Systematic selection of competing metabolomics methods in a metabolite-sensory relationship study

Metabolomics - To study metabolic signatures can be used to identify predictive biomarkers for a patient's therapeutic response. We hypothesized that the characterization of a patients’...     

Agrobacterium-mediated transformation of alfalfa (Medicago sativa) using a synthetic cry3a gene to enhance resistance against alfalfa weevil

To introduce genetic resistance against alfalfa weevil (Hypera postica), leaves and petiole explants of three commercial alfalfa genotypes, including Km-27, Kk-14 and Syn-18 were transformed with Agrobacterium tumefaciens strains GV101, LBA4404 and AGL01. All the Agrobacterium strains used harbored the recombinant binary vector pBI121 containing a synthetic cry3a gene under the control of CaMV35S promoter as well as the nptII gene as selectable marker. Transformed explants were cultured on callus-induction medium, and the germinated somatic embryos were then transferred to the regeneration medium. The primary transformants were evaluated by PCR and Southern blot analysis. The results indicated successful integration of the target gene into the genomes of primary transgenic lines. Moreover, the expression of Cry3a protein in the transgenic plants was confirmed by ELISA method. Three transgenic lines, including TL6, TL8 and TL11 showed significantly higher levels of insect resistance against H. postica larvae (mortality rate of 73–90 % after infestation), in comparison with the control plants during the two-year bioassays. All transgenic plants were fertile and no irregular behavior in terms of growth and the morphological traits were observed. Transgenic plants developed during the course of this study are currently being grown in greenhouse and will be crossed with each other for seed production.     

Extracellular Signal-Regulated Kinase Regulates RhoA Activation and Tumor Cell Plasticity by Inhibiting Guanine Exchange Factor H1 Activity

In certain Ras mutant cell lines, the inhibition of extracellular signal-regulated kinase (ERK) signaling increases RhoA activity and inhibits cell motility, which was attributed to a decrease in Fra-1 levels. Here we report a Fra-1-independent augmentation of RhoA signaling during short-term inhibition of ERK signaling. Using mass spectrometry-based proteomics, we identified guanine exchange factor H1 (GEF-H1) as mediating this effect. ERK binds to the Rho exchange factor GEF-H1 and phosphorylates it on S959, causing inhibition of GEF-H1 activity and a consequent decrease in RhoA activity. Knockdown experiments and expression of a nonphosphorylatable S959A GEF-H1 mutant showed that this site is crucial in regulating cell motility and invasiveness. Thus, we identified GEF-H1 as a critical ERK effector that regulates motility, cell morphology, and invasiveness.     

Physiological,biochemical, and metabolic responses of a Taxus baccata L. callus culture under drought stress

In Vitro Cellular & Developmental Biology - Plant - The metabolic stimulation induced by abiotic stress is an efficient strategy for the production of secondary metabolites in sterile and...     

Design,Synthesis and Enzymatic Inhibition of Novel Unusual Amino Acids as a Transition State Analogue of Amyloid Precursor Protein Peptide

International Journal of Peptide Research and Therapeutics - β-secretase 1 (BACE1) plays a pivotal role in the pathology of Alzheimer?s disease via accumulation beta amyloid in the...     

Role of Zooplankton Diversity in Vibrio cholerae Population Dynamics and in the Incidence of Cholera in the Bangladesh Sundarbans

Vibrio cholerae, a bacterium autochthonous to the aquatic environment, is the causative agent of cholera, a severe watery, life-threatening diarrheal disease occurring predominantly in developing countries. V. cholerae, including both serogroups O1 and O139, is found in association with crustacean zooplankton, mainly copepods, and notably in ponds, rivers, and estuarine systems globally. The incidence of cholera and occurrence of pathogenic V. cholerae strains with zooplankton were studied in two areas of Bangladesh: Bakerganj and Mathbaria. Chitinous zooplankton communities of several bodies of water were analyzed in order to understand the interaction of the zooplankton population composition with the population dynamics of pathogenic V. cholerae and incidence of cholera. Two dominant zooplankton groups were found to be consistently associated with detection of V. cholerae and/or occurrence of cholera cases, namely, rotifers and cladocerans, in addition to copepods. Local differences indicate there are subtle ecological factors that can influence interactions between V. cholerae, its plankton hosts, and the incidence of cholera.     

Serum level and tumor tissue expression of Ribonucleotide-diphosphate Reductase subunit M2 B: a potential biomarker for colorectal cancer

Molecular Biology Reports - This study explored the applicability of serum level and tissue expression of Ribonucleotide-diphosphate Reductase subunit M2 B (RRM2B) as reliable biomarkers for...     

Sympatric morphotypes of the restricted-range Tashan Cave Garra: distinct species or a case of phenotypic plasticity?

Environmental Biology of Fishes - Among Tashan cave barb Garra tashanensis inhabiting a small cave in southwest Iran, two mental disc (sucking mouth disc) forms were observed. To assess their...     

Mechanistic Elucidation of Salicylic Acid and Sulphur-Induced Defence Systems,Nitrogen Metabolism,Photosynthetic, and Growth Potential of Mungbean (Vigna radiata) Under Salt Stress

The potential of plant nutrients (such as sulphur, S) and phytohormones (such as salicylic acid, SA) has been explored in isolated studies by researchers in controlling the impact of abiotic stresses such as salinity in plants. However, information is scanty on the major mechanisms underlying the role of S and/or SA in modulation of enzymes involved in nitrogen (N) assimilation, GOGAT cycle, and antioxidant defence system; the cellular status of N-containing osmolyte proline, glucose, S-containing compounds; and their cumulative role in photosynthesis functions and growth in crop plants. The present study aimed to assess the role of cumulative effect of SA and S (SO₄²⁻) mediated induction of N assimilatory enzymes, GOGAT cycle, N-osmolyte proline and its metabolizing enzymes, glyoxylase enzymes, and antioxidant capacity in mungbean (Vigna radiata L.) exposed to NaCl with or without SO₄²⁻ and SA. Salt-exposed V. radiate showed differential elevations in damage (O^.₂⁻, H₂O₂, lipid peroxidation; glucose) and defence (ascorbate peroxidase, APX; glutathione reductase, GR; superoxide dismutase, SOD; reduced GSH; proline) and inhibitions in the activities of NR and NiR; N content, photosynthesis, photosynthetic N-use-efficiency (NUE), and growth. The separate supplementation of SA and SO₄²⁻ to 50 mM NaCl almost equally strengthened the antioxidant machinery and diminished NaCl-accrued damages. However, combined supply of SA and SO₄²⁻ to NaCl-exposed cultivars led to significant improvements in NR and NiR activities, the accumulation of N, GSH, proline, enhanced activity of APX, GR, and reduced activity of SOD, and also decreases in O^.₂⁻, H₂O₂, lipid peroxidation and glucose. These observations were corroborated with SA, SO₄²⁻ and NaCl-mediated changes in the traits of photosynthesis and growth, stomatal behaviour, and the polypeptide patterns of Rubisco in V. radiata. Overall, in V. radiata, SA-mediated higher enhancements in the activity of N assimilatory enzymes (NR, NiR, and GS), increase in the N and proline, and GSH; and decreases in the contents of Na⁺ and Cl⁻ ions, and glucose (a photosynthesis repressor); maintenance of a fine tuning among SOD, APX, and GR enzymes; and higher minimization of ROS (O^.₂⁻, H₂O₂) and lipid peroxidation finally led to a higher promotion in photosynthesis and growth.

     

The effect of fludrocortisone on the uterine receptivity partially mediated by ERK1/2-mTOR pathway

Implantation of embryos needs endometrial receptivity. Mineralocorticoids is one of the causes influencing the implantation window. This study targeted to evaluation fludrocortisone different properties on endometrial receptivity. The objective of this study was to assess whether treatment with fludrocortisone could impact the expression of diverse genes and proteins that are involved in uterine receptivity in mice. In this study, 40 female adult BALB/c mice were used. The samples were allocated to four groups of ten. Control group (C) received: vehicle; fludrocortisone group (FCA): received 1.5 mg/kg fludrocortisone; PP242 group (PP242): received 30 mg/kg PP242; fludrocortisone+PP242 group (FCA+PP242): received fludrocortisone and PP242. Mice were killed on window implantation day after mating and confirmed pregnancy. The endometrial epithelium of mouse was collected to assess mRNA expression of leukemia inhibitory factor (LIF), mucin-1 (MUC1), heparin-binding epidermal growth factor (HB-EGF), (Msx.1), miRNA Let-7a, and miRNA 223-3p as well as protein expression of extracellular signal-regulated kinase 1/2 (ERK1/2), mammalian target of rapamycin (mTOR), and eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1) in the uterine using real-time PCR and western blot, respectively. In comparison with the control group, fludrocortisone administration upregulated the expression of LIF, HB-EGF, Msx.1, miRNA Let-7a, ERK1/2, and mTOR in the epithelial endometrium. The PP242-treated group demonstrated a significant rise in the expression of MUC1, miRNA 223-3p and a remarkable decline in ERK1/2 and p-4E-BP1 levels in comparison with the control group. Combination therapy of (FCA+PP242) resulted in a remarkable rise in LIF, Msx-1, HB-EGF, ERK1/2, and mTOR levels, in comparison with the PP242 group. Furthermore, combination therapy of (FCA+PP242) downregulated the expression of MUC1 in comparison with the PP242-treated group. According to the results, fludrocortisone affected uterine receptivity possibly by means of modulating the expression of genes involved in the uterine receptivity and activation of the ERK1/2-mTOR pathway.