Synergistic roles of leaf boron and calcium during the growing season in affecting sugar and starch accumulation in ripening apple fruit

Fruit sugar content is one of the most important flavor quality traits in the fresh market. Minerals, such as boron (B) and calcium (Ca), are associated with fruit sugar and starch accumulation in many plant species. To better understand the roles of B and Ca in affecting sugar and starch accumulation in apples, 2 g L^?1 Na₂B₄O₇·10H₂O or 10 g L^?1 CaCl₂ was supplied by foliar spray to 20-year-old ‘Fuji’ (Malus domestica Borkh. cv. Fuji) trees at four developmental stages (fruit set, onset of rapid fruit growth, rapid fruit growth and the end of rapid fruit growth), in 2010–2011. The most effective treatment significantly increasing soluble sugar and starch levels in ripening fruit was the foliar application of 2 g L^?1 Na₂B₄O₇·10H₂O during rapid fruit growth, and the robustness of the effects was confirmed for two cultivars, ‘Fuji’ and ‘Orin’, at three orchards in 2011. Foliar applications of B during the onset of rapid fruit growth and rapid fruit growth, as well as the foliar application of Ca at fruit set, significantly increased the soluble sugar content in ripening fruit. In addition, the B application was effective in increasing the fruit starch content, but Ca was not. Both B and Ca treatments significantly increased the leaf concentrations of the other element at least transiently. However, B and Ca effects on fruit sugar/starch did not seem to depend on higher leaf B or Ca levels. In conclusion, B and Ca interact in enhancing fruit sugar and starch contents at the fruit ripening stage.     

Mechanisms for L-channel-mediated increase in [Ca]i and its reduction by anti-bipolar drugs in cultured astrocytes combined with its mRNA expression in freshly isolated cells support the importance of astrocytic L-channels

The importance of Ca²⁺ signaling in astrocytes is undisputed but a potential role of Ca²⁺ influx via L-channels in the brain in vivo is disputed, although expression of these channels in cultured astrocytes is recognized. This study shows that an increase in free cytosolic Ca²⁺ concentration ([Ca²⁺]_i) in astrocytes in primary cultures in response to an increased extracellular K⁺ concentration (45 mM) is inhibited not only by nifedipine (confirming previous observations) but also to a very large extent by ryanodine, inhibiting ryanodine receptor-mediated release of Ca²⁺, known to occur in response to an elevation in [Ca²⁺]_i. This means that the actual influx of Ca²⁺ is modest, which may contribute to the difficulty in demonstrating L-channel-mediated Ca²⁺ currents in astrocytes in intact brain tissue. Chronic treatment with any of the 3 conventional anti-bipolar drugs lithium, carbamazepine or valproic acid similarly causes a pronounced inhibition of K⁺-mediated increase in [Ca²⁺]_i. This is shown to be due to an inhibition of capacitative Ca²⁺ influx, reflected by decreased mRNA and protein expression of the ‘transient receptor potential channel’ (TRPC1), a constituent of store-operated channels (SOCEs). Literature data are cited (i) showing that depolarization-mediated Ca²⁺ influx in response to an elevated extracellular K⁺ concentration is important for generation of Ca²⁺ oscillations and for the stimulatory effect of elevated K⁺ concentrations in intact, non-cultured brain tissue, and (ii) that Ca²⁺ channel activity is dependent upon availability of metabolic substrates, including glycogen. Finally, expression of mRNA for Ca_v1.3 is demonstrated in freshly separated astrocytes from normal brain.     

Detection of Biosignatures by Geomatrix-Assisted Laser Desorption/Ionization (GALDI) Mass Spectrometry

Identification of mineral-associated biosignatures is of significance for retrieving biochemical information from geological records here on Earth and for detecting signs of life on other planets, such as Mars. An investigation using laser desorption Fourier transform mass spectrometry was conducted to determine whether geomatrix-assisted laser desorption/ionization (GALDI) can be used to detect amino acids (e.g., histidine, threonine, and cysteine) and small proteins (e.g., gramicidin S) associated with mineral phases and whether the geomatrix impacts detection. Iron oxide (Fe₂ O ₃ ) and sodium chloride (NaCl) were investigated as clean chemical analogues of hematite and halite, respectively, which have both been detected on the surface of Mars. Samples were prepared by 2 methods: (1) application of analyte solution to the geomatrix surface with subsequent drying; and (2) physical mixing of analyte and geomatrix. Amino acids incorporated within NaCl by physical mixing yielded a better signal-to-noise ratio than those that were applied to the surface of a NaCl pellet. The composition of the geomatrix had an influence on the detection of biomolecules. Peaks corresponding to the cation-attached biomolecular ions were observed for the NaCl prepared samples. However, no biomolecular ion species were observed in samples using Fe ₂ O ₃ as geomatrix. Instead, only minor peaks that may correspond to ions derived from fragments of the biomolecules were obtained.     

Struvite Precipitation Induced by a Novel Sulfate-Reducing Bacterium Acinetobacter calcoaceticus SRB4 Isolated from River Sediment

This article presents a study of struvite formation in liquid medium induced by the sulfate-reducing bacterium Acinetobacter calcoaceticus SRB4, a strain isolated from river sediment. We identified the bacterial strain A. calcoaceticus SRB4 and analyzed its micromorphology. The minerals formed were studied with an electroprobe microanalyzer, Fourier transform infrared spectroscopy, high-resolution transmission electron microscopy, selected-area electron diffraction, X-ray diffraction, thermogravimetry, differential thermogravimetry, and differential scanning calorimetry. Acinetobacter calcoaceticus SRB4 was found to induce struvite precipitation, whereas sterile control cultures did not. Many transparent stick-shaped struvite precipitates were distributed at the bottom of the conical flasks in the experimental group. Most bacteria were spherical and a large quantity of spherical struvite particles (less than 200 nm in diameter) adhered to the bacterial surface. An electron probe microanalysis showed that the precipitates contained C, O, P, Mg, and other elements. Fourier transformation infrared spectra showed that the precipitates contained crystalline water, NH₄⁺, and PO₄^3? groups. X-ray diffraction spectra showed that the precipitates were struvite crystals, with preferential orientation and lattice distortion. Thermogravimetry showed that the weight loss was caused by the evaporation of crystalline water at temperatures lower than 136°C and the release of ammonia from struvite at temperatures of 136–228.5°C. In this article, we discuss the possible mechanism of struvite formation and the possible role played by A. calcoaceticus SRB4. Our study extends our understanding of the phosphate biomineralization mechanism and should prove useful in recycling phosphorus in wastewater.     

Protective Effects of Mangiferin in Subchronic Developmental Lead-Exposed Rats

Lead is a ubiquitous environmental and industrial pollutant. Exposure to excessive amounts of lead is especially harmful to the central nervous systems of infants and young children, and oxidative stress has been reported as a major mechanism of lead-induced toxicity. To evaluate the ameliorative potential of antioxidant mangiferin (MGN) on lead-induced toxicity, Morris water maze test, determination of blood and bone lead concentration, determination of antioxidant status in plasma, as well as observation of ultrastructural changes in the hippocampus were carried out. In the present study, under a transmission electron microscope, ameliorated morphological damages in the hippocampus were observed in MGN-treated groups. Blood and bone lead concentration in MGN-treated groups lowered to some extent (p?<?0.05, p?<?0.01). The activities of antioxidant enzymes, glutathione (GSH) content, and the GSH/oxidized glutathione ratio in MGN-treated groups were increased, respectively. Further studies are needed to establish whether the observed differences were a direct cause of mangiferin on lead-induced toxicity or not. This study might provide clues for the treatment of lead-induced toxicity.     

Iodine Excess Induces Hepatic Steatosis Through Disturbance of Thyroid Hormone Metabolism Involving Oxidative Stress in BaLB/c Mice

Iodine excess is emerging as a new focus. A better understanding of its hazardous effects on the liver will be of great benefit to health. The aim of this study is to illustrate the effects of iodine excess on hepatic lipid homeostasis and explore its possible mechanisms. One hundred twenty BaLB/c mice were given iodine at different levels (0, 0.3, 0.6, 1.2, 2.4, and 4.8 mg I/L) in drinking water for 1 or 3 months. Lipid parameters and serum thyroid hormones were measured. Hepatic type 1 deiodinase activity and oxidative stress parameters were evaluated. The mRNA expression of sterol regulatory element-binding protein-1c (SREBP-1c) and fatty acid synthase (FAS) was detected by real-time polymerase chain reaction. Dose-dependent increase of hepatic triglyceride content was detected (r?=?0.680, P?<?0.01) in iodine-loaded groups. Evident hepatic steatosis was observed in 2.4 and 4.8 mg I/L iodine-loaded groups. The activities of antioxidant enzymes (glutathione peroxidase and superoxide dismutase) were decreased, and the malondialdehyde level was increased by excessive iodine in both serum and liver in a dose-dependent manner, accompanying the decrease of hepatic D1 activity. That resulted in the increase of serum total thyroxine and the decrease of serum total triiodothyronine in iodine-loaded groups. The mRNA expression of SREBP-1c and FAS was increased in iodine-loaded groups in response to the change of serum triiodothyronine. Present findings demonstrated that iodine excess could dose dependently induce hepatic steatosis. Furthermore, our data suggested that the disturbance of thyroid hormone metabolism involving oxidative stress may play a critical role in iodine excess-induced hepatic steatosis.     

Arsenic Resistance and Bioaccumulation of an Indigenous Bacterium Isolated from Aquifer Sediments of Datong Basin,Northern China

To obtain bacteria with arsenic accumulation potential that can be used to remove arsenic from contaminated waters, experiments were made to investigate the tolerance and accumulation to arsenic of an indigenous bacterium XZM002 isolated from aquifer sediments of Datong Basin, northern China. The results showed that strain XZM002 belongs to the genus Bacillus and has evolved defense mechanisms to reduce arsenic injury: the change of cellular shape from initial rod to oval and then to round with increment of arsenic toxicity. The effect of arsenate or arsenite on the bacterial growth was also investigated. Results showed that growth of the strain was inhibited under As(III) and high concentration As(V) (over 1200 μg l^?1) conditions in the first 2 days and promoted under low concentration As(V) (under 400 μg l^?1) condition. Its arsenic bioaccumulation potential was surveyed by monitoring the concentration changes of total arsenic and arsenic speciation in the medium and in the cytoplasm, and those of total arsenic on the membrane. Methylated arsenic species were not detected throughout the experiment. The results indicated that 11.5% of arsenic was removed from liquid medium into the bacterial cells and 9.22% of As(V) in the medium was transformed gradually to As(III) during 4 d of incubation. Approximately 80% of the total accumulated arsenic was adsorbed onto the membrane instead of into cytoplasm; and the arsenic accumulation almost approached saturation after incubation for 72 h.     

Influence of Arsenate on Lipid Peroxidation Levels and Antioxidant Enzyme Activities in Bacillus cereus Strain XZM002 Isolated from High Arsenic Aquifer Sediments

Bacillus cereus strain XZM002 isolated from high arsenic aquifer sediments of Datong Basin was applied to examine the effects of arsenate stress on antioxidant enzyme activities, lipid peroxidation levels and cell growth inhibition rate. After 2 d exposure, the cell growth inhibition rate enhanced with an increase of As(V) concentrations (0, 800, 1600 μg/l). Reactive oxygen species and glutathione contents, lipid peroxidation levels, and antioxidant enzymes (glutathione peroxidase, and other three) activities of the treated cells were significantly higher than those of the controls during 3 d exposure (p < 0.05). Besides, the levels of nine parameters reached maximum after 2 d exposure and increased significantly with increasing arsenate stress (p < 0.05). However, they returned to levels similar to those of the control on the fourth day of exposure. The results suggested that the antioxidant defense system in B. cereus strain XZM002 could protect the cells from oxidative damage induced by arsenate.     

Insights into Distinct Modulation of α7 and α7β2 Nicotinic Acetylcholine Receptors by the Volatile Anesthetic Isoflurane

Nicotinic acetylcholine receptors (nAChRs) are targets of general anesthetics, but functional sensitivity to anesthetic inhibition varies dramatically among different subtypes of nAChRs. Potential causes underlying different functional responses to anesthetics remain elusive. Here we show that in contrast to the α7 nAChR, the α7β2 nAChR is highly susceptible to inhibition by the volatile anesthetic isoflurane in electrophysiology measurements. Isoflurane-binding sites in β2 and α7 were found at the extracellular and intracellular end of their respective transmembrane domains using NMR. Functional relevance of the identified β2 site was validated via point mutations and subsequent functional measurements. Consistent with their functional responses to isoflurane, β2 but not α7 showed pronounced dynamics changes, particularly for the channel gate residue Leu-249(9′). These results suggest that anesthetic binding alone is not sufficient to generate functional impact; only those sites that can modulate channel dynamics upon anesthetic binding will produce functional effects.     

Synaptic mutant huntingtin inhibits synapsin-1 phosphorylation and causes neurological symptoms

Many genetic mouse models of Huntington’s disease (HD) have established that mutant huntingtin (htt) accumulates in various subcellular regions to affect a variety of cellular functions, but whether and how synaptic mutant htt directly mediates HD neuropathology remains to be determined. We generated transgenic mice that selectively express mutant htt in the presynaptic terminals. Although it was not overexpressed, synaptic mutant htt caused age-dependent neurological symptoms and early death in mice as well as defects in synaptic neurotransmitter release. Mass spectrometry analysis of synaptic fractions and immunoprecipitation of synapsin-1 from HD CAG150 knockin mouse brains revealed that mutant htt binds to synapsin-1, a protein whose phosphorylation is critical for neurotransmitter release. We found that polyglutamine-expanded exon1 htt binds to the C-terminal region of synapsin-1 to reduce synapsin-1 phosphorylation. Our findings point to a critical role for synaptic htt in the neurological symptoms of HD, providing a new therapeutic target.