JMJ704 positively regulates rice defense response against Xanthomonas oryzae pv. oryzae infection via reducing H3K4me2/3 associated with negative disease resistance regulators

A schematic representation showing the genomic regions of the three genes for ChIP-PCR assay. White box indicates untranslated region, black box indicates coding sequence, line through the box indicates intron region of the genes, lines and numbers above the gene indicate the regions and positions used for ChIP-PCR assay. (TIF 2795 kb

Increased Expression and Altered Methylation of HERVWE1 in the Human Placentas of Smaller Fetuses from Monozygotic, Dichorionic, Discordant Twins

<div><h3>Background</h3><p>The human endogenous retroviral family W, Env(C7), member 1 gene (<em>HERVWE1</em>) is thought to participate in trophoblast cell fusion, and its expression is diminished in the placentas of singleton intrauterine growth-retarded pregnancies. However, there is limited information about the role of <em>HERVWE1</em> in discordant fetal growth in twins. This study was to compare <em>HERVWE1</em> gene expression between the placentas of discordant monozygotic twins and to identify its regulation by methylation.</p> <h3>Methodology/Principal Findings</h3><p>Fetuses from twenty-one pairs of monozygotic, dichorionic, discordant twins were marked as “smaller” or “larger” according to birth weight. Placental <em>HERVWE1</em> mRNA and protein expression profiles were analyzed using quantitative RT-PCR and immunohistochemistry (IHC) staining. Methylation profiles of the <em>HERVWE1</em> promoter region were analyzed using a pyrosequencing assay. DNA methyltransferase (<em>DNMT</em>) transcript levels were analyzed by RT-PCR. 5-methyl cytosine (5-MC) was stained using an immunohistochemical assay. There was a significant negative correlation between <em>HERVWE1</em> mRNA levels and birth weight in twins (<em>P</em><0.01). Whereas the mean methylation level of the <em>HERVWE1</em> promoter region was diminished in the smaller group in discordant twins(<em>P</em><0.01), increased mRNA and protein levels of <em>HERVWE1</em> were found in smaller fetuses compared with larger fetuses in discordant twins(<em>P</em><0.01). There was no significant difference in 5-MC staining intensity between discordant twins (<em>P</em>>0.05). The <em>DNMT3b3</em> mRNA levels in the smaller group were significantly downregulated compared with the larger group in discordant twins(<em>P</em><0.05), whereas the <em>DNMT3b7</em> mRNA levels in the smaller group were significantly upregulated compared with the larger group in discordant twins(<em>P</em><0.05).</p> <h3>Conclusions/Significance</h3><p>In discordant, monozygotic, dichorionic twins, <em>HERVWE1</em> expression was higher in smaller fetuses and lower in larger fetuses. Methylation of the <em>HERVWE1</em> gene promoter region may participate in the regulation of <em>HERVWE1</em> gene expression in discordant twin pregnancies.</p> </div

SIRT5 promotes IDH2 desuccinylation and G6PD deglutarylation to enhance cellular antioxidant defense

Abstract Excess in mitochondrial reactive oxygen species (ROS) is considered as a major cause of cellular oxidative stress. NADPH, the main intracellular reductant, has a key role in keeping glutathione in its reduced form GSH, which scavenges ROS and thus protects the cell from oxidative damage. Here, we report that SIRT5 desuccinylates and deglutarylates isocitrate dehydrogenase 2 (IDH2) and glucose‐6‐phosphate dehydrogenase (G6PD), respectively, and thus activates both NADPH‐producing enzymes. Moreover, we show that knockdown or knockout of SIRT5 leads to high levels of cellular ROS. SIRT5 inactivation leads to the inhibition of IDH2 and G6PD, thereby decreasing NADPH production, lowering GSH, impairing the ability to scavenge ROS, and increasing cellular susceptibility to oxidative stress. Our study uncovers a SIRT5‐dependent mechanism that regulates cellular NADPH homeostasis and redox potential by promoting IDH2 desuccinylation and G6PD deglutarylation

Indigo: a natural molecular passivator for efficient perovskite solar cells

Organic–inorganic hybrid lead halide perovskite solar cells have made unprecedented progress in improving photovoltaic efficiency during the past decade, while still facing critical stability challenges. Herein, the natural organic dye Indigo is explored for the first time to be an efficient molecular passivator that assists in the preparation of high-quality hybrid perovskite film with reduced defects and enhanced stability. The Indigo molecule with both carbonyl and amino groups can provide bifunctional chemical passivation for defects. In-depth theoretical and experimental studies show that the Indigo molecules firmly binds to the perovskite surfaces, enhancing the crystallization of perovskite films with improved morphology. Consequently, the Indigo-passivated perovskite film exhibits increased grain size with better uniformity, reduced grain boundaries, lowered defect density, and retarded ion migration, boosting the device efficiency up to 23.22%, and ˜21% for large-area device (1 cm2). Furthermore, the Indigo passivation can enhance device stability in terms of both humidity and thermal stress. These results provide not only new insights into the multipassivation role of natural organic dyes but also a simple and low-cost strategy to prepare high-quality hybrid perovskite films for optoelectronic applications based on Indigo derivatives.Peer ReviewedPostprint (author's final draft

An emerging recombinant human enterovirus 71 responsible for the 2008 outbreak of Hand Foot and Mouth Disease in Fuyang city of China

Hand, foot and mouth disease (HFMD), a common contagious disease that usually affects children, is normally mild but can have life-threatening manifestations. It can be caused by enteroviruses, particularly Coxsackieviruses and human enterovirus 71 (HEV71) with highly variable clinical manifestations. In the spring of 2008, a large, unprecedented HFMD outbreak in Fuyang city of Anhui province in the central part of southeastern China resulted in a high aggregation of fatal cases. In this study, epidemiologic and clinical investigations, laboratory testing, and genetic analyses were performed to identify the causal pathogen of the outbreak. Of the 6,049 cases reported between 1 March and 9 May of 2008, 3023 (50%) were hospitalized, 353 (5.8%) were severe and 22 (0.36%) were fatal. HEV71 was confirmed as the etiological pathogen of the outbreak. Phylogenetic analyses of entire VP1 capsid protein sequence of 45 Fuyang HEV71 isolates showed that they belong to C4a cluster of the C4 subgenotype. In addition, genetic recombinations were found in the 3D region (RNA-dependent RNA polymerase, a major component of the viral replication complex of the genome) between the Fuyang HEV71 strain and Coxsackievirus A16 (CV-A16), resulting in a recombination virus. In conclusion, an emerging recombinant HEV71 was responsible for the HFMD outbreak in Fuyang City of China, 2008