title: Hydrogen sulfide is involved in maintaining ion homeostasis via regulating plasma membrane Na+/H+ antiporter system in the hydrogen peroxide-dependent manner in salt-stress Arabidopsis thaliana root.
abstract: 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.
authors: College of Life Sciences, Northwest A&F University, Yangling, Shaanxi, 712100, China, lijsh2011@163.com.
authors: Jisheng
authors: J
authors: Li
authors: Honglei
authors: H
authors: Jia
authors: Jue
authors: J
authors: Wang
authors: Qianhua
authors: Q
authors: Cao
authors: Zichao
authors: Z
authors: Wen
mesh_terms: D062646:Acid Sensing Ion Channel Blockers / Q000494:pharmacology; D000584:Amiloride / Q000494:pharmacology; D017360:Arabidopsis / Q000187:drug effects* / Q000378:metabolism*; D002462:Cell Membrane / Q000187:drug effects / Q000378:metabolism; D005990:Glycerol / Q000494:pharmacology; D006861:Hydrogen Peroxide / Q000378:metabolism; D006862:Hydrogen Sulfide / Q000378:metabolism*; D019255:NADPH Oxidases / Q000378:metabolism; D009861:Onium Compounds / Q000494:pharmacology; D012965:Sodium Chloride; D013440:Sulfides / Q000494:pharmacology; D013890:Thiourea / Q000031:analogs & derivatives / Q000494:pharmacology; D014638:Vanadates / Q000494:pharmacology
chemical_list: D062646:Acid Sensing Ion Channel Blockers; D009861:Onium Compounds; D013440:Sulfides; D014638:Vanadates; D012965:Sodium Chloride; C007517:diphenyleneiodonium; D000584:Amiloride; C038983:1,3-dimethylthiourea; D006861:Hydrogen Peroxide; D019255:NADPH Oxidases; C025451:sodium bisulfide; D013890:Thiourea; D005990:Glycerol; D006862:Hydrogen Sulfide