Adsorption mechanism of Ca2+, Mg2+, Fe3+, and Al3+ ions in phosphoric acid-nitric acid solution on 001 × 7 and S957 resins.

Selective removal of Ca2+ and Mg2+ ions using the 001 × 7 resin and Fe3+ and Al3+ ions using the S957 resin is able to achieve the deep purification of the phosphoric acid-nitric acid solution, but the adsorption behaviors of Fe3+ and Al3+ ions are seriously suppressed by phosphoric acid. In order to understand the interaction mechanism of separation processes and the influence of phosphoric acid, we first studied the bonding form of Ca2+, Mg2+, Fe3+, and Al3+ ions on 001 × 7 and S957 resins using FT-IR and XPS techniques; subsequently, quantum chemistry computation was carried out to further explore the bonding mechanism between the functional groups on resins and metal ions. FT-IR and XPS results reveal that for the adsorption process on the 001 × 7 resin, hydroxyls from sulfonic acid groups combine with Ca2+ and Mg2+ ions. Whereas Fe3+ and Al3+ ions are adsorbed on the S957 resin through an exchange reaction with hydroxyls on the phosphonic acid group but not on the sulfonic acid group. Quantum chemistry computation results reveal that the phosphonic acid group has a larger binding energy with Fe3+ and Al3+ ions. Thus, the S957 resin still presents great adsorption performance for Fe3+ and Al3+ ions despite the influence of dihydrogen phosphate ions in the phosphoric acid-nitric acid solution.

Enhanced Arabidopsis disease resistance against Botrytis cinerea induced by sulfur dioxide.

Sulfur dioxide (SO2) is a common air pollutant that has complex impacts on plants. The effect of prior exposure to 30mgm-3 SO2 on defence against Botrytis cinerea (B. cinerea) in Arabidopsis thaliana and the possible mechanisms of action were investigated. The results indicated that pre-exposure to 30mgm-3 SO2 resulted in significantly enhanced resistance to B. cinerea infection. SO2 pre-treatment significantly enhanced the activities of defence-related enzymes including phenylalanine ammonia-lyase (PAL), polyphenol oxidase (PPO), ß-1,3-glucanase (BGL) and chitinase (CHI). Transcripts of the defence-related genes PAL, PPO, PR2, and PR3, encoding PAL, PPO, BGL and CHI, respectively, were markedly elevated in Arabidopsis plants pre-exposed to SO2 and subsequently inoculated with B. cinerea (SO2+ treatment group) compared with those that were only treated with SO2 (SO2) or inoculated with B. cinerea (CK+). Moreover, SO2 pre-exposure also led to significant increases in the expression levels of MIR393, MIR160 and MIR167 in Arabidopsis. Meanwhile, the expression of known targets involved in the auxin signalling pathway, was negatively correlated with their corresponding miRNAs. Additionally, the transcript levels of the primary auxin-response genes GH3-like, BDL/IAA12, and AXR3/IAA17 were markedly repressed. Our findings indicate that 30mgm-3 SO2 pre-exposure enhances disease resistance against B. cinerea in Arabidopsis by priming defence responses through enhancement of defence-related gene expression and enzyme activity, and miRNA-mediated suppression of the auxin signalling pathway.

miR398 and miR395 are involved in response to SO2 stress in Arabidopsis thaliana.

Sulfur dioxide (SO2) is a common air pollutant that has adverse effects on plants. MicroRNAs (miRNAs) are small noncoding RNA that play critical roles in plant development and stress response. In this study, we found that two miRNAs, miR398 and miR395, were differentially expressed in Arabidopsis shoots under SO2 stress. The expression of miR398 was down-regulated, and the transcript levels of its target genes, Cu/Zn superoxide dismutases (CSD1 and CSD2), were increased during SO2 exposure. The activity of superoxide dismutase (SOD), one of the major antioxidant enzymes, was enhanced with the increase in the CSD transcript level, suggesting an important role of miR398 in response to SO2-induced oxidative stress. Meanwhile, the expression of miR395 was increased, and the transcript levels of its target genes, ATP sulfurylases (APS3 and APS4) and a low-affinity sulfate transporter (SULTR2;1), were decreased in Arabidopsis shoots, showing that miR395 played important roles in the regulation of sulfate assimilation and translocation during SO2 exposure. The content of glutathione (GSH), an important sulfur-containing antioxidant, was enhanced with the changes in sulfur metabolism in Arabidopsis shoots under SO2 stress. These results showed that both miR398 and miR395 were involved in protecting plants from oxidative damage during SO2 exposure. Many stress-responsive cis-elements were found in the promoter regions of MIR398 and MIR395, suggesting that these miRNAs might respond to various environmental conditions, including SO2 stress. Overall, our study provides an insight into the regulatory roles of miRNAs in response to SO2 stress in plants, and highlights the molecular mechanisms of plant adaptation to environmental stress.

NO and H2O2 contribute to SO2 toxicity via Ca2+ signaling in Vicia faba guard cells.

NO and H2O2 have been implicated as important signals in biotic and abiotic stress responses of plants to the environment. Previously, we have shown that SO2 exposure increased the levels of NO and H2O2 in plant cells. We hypothesize that, as signaling molecules, NO and H2O2 mediate SO2-caused toxicity. In this paper, we show that SO2 hydrates caused guard cell death in a concentration-dependent manner in the concentration range of 0.25 to 6 mmol L-1, which was associated with elevation of intracellular NO, H2O2, and Ca2+ levels in Vicia faba guard cells. NO donor SNP enhanced SO2 toxicity, while NO scavenger c-PTIO and NO synthesis inhibitors L-NAME and tungstate significantly prevented SO2 toxicity. ROS scavenger ascorbic acid (AsA) and catalase (CAT), Ca2+ chelating agent EGTA, and Ca2+ channel inhibitor LaCl3 also markedly blocked SO2 toxicity. In addition, both c-PTIO and AsA could completely block SO2-induced elevation of intracellular Ca2+ level. Moreover, c-PTIO efficiently blocked SO2-induced H2O2 elevation, and AsA significantly blocked SO2-induced NO elevation. These results indicate that extra NO and H2O2 are produced and accumulated in SO2-treated guard cells, which further activate Ca2+ signaling to mediate SO2 toxicity. Our findings suggest that both NO and H2O2 contribute to SO2 toxicity via Ca2+ signaling.

Uncovering microRNA-mediated response to SO2 stress in Arabidopsis thaliana by deep sequencing.

Sulfur dioxide (SO2) is a major air pollutant and has significant impacts on plants. MicroRNAs (miRNAs) are a class of gene expression regulators that play important roles in response to environmental stresses. In this study, deep sequencing was used for genome-wide identification of miRNAs and their expression profiles in response to SO2 stress in Arabidopsis thaliana shoots. A total of 27 conserved miRNAs and 5 novel miRNAs were found to be differentially expressed under SO2 stress. qRT-PCR analysis showed mostly negative correlation between miRNA accumulation and target gene mRNA abundance, suggesting regulatory roles of these miRNAs during SO2 exposure. The target genes of SO2-responsive miRNAs encode transcription factors and proteins that regulate auxin signaling and stress response, and the miRNAs-mediated suppression of these genes could improve plant resistance to SO2 stress. Promoter sequence analysis of genes encoding SO2-responsive miRNAs showed that stress-responsive and phytohormone-related cis-regulatory elements occurred frequently, providing additional evidence of the involvement of miRNAs in adaption to SO2 stress. This study represents a comprehensive expression profiling of SO2-responsive miRNAs in Arabidopsis and broads our perspective on the ubiquitous regulatory roles of miRNAs under stress conditions.