₂S）和过氧化氢（H₂O₂）作为植物响应盐胁迫的信号分子发挥作用。本研究提出了一个拟南芥根抗盐途径中涉及H₂S和H₂O₂的信号网络。拟南芥根对100 mM NaCl处理敏感，在盐胁迫下其电解质渗漏（EL）和Na⁺/K⁺比值大幅增加。H₂S供体硫氢化钠（NaHS）处理通过维持较低的Na⁺/K⁺比值增强了耐盐性。此外，H₂S消除了盐胁迫下对根生长的抑制。进一步研究表明，H₂O₂参与了H₂S诱导的耐盐途径。H₂S通过调节6-磷酸葡萄糖脱氢酶（G6PDH）和质膜（PM）NADPH氧化酶的活性诱导内源性H₂O₂的产生，用二甲基硫脲（DMTU，一种活性氧清除剂）、二苯基碘鎓（DPI，一种PM NADPH氧化酶抑制剂）或甘油（G6PDH抑制剂）处理可消除H₂S的作用。用氨氯地平（一种PM Na⁺/H⁺反向转运蛋白抑制剂）和钒酸盐（一种PM H⁺-ATP酶抑制剂）处理也抑制了H₂S对Na⁺/K⁺比值的作用。通过定量实时聚合酶链反应和蛋白质免疫印迹分析，我们发现H₂S促进了PM H⁺-ATP酶的基因表达和磷酸化水平以及Na⁺/H⁺反向转运蛋白的蛋白水平。然而，当内源性H₂O₂水平被DPI或DMTU抑制时，H₂S对PM Na⁺/H⁺反向转运蛋白系统的作用被消除。综上所述，在盐胁迫的拟南芥根中，H₂S以H₂O₂依赖的方式维持离子稳态。
