The bZIP Transcription Factor MoAP1 Mediates the Oxidative Stress Response and Is Critical for Pathogenicity of the Rice Blast Fungus Magnaporthe oryzae

Saccharomyces cerevisiae Yap1 protein is an AP1-like transcription factor involved in the regulation of the oxidative stress response. An ortholog of Yap1, MoAP1, was recently identified from the rice blast fungus Magnaporthe oryzae genome. We found that MoAP1 is highly expressed in conidia and during invasive hyphal growth. The Moap1 mutant was sensitive to H2O2, similar to S. cerevisiae yap1 mutants, and MoAP1 complemented Yap1 function in resistance to H2O2, albeit partially. The Moap1 mutant also exhibited various defects in aerial hyphal growth, mycelial branching, conidia formation, the production of extracellular peroxidases and laccases, and melanin pigmentation. Consequently, the Moap1 mutant was unable to infect the host plant. The MoAP1-eGFP fusion protein is localized inside the nucleus upon exposure to H2O2, suggesting that MoAP1 also functions as a redox sensor. Moreover, through RNA sequence analysis, many MoAP1-regulated genes were identified, including several novel ones that were also involved in pathogenicity. Disruption of respective MGG_01662 (MoAAT) and MGG_02531 (encoding hypothetical protein) genes did not result in any detectable changes in conidial germination and appressorium formation but reduced pathogenicity, whereas the mutant strains of MGG_01230 (MoSSADH) and MGG_15157 (MoACT) showed marketed reductions in aerial hyphal growth, mycelial branching, and loss of conidiation as well as pathogenicity, similar to the Moap1 mutant. Taken together, our studies identify MoAP1 as a positive transcription factor that regulates transcriptions of MGG_01662, MGG_02531, MGG_01230, and MGG_15157 that are important in the growth, development, and pathogenicity of M. oryzae

A comprehensive review of circRNA: from purification and identification to disease marker potential

Circular RNA (circRNA) is an endogenous noncoding RNA with a covalently closed cyclic structure. Based on their components, circRNAs are divided into exonic circRNAs, intronic circRNAs, and exon-intron circRNAs. CircRNAs have well-conserved sequences and often have high stability due to their resistance to exonucleases. Depending on their sequence, circRNAs are involved in different biological functions, including microRNA sponge activity, modulation of alternative splicing or transcription, interaction with RNA-binding proteins, and rolling translation, and are a derivative of pseudogenes. CircRNAs are involved in the development of a variety of pathological conditions, such as cardiovascular diseases, diabetes, neurological diseases, and cancer. Emerging evidence has shown that circRNAs are likely to be new potential clinical diagnostic markers or treatments for many diseases. Here we describe circRNA research methods and biological functions, and discuss the potential relationship between circRNAs and disease progression

piR-hsa-211106 Inhibits the Progression of Lung Adenocarcinoma Through Pyruvate Carboxylase and Enhances Chemotherapy Sensitivity

Although the importance of PIWI-interacting RNAs (piRNAs) in cancer has recently been recognized, studies on the role and functional mechanism of piRNAs in lung adenocarcinoma (LUAD) development and progression are limited. In this study, we identified 10 differently expressed piRNAs in LUAD tissues compared to normal tissues, among which, piR-hsa-211106 expression levels were downregulated in LUAD tissues and cell lines. Furthermore, the effects of piR-hsa-211106 on the malignant phenotypes and chemosensitivity of LUAD cells were detected by gain- and loss-of-function analyses in vitro and in vivo, which showed that piR-hsa-211106 inhibited LUAD cell proliferation, tumor growth, and migration, but promoted apoptosis. Moreover, our finding indicated that piR-hsa-211106 is a potential therapeutic target that synergistically imparts anticancer effects with a chemotherapeutic agent for LUAD-cisplatin. Further mechanistic investigation indicated that piR-hsa-211106 could bind to pyruvate carboxylase (PC) by RNA pull down and RNA immunoprecipitation assays and inhibited PC mRNA and protein expression. Our study demonstrates that piR-hsa-211106 inhibits LUAD progression by hindering the expression and function of PC and enhances chemotherapy sensitivity, suggesting that piR-hsa-211106 is a novel diagnostic and therapeutic target for LUAD

Melting Curve of Potassium Chloride from in situ Ionic Conduction Measurements

We report experimental constraints on the melting curve of potassium chloride (KCl) between 3.2 and 9 GPa from in situ ionic conduction measurements using a multi-anvil apparatus. On the basis of concurrent measurements of KCl and sodium chloride (NaCl) at 1 bar using the differential thermal analysis (DTA) method and Pt sphere marker, we show that the peak rate of increase in ionic current with temperature upon heating coincides with latent heat ledge and fall of Pt sphere, thus establishing the criterion for melting detection from ionic conduction measurements. Applying this criterion to high pressures, we found that the melting point of KCl rose steeply with increasing pressure to exceed 2443 ± 100 K at 9 GPa. Fitting the results of this study together with existing data at pressures below 4 GPa and above 20 GPa, we obtained the Simon’s melting equation for KCl in the simple cubic B2 structure between 1.8 and 50 GPa: T m = 1323 ( P − 1.87 2.2 ( 1 ) + 1 ) 1 2.7 ( 1 ) , where T is in K and P is in GPa. Starting at 1 bar, the melting point of KCl increases at an average rate of ~150 K/GPa to cross that of Pt near 9 GPa. The highly refractory nature of KCl makes it a sensitive pressure calibrant for the large-volume pressure at moderate pressures and a potential sample container for experiments at moderate pressures and very high temperatures

The Flexural Strength and Fracture Toughness of TC4-Based Laminated Composites Reinforced with Ti Aluminide and Carbide

TiC–Ti–Al mixed powders and TC4 titanium alloy foils were overlapped layer-by-layer in the graphite die. The TC4-based laminated composite sheets reinforced by Ti aluminide and carbide were successfully fabricated via spark plasma sintering (SPS) at 1100 °C with a well-bonded interface. The composite layers were mainly composed of TiAl, Ti3Al, Ti2AlC, and Ti3AlC2 phases. The carbides particles distributed in the matrix played an important role in the deflection of cracks and the passivation of microcracks. TC4 titanium alloy layers had an obvious effect on the stress distribution during the loading process, and provided an energy dissipation mechanism, which could improve the mechanical properties of the laminated composite sheets obviously. When the theoretical amount of Ti2AlC was 20 wt %, the flexural strength and fracture toughness of the laminated composite sheets reached the maximum value in the arrester direction, which were 1428.79 MPa and 64.08 MPa·m1/2, respectively

Correction to: MoMyb1 is required for asexual development and tissue-specific infection in the rice blast fungus Magnaporthe oryzae

Following the publication of this article [1], the authors noticed that they mistakenly introduced duplicate images in Figure 6A during the preparation of figures. They apologize for any confusion that brought to the readers and have corrected the figure. This correction does not change any statement or conclusion drawn from the data

Effects of REDOX in Regulating and Treatment of Metabolic and Inflammatory Cardiovascular Diseases

Reduction oxidation (REDOX) reaction is crucial in life activities, and its dynamic balance is regulated by ROS. Reactive oxygen species (ROS) is associated with a variety of metabolic diseases involving in multiple cellular signalling in pathologic and physiological signal transduction. ROS are the by-products of numerous enzymatic reactions in various cell compartments, including the cytoplasm, cell membrane, endoplasmic reticulum (ER), mitochondria, and peroxisome. ROS signalling is not only involved in normal physiological processes but also causes metabolic dysfunction and maladaptive responses to inflammatory signals, which depends on the cell type or tissue environment. Excess oxidants are able to alter the normal structure and function of DNA, lipids, and proteins, leading to mutations or oxidative damage. Therefore, excessive oxidative stress is usually regarded as the cause of various pathological conditions, such as cancer, neurodegeneration, cardiovascular diseases (CVDs), diabetes, and kidney diseases. Currently, it has been possible to detect diabetes and other cardiac diseases by detecting derivatives accompanied by oxidative stress in vivo as biomarkers, but there is no effective method to treat these diseases. In consequence, it is essential for us to seek new therapy targeting these diseases through understanding the role of ROS signalling in regulating metabolic activity, inflammatory activation, and cardiac diseases related to metabolic dysfunction. In this review, we summarize the current literature on REDOX and its role in the regulation of cardiac metabolism and inflammation, focusing on ROS, local REDOX signalling pathways, and other mechanisms