Hydrogen sulfide enhances salt tolerance through nitric oxide-mediated maintenance of ion homeostasis in barley seedling roots

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作者
Juan Chen
Wen-Hua Wang
Fei-Hua Wu
En-Ming He
Xiang Liu
Zhou-Ping Shangguan
Hai-Lei Zheng
机构
[1] State Key Laboratory of Soil Erosion and Dryland Farming on the Loess Plateau,
[2] Northwest A&F University,undefined
[3] Key Laboratory for Subtropical Wetland Ecosystem Research of MOE,undefined
[4] College of the Environment and Ecology,undefined
[5] Xiamen University,undefined
[6] Fujian Key Laboratory of Subtropical Plant Physiology and Biochemistry,undefined
[7] Fujian Institute of Subtropical Botany,undefined
[8] College of Life and Environmental Sciences,undefined
[9] Hangzhou Normal University,undefined
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摘要
Hydrogen sulfide (H2S) and nitric oxide (NO) are emerging as messenger molecules involved in the modulation of plant physiological processes. Here, we investigated a signalling network involving H2S and NO in salt tolerance pathway of barley. NaHS, a donor of H2S, at a low concentration of either 50 or 100 μM, had significant rescue effects on the 150 mM NaCl-induced inhibition of plant growth and modulated the K+/Na+ balance by decreasing the net K+ efflux and increasing the gene expression of an inward-rectifying potassium channel (HvAKT1) and a high-affinity K+ uptake system (HvHAK4). H2S and NO maintained the lower Na+ content in the cytoplast by increasing the amount of PM H+-ATPase, the transcriptional levels of PM H+-ATPase (HvHA1) and Na+/H+ antiporter (HvSOS1). H2S and NO modulated Na+ compartmentation into the vacuoles with up-regulation of the transcriptional levels of vacuolar Na+/H+ antiporter (HvVNHX2) and H+-ATPase subunit β (HvVHA-β) and increased in the protein expression of vacuolar Na+/H+ antiporter (NHE1). H2S mimicked the effect of sodium nitroprusside (SNP) by increasing NO production, whereas the function was quenched with the addition of NO scavenger. These results indicated that H2S increased salt tolerance by maintaining ion homeostasis, which were mediated by the NO signal.
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