Green Environmentally Friendly "Zn(CH3SO3)2" Electrolyte for Aqueous Zinc-Ion Batteries.

Aqueous zinc-ion batteries are considered as an ideal substitute for lithium-ion batteries due to their abundant resource storage, high safety, and low price. However, zinc anodes exhibit poor reversibility and cyclic stability in most conventional aqueous electrolytes. Herein, an environmentally friendly Zn(CH3SO3)2 electrolyte is proposed to solve the problems of common aqueous electrolytes. The bulky CH3SO3- anions can regulate the solvation structure of Zn2+ by replacing some water molecules in the primary solvation sheath of Zn2+, thus slowing the hydrogen evolution side reactions and formation of zinc dendrite. Additionally, the changing solvation structure weakens the bonding between Zn2+ and the surrounding water molecules, which is conducive to the transport and charge transfer of Zn2+, thus improving the battery capacity. In the Zn(CH3SO3)2 electrolyte, Zn plating/stripping exhibits a high Coulombic efficiency of >98% and long-term cyclic stability over 800 h. The specific capacity of the assembled Zn//V2O5 cell in 3 mol L-1 Zn(CH3SO3)2 reaches 350 mA h g-1 at 0.1 A g-1, much higher than that in the ZnSO4 electrolyte (213 mA h g-1). In conclusion, this work offers insights into the exploration of advanced green electrolyte systems for zinc-ion batteries.

A facile morphology tunable strategy of Zn-MOF derived hierarchically carbon materials with enhanced supercapacitive performance through the solvent effect.

Metal-organic framework (MOF) derived porous carbon materials have been widely applied as active materials for supercapacitors due to their large specific surface area and ordered pore structure. This paper presents a facile and effective strategy to regulate the morphology of a zinc-based metal-organic framework (Zn-trimesic acid, Zn-BTC) by adjusting the ethanol content in a solvent, which can effectively change the pore structure of Zn-BTC derived porous carbon (PC). The optimal PC prepared in 50% ethanol displays a rodlike structure with a large specific surface area (SSA) of 1930 m2 g-1 and an average pore size of 2.9 nm. This material shows an excellent rate performance with 78.8% capacitance retention when the current density increases from 1 A g-1 to 100 A g-1 and outstanding electrochemical stability with only 2.2% decline of capacitance after 200 000 cycles at 50 A g-1. Moreover, the assembled symmetrical capacitor shows a high energy density of 16.09 W h kg-1 at 698 W kg-1 and 11.89 W h kg-1 at a high power density of 41.56 kW kg-1. This method would provide a new pathway for the preparation of carbon materials with an adjustable pore size for high-performance supercapacitors.

MxRop1-MxrbohD1 interaction mediates ROS signaling in response to iron deficiency in the woody plant Malus xiaojinensis.

Iron (Fe) deficiency affects crop production and quality. Rho of plants (ROPs) involves in multiple physiological processes in plants. While it has not been well characterized under Fe deficiency, especially in perennial woody plants. In our study, we cloned ROP homologous gene MxRop1 from Malus xiaojinenesis, then overexpressed it in Arabidopsis, showing enhanced plant tolerance to Fe deficiency, which demonstrated its gene function during this stress. Overexpression of MxRop1 also increased reactive oxygen species (ROS) levels. Moreover, active state of MxRop1 (CA-MxRop1) interacted with N-terminal region of MxrbohD1, one ROS synthesis gene. When MxrbohD1 was overexpressed in apple calli, it showed significantly increased H2O2 content, fresh weight and FCR activity, while ROS inhibitor application dramatically inhibited FCR activity, demonstrating ROS produced by MxrbohD1 regulated Fe deficiency responses. Furthermore, using Agrobacterium rhizogenes transformation, MxrbohD1 was overexpressed in apple roots, with increased expression of Fe deficiency-induced genes and increased root FCR activity. Under Fe deficiency, it exhibited slight leaf yellowing phenotype. Co-expression of CA-MxRop1 and MxrbohD1 significantly induced ROS generation. Finally, we proposed that MxRop1 interacted with MxrbohD1 to modulate ROS mediated Fe deficiency adaptive responses in Malus xiaojinensis, which will provide a guidance of cultivation of Fe-deficiency tolerant apple plant.

AtROP6 is involved in reactive oxygen species signaling in response to iron-deficiency stress in Arabidopsis thaliana.

Understanding the mechanism of iron (Fe)-deficiency responses is crucial for improving plant Fe bioavailability. Here, we found that the Arabidopsis Rho-like GTPase 6 mutant (rop6) is less sensitive to Fe-deficiency responses and has reduced levels of reactive oxygen species (ROS) compared to wild-type (WT), while AtROP6-overexpressing seedlings exhibit more sensitivity to Fe-deficiency responses and has higher levels of ROS compared to WT. Moreover, treatment with H2 O2 improves the sensitivity to Fe-deficiency responses in rop6 mutants. By using the yeast two-hybrid system, we further demonstrate the direct interaction between AtROP6 and Arabidopsis respiratory burst oxidase homolog D (AtRBOHD), which controls the generation of ROS. Overall, we suggest that AtROP6 is involved in AtRBOHD-mediated ROS signaling to modulate Fe-deficiency responses in Arabidopsis thaliana.

Reactive Oxygen Species Function to Mediate the Fe Deficiency Response in an Fe-Efficient Apple Genotype: An Early Response Mechanism for Enhancing Reactive Oxygen Production.

Reactive oxygen species (ROS) are important signaling molecules in plants that contribute to stress acclimation. This study demonstrated that ROS play a critical role in Fe deficiency-induced signaling at an early stage in Malus xiaojinensis. Once ROS production has been initiated, prolonged Fe starvation leads to activation of ROS scavenging mechanisms. Further, we demonstrated that ROS scavengers are involved in maintaining the cellular redox homeostasis during prolonged Fe deficiency treatment. Taken together, our results describe a feedback repression loop for ROS to preserve redox homeostasis and maintain a continuous Fe deficiency response in the Fe-efficient woody plant M. xiaojinensis. More broadly, this study reveals a new mechanism in which ROS mediate both positive and negative regulation of plant responses to Fe deficiency stress.

Nitric oxide signaling is involved in the response to iron deficiency in the woody plant Malus xiaojinensis.

To cope with iron (Fe) deficiency, plants have evolved a wide range of adaptive responses from changes in morphology to altered physiological responses. Recent studies have demonstrated that nitric oxide (NO) is involved in the Fe-deficiency response through hormonal signaling pathways. Here, we report that NO plays a significant role in Malus xiaojinensis, an Fe-efficient woody plant. Fe deficiency triggered significant accumulation of NO in the root system, predominantly in the outer cortical and epidermal cells of the elongation zone. The NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide potassium salt (cPTIO) completely arrested Fe deficiency-induced root hair formation, blocked the increase in root ferric-chelate reductase activity and in root H+ excretion, further reduced the active iron content in young leaves and roots, and prevented the upregulation of the critical Fe-related genes, FIT, MxFRO2-like, and MxIRT1. These conditions were restored under Fe deficiency by treatment with the NO donor, sodium nitroprusside (SNP). Additionally, chlorophyll content and relative expression levels of the genes chlorophyll a deoxygenase (MxCAO) and polyamine oxidase (MxPAO) were not changed significantly following Fe deficiency for 6 d; however, SNP treatment increased MxHEMA gene expression. Interestingly, the Fv/Fm ratio, the maximum quantum yield of photosystem II (PSII), decreased significantly following cPTIO treatment. We observed more severe chlorosis under Fe deficiency with cPTIO treatment for 9 d. These results strongly suggest that NO mediates a range of responses to Fe deficiency in M. xiaojinensis, from morphological changes to the regulation of physiological processes and gene expression.