The objective of this study was to evaluate the ability of the phytohormone S-abscisic acid (S-ABA) to protect maize seedlings grown under drought stress and to measure their increased drought tolerance. The maize hybrids ‘Zhengdan 958’ (ZD958; drought tolerant) and ‘Xundan 20’ (XD20; drought sensitive) were treated with nutrient solutions of different concentrations (1, 2, 4, 8, and 10 mg/kg) of S-ABA under polyethylene glycol (PEG, 15% w/v, MW 6000) simulated drought stress. Optimal concentrations of S-ABA were designed to be sprayed onto the leaves of seedlings, and their effect on endogenous ABA, malondialdehyde (MDA), osmotic substances, antioxidant enzyme activities, and Asr1 gene expression in seedlings were studied. Results indicated that, under drought stress, S-ABA treatment significantly improved maize seed germination rate (GR), germination energy (GE), and seedling biomass (p < 0.05). After spraying 4 mg/kg S-ABA onto leaves, the endogenous hormone ABA, osmotic substances, antioxidant enzyme activities, and expressive quantity of the Asr1 gene were extended and MDA content dropped significantly (p < 0.05). Moreover, ZD 958 endogenous ABA content, osmotic substances content, antioxidant enzyme activity and Asr1 gene expressive quantity were higher than that of XD 20 (p < 0.05). In conclusion, S-ABA treatment increased the content of endogenous ABA, induced an increase in antioxidant enzyme activity and Asr1 gene expression level, reduced the oxidative damage caused by drought to maize leaves, and improved the adaptability of maize seedlings to withstand drought stress. The promoting effect of S-ABA on the drought-tolerant variety ZD 958 was more obvious (p < 0.05). These results serve as a reference for the use of S-ABA in mitigating drought stress in maize.
Ligupurpuroside A is a glycoside extracted from Ku-Ding tea. As extracts from Ku-Ding tea exhibit anti-inflammatory property, we hypothesize that Ligupurpuroside A may be an active compound which inhibits trypsin activity during the anti-inflammatory process. The mechanism and nature of inhibition of trypsin by Ligupurpuroside A have been studied by multi-spectroscopic method, enzyme-activity assay and molecular docking. Enzyme activity assay reveals that Ligupurpuroside A significantly inhibits the activity of trypsin through a competitive manner with an IC50 value of 3.08 × 10?3 mol L?1. Fluorescence titration together with thermodynamic analysis indicate that a Ligupurpuroside A-trypsin complex is formed, and that hydrophobic force and hydrogen bonding are the main forces stabilizing the complex. UV-vis absorption, synchronous fluorescence and circular dichroism spectra show that the interaction between Ligupurpuroside A and trypsin induces conformational changes of trypsin with a decrease in the contents of α-helix and β-sheet. Finally, molecular docking further suggests that Ligupurpuroside A molecule binds within the active pocket of trypsin via hydrophobic force and hydrogen bond. Results from this study of the interaction of trypsin with its natural inhibitor should be useful to minimize the antinutritional effects and make full use of tea extracts in the food industry, and be also helpful to the design of the drugs for the diseases related to overexpression of trypsin. 相似文献
Long interspersed element type 1 (LINE-1, also L1 for short) is the only autonomously transposable element in the human genome. Its insertion into a new genomic site may disrupt the function of genes, potentially causing genetic diseases. Cells have thus evolved a battery of mechanisms to tightly control LINE-1 activity. Here, we report that a cellular antiviral protein, myxovirus resistance protein B (MxB), restricts the mobilization of LINE-1. This function of MxB requires the nuclear localization signal located at its N-terminus, its GTPase activity and its ability to form oligomers. We further found that MxB associates with LINE-1 protein ORF1p and promotes sequestration of ORF1p to G3BP1-containing cytoplasmic granules. Since knockdown of stress granule marker proteins G3BP1 or TIA1 abolishes MxB inhibition of LINE-1, we conclude that MxB engages stress granule components to effectively sequester LINE-1 proteins within the cytoplasmic granules, thus hindering LINE-1 from accessing the nucleus to complete retrotransposition. Thus, MxB protein provides one mechanism for cells to control the mobility of retroelements. 相似文献
The mitochondrial DNA m.3243A > G mutation is well-known to cause a variety of clinical phenotypes, including diabetes, deafness, and osteoporosis. Here, we report isolation and expansion of urine-derived stem cells (USCs) from patients carrying the m.3243A > G mutation, which demonstrate bimodal heteroplasmy. USCs with high levels of m.3243A > G mutation displayed abnormal mitochondrial morphology and function, as well as elevated ATF5-dependent mitochondrial unfolded protein response (UPRmt), together with reduced Wnt/β-catenin signaling and osteogenic potentials. Knockdown of ATF5 in mutant USCs suppressed UPRmt, improved mitochondrial function, restored expression of GSK3B and WNT7B, and rescued osteogenic potentials. These results suggest that ATF5-dependent UPRmt could be a core disease mechanism underlying mitochondrial dysfunction and osteoporosis related to the m.3243A > G mutation, and therefore could be a novel putative therapeutic target for this genetic disorder.Subject terms: Mechanisms of disease, Diabetes相似文献
Lentiviral Nef proteins have multiple functions and are important for viral pathogenesis. Recently, Nef proteins from many simian immunodefiency viruses were shown to antagonize a cellular antiviral protein, named Tetherin, that blocks release of viral particles from the cell surface. However, the mechanism by which Nef antagonizes Tetherin is unknown. Here, using related Nef proteins that differ in their ability to antagonize Tetherin, we identify three amino-acids in the C-terminal domain of Nef that are critical specifically for its ability to antagonize Tetherin. Additionally, divergent Nef proteins bind to the AP-2 clathrin adaptor complex, and we show that residues important for this interaction are required for Tetherin antagonism, downregulation of Tetherin from the cell surface and removal of Tetherin from sites of particle assembly. Accordingly, depletion of AP-2 using RNA interference impairs the ability of Nef to antagonize Tetherin, demonstrating that AP-2 recruitment is required for Nef proteins to counteract this antiviral protein. 相似文献