Biocontrol of Fusarium wilt disease in muskmelon with Bacillus subtilis Y-IVI

Muskmelon (Cucumis melo L.) wilt caused by Fusarium oxysporum f. sp. melonis leads to severe economic losses. A bio-organic fertilizer (BIO) fortified with an antagonistic strain of Bacillus subtilis Y-IVI was used to control this disease. Pot experiments were carried out to investigate the efficacy and to elucidate biocontrol mechanisms for the disease. BIO significantly reduced the disease incidence. Population of F. oxysporum in plant shoots of the BIO treatment were about 1000-fold lower than the control. Population of Y-IVI remained high in muskmelon rhizosphere of the BIO treatment during the experiment. Concentration of antifungal lipopeptides, iturin A, in the BIO treatment was significantly higher than other treatments. Ten days after transplantation, the salicylic acid content in BIO-treated plant leaves was significantly higher than control. In conclusion, BIO effectively controlled muskmelon wilt, possibly because the antagonistic microbes effectively colonize the plant rhizosphere and shoots to preclude pathogen invasion. Furthermore, Y-IVI produces antifungal lipopeptides in the rhizosphere.     

Vildagliptin improves high glucose‐induced endothelial mitochondrial dysfunction via inhibiting mitochondrial fission

The dipeptidyl peptidase 4 inhibitor vildagliptin (VLD), a widely used anti‐diabetic drug, exerts favourable effects on vascular endothelium in diabetes. We determined for the first time the improving effects of VLD on mitochondrial dysfunction in diabetic mice and human umbilical vein endothelial cells (HUVECs) cultured under hyperglycaemic conditions, and further explored the mechanism behind the anti‐diabetic activity. Mitochondrial ROS (mtROS) production was detected by fluorescent microscope and flow cytometry. Mitochondrial DNA damage and ATP synthesis were analysed by real time PCR and ATPlite assay, respectively. Mitochondrial network stained with MitoTracker Red to identify mitochondrial fragmentation was visualized under confocal microscopy. The expression levels of dynamin‐related proteins (Drp1 and Fis1) were determined by immunoblotting. We found that VLD significantly reduced mtROS production and mitochondrial DNA damage, but enhanced ATP synthesis in endothelium under diabetic conditions. Moreover, VLD reduced the expression of Drp1 and Fis1, blocked Drp1 translocation into mitochondria, and blunted mitochondrial fragmentation induced by hyperglycaemia. As a result, mitochondrial dysfunction was alleviated and mitochondrial morphology was restored by VLD. Additionally, VLD promoted the phosphorylation of AMPK and its target acetyl‐CoA carboxylase in the setting of high glucose, and AMPK activation led to a decreased expression and activation of Drp1. In conclusion, VLD improves endothelial mitochondrial dysfunction in diabetes, possibly through inhibiting Drp1‐mediated mitochondrial fission in an AMPK‐dependent manner.     

Individualism in plant populations: using stochastic differential equations to model individual neighbourhood-dependent plant growth

We study individual plant growth and size hierarchy formation in an experimental population of Arabidopsis thaliana, within an integrated analysis that explicitly accounts for size-dependent growth, size- and space-dependent competition, and environmental stochasticity. It is shown that a Gompertz-type stochastic differential equation (SDE) model, involving asymmetric competition kernels and a stochastic term which decreases with the logarithm of plant weight, efficiently describes individual plant growth, competition, and variability in the studied population. The model is evaluated within a Bayesian framework and compared to its deterministic counterpart, and to several simplified stochastic models, using distributional validation. We show that stochasticity is an important determinant of size hierarchy and that SDE models outperform the deterministic model if and only if structural components of competition (asymmetry; size- and space-dependence) are accounted for. Implications of these results are discussed in the context of plant ecology and in more general modelling situations.     

De-dimerization of PTB is catalyzed by PDI and is involved in the regulation of p53 translation

Polypyrimidine tract-binding protein (PTB) is an RNA binding protein existing both as dimer and monomer and shuttling between nucleus and cytoplasm. However, the regulation of PTB dimerization and the relationship between their functions and subcellular localization are unknown. Here we find that PTB presents as dimer and monomer in nucleus and cytoplasm respectively, and a disulfide bond involving Cysteine 23 is critical for the dimerization of PTB. Additionally, protein disulfide isomerase (PDI) is identified to be the enzyme that catalyzes the de-dimerization of PTB, which is dependent on the CGHC active site of the a’ domain of PDI. Furthermore, upon DNA damage induced by topoisomerase inhibitors, PTB is demonstrated to be de-dimerized with cytoplasmic accumulation. Finally, cytoplasmic PTB is found to associate with the ribosome and enhances the translation of p53. Collectively, these findings uncover a previously unrecognized mechanism of PTB dimerization, and shed light on the de-dimerization of PTB functionally linking to cytoplasmic localization and translational regulation.     

Genome-Wide QTL Analysis Identified Significant Associations Between Hypoxia Tolerance and Mutations in the GPR132 and ABCG4 Genes in Nile Tilapia

Exposure to hypoxia induces both acute and chronic stress responses, which plays an important role in health of cultured organisms including growth, reproduction, immunity, and other energy demanding activities. Application of advanced genomic technologies allows rapid identification of hypoxia trait-associated genes and precise selection of superior brood stocks with high tolerance in tilapia. By applying QTL-seq and double-digest restriction-site associated DNA sequencing (ddRAD-seq) techniques, we identified four genome-wide significant quantitative trait loci (QTLs) for hypoxia tolerance and many suggestive QTLs in Nile tilapia. These QTLs explained 6.6–14.7% of the phenotypic variance. Further analysis revealed that single nucleotide polymorphisms (SNPs) in exons of both GPR132 and ABCG4 genes located in genome-wide QTL intervals were significantly associated with hypoxia-tolerant traits. Expression analysis of both genes suggested that they were strong candidate genes involved into hypoxia tolerance in tilapia. Our findings suggest that both QTL-seq and ddRAD-seq techniques can be effectively utilized in QTL mapping of hypoxia traits in fish. Our data supply a basis for further marker-assisted selection of super lines with a high level of tolerance against low oxygen stress in the tilapia.     

A new natural α-helical peptide from the venom of the scorpion Heterometrus petersii kills HCV

Hepatitis C virus (HCV) is a major cause of chronic liver disease, cirrhosis, and hepatocellular carcinoma. There is no vaccine available for HCV, and almost half of patients cannot be cured using standard combination therapy. Thus, new anti-HCV strategies and drugs are urgently needed. Here, the gene encoding a new α-helical peptide, Hp1090, was screened from the venomous gland cDNA library of the scorpion Heterometrus petersii. Structural analysis showed that Hp1090 is an amphipathic α-helical peptide. In vitro HCV RNA inhibitory assays indicated that Hp1090 peptide inhibited HCV infection with an IC₅₀ of 7.62 μg/ml (5.0 μM), whereas Hp1035 peptide, showing high homology to Hp1090, exhibited no anti-HCV activity. Hp1090 acted as a viricide against HCV particles in vitro and prevented the initiation of HCV infection. Furthermore, this peptide interacted with HCV particles directly and rapidly permeabilized phospholipid membranes. Collectively, it seems that Hp1090 is virocidal for HCV in vitro, directly interacting with the viral membrane and decreasing the virus infectivity. These results suggest that Hp1090 could be considered an anti-HCV lead compound with virocidal mechanism that offers a potential therapeutic approach to HCV infection. Our work opens a new avenue for antiviral drug discovery in natural scorpion venom.     

Identification of changes in Triticum aestivum L. leaf proteome in response to drought stress by 2D-PAGE and MALDI-TOF/TOF mass spectrometry

Drought is an abiotic stress that strongly influences plant growth, development and productivity. To gain a better understanding of the drought-stress responses at physiological and molecular level in wheat plants (Triticum aestivum cv. KTC86211), we performed a comparative physiological and proteomics analysis. Eight-day-old wheat seedlings were treated with polyethylene glycol-simulated drought stress for 0, 24, 48 and 72 h. Drought treatment resulted in alterations of morphology, increased relative electrolyte leakage and reduced length and weight on leaf and root. Stress-induced proteome changes were analyzed by two-dimensional gel electrophoresis in conjunction with MALDI-TOF/TOF. Twenty-three spots differed significantly between control and treated plants following 48 h of drought stress, with 19 upregulated, and 4 downregulated, in leaf tissues. All of the differentially expressed protein spots were identified, revealing that the majority of proteins altered by drought treatment were involved in reactive oxygen species scavenging enzymes and photosynthesis. Other proteins identified were involved in protein metabolism, cytoskeleton structure, defense response, acid metabolism and signal transduction. All proteins might contribute cooperatively to reestablish cellular homeostasis under drought stress. The present study not only provides new insights into the mechanisms of acclimation and tolerance to drought stress in wheat plants, but also provides clues for improving wheat’s drought tolerance through breeding or genetic engineering.     

<Emphasis Type=Italic>Clavispora lusitaniae</Emphasis> and <Emphasis Type=Italic>Chaetomium atrobrunneum</Emphasis> as Rare Agents of Cutaneous Infection

We describe the first case of cutaneous infection caused by Chaetomium atrobrunneum and Clavispora lusitaniae in a one-and-a-half-year-old boy with acute and severe inflammation around his left eyelid. He presented to our outpatient center with a 6-day history and previously ineffective antibacterial therapy. Scanning electron microscopy (SEM) revealed hyphae and spores were on the surface of the crusty exudates and also penetrated into it, and the microbiology study further showed their characteristic cultural features. Fungal isolates were identified by the amplification and sequencing of the 26S RNA gene and of the ITS region, as C. lusitaniae and C. atrobrunneum. Up until now, most known clinical records of these rare species have shown them as agents of deep mycosis. Due to the emergency situation, medications were administered promptly and confirmed by subsequent fungal identification and successful therapeutic outcome. This article illustrates the importance of recognizing fungal infections, especially those caused by uncommon pathogens. Limitations in the routine identification procedures and therapeutic options of this emerging opportunistic agent are also discussed in this report.     

Small Peptide Inhibitor of JNK3 Protects Dopaminergic Neurons from MPTP Induced Injury via Inhibiting the ASK1-JNK3 Signaling Pathway

Introduction and Aims

The ASK1-JNK3 signaling pathway plays a pivotal role in the pathogenesis of Parkinson''s disease (PD). The specific binding of β-arrestin2 to JNK3 is essential for activation of the ASK1-JNK3 cascade, representing a potential therapeutic target for preventing dopaminergic neuronal death in PD. The aim of this study was to identify a novel strategy for the prevention of dopaminergic neuronal death in PD.

Methods

Based on the specific binding of β-arrestin2 to JNK3, a 21-amino-acid fusion peptide, termed JNK3-N-Tat, was synthesized. We evaluated the ability of this peptide to inhibit the binding of β-arrestin2 to its target domain in JNK3 in vitro and in vivo.

Results

The JNK3-N-Tat peptide inhibited activation of the ASK1-JNK3 cascade by disrupting the interaction between β-arrestin2 and JNK3. JNK3-N-Tat exerted beneficial effects through pathways downstream of JNK3 and improved mitochondrial function, resulting in attenuated MPP+/MPTP-induced damage. JNK3-N-Tat protected mesencephalic dopaminergic neurons against MPTP-induced toxicity.

Conclusions

JNK3-N-Tat, a JNK3-inhibitory peptide, protects dopaminergic neurons against MPP+/MPTP-induced injury by inhibiting the ASK1-JNK3 signaling pathway.