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In tomato (Solanum lycopersicum), as in other plants, the immunity hormone jasmonate (JA) triggers genome-wide transcriptional changes in response to pathogen and insect attack. These changes are largely regulated by the basic helix-loop-helix (bHLH) transcription factor MYC2. The function of MYC2 depends on its physical interaction with the MED25 subunit of the Mediator transcriptional coactivator complex. Although much has been learned about the MYC2-dependent transcriptional activation of JA-responsive genes, relatively less studied is the termination of JA-mediated transcriptional responses and the underlying mechanisms. Here, we report an unexpected function of MYC2 in regulating the termination of JA signaling through activating a small group of JA-inducible bHLH proteins, termed MYC2-TARGETED BHLH1 (MTB1), MTB2, and MTB3. MTB proteins negatively regulate JA-mediated transcriptional responses via their antagonistic effects on the functionality of the MYC2-MED25 transcriptional activation complex. MTB proteins impair the formation of the MYC2-MED25 complex and compete with MYC2 to bind to its target gene promoters. Therefore, MYC2 and MTB proteins form an autoregulatory negative feedback circuit to terminate JA signaling in a highly organized manner. We provide examples demonstrating that gene editing tools such as CRISPR/Cas9 open up new avenues to exploit MTB genes for crop protection.

Constructing a LiF-rich solid electrolyte interphase (SEI) is a feasible strategy for inhibiting lithium (Li) dendrites of Li metal anodes (LMAs). However, selecting appropriate F-containing additives with efficient LiF contribution is still under active research. Herein, a series of fluorinated additives with diverse F/C molar ratios are investigated, and we demonstrate that the hexafluoroglutaric anhydride (F 6−0 ) holds the best capability to derive the LiF-rich SEI in regular carbonate electrolytes (RCEs). To ameliorate the decomposition kinetics of the F 6−0 , LiNO 3 (LNO) as an adjuvant is further introduced in the system. As a result, the reduction efficiency of F 6−0 is increased to 91% under the F 6−0 /LNO synergistic effect, enabling the LMA with a uniform LiF-rich SEI in the RCE with merely 4 vol. % F 6−0 /LNO (F6L) addition. The LiNi 0.8 Co 0.1 Mn 0.1 O 2 ||Li-20μm full-cell with the F6L also showcases better cycling and rate performances than the cases with other F-containing additives. A F-containing additive with efficient LiF contribution is urgent for Li metal batteries. The authors report a hexafluoroglutaric anhydride additive with a 91% conversion, enabling the Li metal anode with a LiF-rich interphase in regular electrolyte.

The operating temperatures of commercial lithium‐ion batteries (LIBs) are generally restricted to a narrow range of −20 to 55 °C because the electrolyte is composed of highly volatile and flammable organic solvents and thermally unstable salts. Herein, the use of concentrated electrolytes is proposed to widen the operating temperature to −20 to 100 °C. It is demonstrated that a 4.0 mol L−1 LiN(SO2F)2/dimethyl carbonate electrolyte enables the stable charge–discharge cycling of a graphite anode and a high‐capacity LiNi0.6Co0.2Mn0.2O2 cathode and the corresponding full cell in a wide temperature range from −20 to 100 °C owing to the highly thermal stable solvation structure of the concentrated electrolyte together with the robust and Li+‐conductive passivation interphase it offered that alleviate various challenges at high temperatures. This work demonstrates the potential for the development of safe LIBs without the need for bulky and heavy thermal management systems, thus significantly increasing the overall energy density. Owing to the highly stable solvation structure, concentrated electrolyte enables the stable operation of LiNi0.6Co0.2Mn0.2O2|graphite full cells in a wide temperature range from −20 to 100 °C, which alleviates various challenges faced by commercial dilute electrolytes. This study demonstrates the potential to build a safe battery system without the bulky and heavy thermal management system, thus significantly increasing the overall energy density.

Malignant lung cancer cells are characterized by uncontrolled proliferation and migration. Aberrant lung cancer cell proliferation and migration are programmed by altered cancer transcriptome. The underlying epigenetic mechanism is unclear. Here we report that expression levels of BRG1, a chromatin remodeling protein, were significantly up-regulated in human lung cancer biopsy specimens of higher malignancy grades compared to those of lower grades. Small interfering RNA mediated depletion or pharmaceutical inhibition of BRG1 suppressed proliferation and migration of lung cancer cells. BRG1 depletion or inhibition was paralleled by down-regulation of cyclin B1 (CCNB1) and latent TGF-β binding protein 2 (LTBP2) in lung cancer cells. Further analysis revealed that BRG1 directly bound to the CCNB1 promoter to activate transcription in response to hypoxia stimulation by interacting with E2F1. On the other hand, BRG1 interacted with Sp1 to activate LTBP2 transcription. Mechanistically, BRG1 regulated CCNB1 and LTBP2 transcription by altering histone modifications on target promoters. Specifically, BRG1 recruited KDM3A, a histone H3K9 demethylase, to remove dimethyl H3K9 from target gene promoters thereby activating transcription. KDM3A knockdown achieved equivalent effects as BRG1 silencing by diminishing lung cancer proliferation and migration. Of interest, BRG1 directly activated KDM3A transcription by forming a complex with HIF-1α. In conclusion, our data unveil a novel epigenetic mechanism whereby malignant lung cancer cells acquired heightened ability to proliferate and migrate. Targeting BRG1 may yield effective interventional strategies against malignant lung cancers.

Macrophage-dependent inflammatory response is considered a pivotal biological process that contributes to a host of diseases when aberrantly activated. The underlying epigenetic mechanism is not completely understood. We report here that MKL1 was both sufficient and necessary for p65-dependent pro-inflammatory transcriptional program in immortalized macrophages, in primary human and mouse macrophages, and in an animal model of systemic inflammation (endotoxic shock). Extensive chromatin immunoprecipitation (ChIP) profiling and ChIP-seq analyses revealed that MKL1 deficiency erased key histone modifications synonymous with transactivation on p65 target promoters. Specifically, MKL1 defined histone H3K4 trimethylation landscape for NF-κB dependent transcription. MKL1 recruited an H3K4 trimethyltransferase SET1 to the promoter regions of p65 target genes. There, our work has identified a novel modifier of p65-dependent pro-inflammatory transcription, which may serve as potential therapeutic targets in treating inflammation related diseases.

Myocardial infarction (MI) dampens heart function and poses a great health risk. The class III deacetylase sirtuin 1 (SIRT1) is known to confer cardioprotection. SIRT1 expression is downregulated in the heart by a number of stress stimuli that collectively drive the pathogenesis of MI, although the underlying mechanism remains largely obscure. Here we show that in primary rat neonatal ventricular myocytes (NRVMs), ischaemic or oxidative stress leads to a rapid upregulation of SUV39H, the mammalian histone H3K9 methyltransferase, paralleling SIRT1 downregulation. Compared to wild-type littermates, SUV39H knockout mice are protected from MI. Likewise, suppression of SUV39H activity with chaetocin attenuates cardiac injury following MI. Mechanistically, SUV39H cooperates with heterochromatin protein 1 gamma (HP1γ) to catalyse H3K9 trimethylation on the SIRT1 promoter and represses SIRT1 transcription. SUV39H augments intracellular ROS levels in a SIRT1-dependent manner. Our data identify a previously unrecognized role for SUV39H linking SIRT1 trans-repression to myocardial infarction. The molecular pathways regulating the cardioprotective activity of deacetylase sirtuin-1 are unknown. Here, Yang et al . show that histone H3K9 methyltransferase SUV39H and HP1gamma cooperatively methylate H3K9 on the sirtuin-1 promoter and inhibit sirtuin-1 transcription, and show that inhibition of SUV39H in mice is cardioprotective.

Rotating stall is an abnormal flow phenomenon in pumps and pump-turbines, which can cause severe vibration, noise, and even cause head hump. A pump-turbine model under pump mode is researched in this study to reveal the formation mechanism of rotating stall. The causes, development laws, and influencing factors of rotating stall is revealed, which can help professionals achieve a deeper understanding of the rotating stall mechanism and suppress it through optimized design. The flow simulation method is mainly adopted in the study, and it is verified through experiment. The research results show that stall in the guide vanes is often caused, maintained and aggravated by rotor–stator interaction (RSI). A stall cell is often difficult to cause the adjacent flow channel to stall. However, under the action of RSI, stall can be induced in the adjacent flow channel, and then rotating stall is gradually formed. Rotating stall can be suppressed by various methods of reducing RSI. To a certain extent, the research makes up for the problem that conventional theory does not fully consider non-uniform and unsteady complex incoming flow when analyzing rotating stall. A connection between rotating stall and RSI is established, which can provide an important basis for further research on how to eliminate rotating stall.

This study investigates the thermal–hydraulic behavior and deposition characteristics of a shell and tube exhaust heat exchanger using a CFD-based predictive model of soot deposition. Firstly, considering the influences of thermophoretic, wall shear stress, and other deposition and removal mechanisms, a predictive model is developed for long-term performance of heat exchangers under soot deposition. Then, the variations in exhaust heat exchanger performance during a 4 h deposition period are simulated based on the model. Subsequently, the variation of deposition distribution and different deposition velocities are also evaluated. Finally, an analysis of the long-term performance of the exhaust heat exchanger under varying gas velocities and temperature gradients is conducted, revealing the performance variations under all engine-operating conditions. Results show that the deterioration in normalized relative j/f1/2 varies from 5.26% to 24.91% under different work conditions, and the exhaust heat exchanger with high gas velocity and low temperature gradient exhibits optimal long-term performance.

Cardiac fibrosis is a key pathophysiological process that contributes to heart failure. Cardiac resident fibroblasts, exposed to various stimuli, are able to trans- differentiate into myofibroblasts and mediate the pro-fibrogenic response in the heart. The present study aims to investigate the mechanism whereby transcription of chloride channel accessory 2 (Clca2) is regulated in cardiac fibroblast and its potential implication in fibroblast-myofibroblast transition (FMyT). We report that Clca2 expression was down-regulated in activated cardiac fibroblasts (myofibroblasts) compared to quiescent cardiac fibroblasts in two different animal models of cardiac fibrosis. Clca2 expression was also down-regulated by TGF-β, a potent inducer of FMyT. TGF-β repressed Clca2 expression at the transcriptional level likely via the E-box element between −516 and −224 of the Clca2 promoter. Further analysis revealed that Twist1 bound directly to the E-box element whereas Twist1 depletion abrogated TGF-β induced Clca2 trans- repression. Twist1-mediated Clca2 repression was accompanied by erasure of histone H3/H4 acetylation from the Clca2 promoter. Mechanistically Twist1 interacted with HDAC1 and recruited HDAC1 to the Clca2 promoter to repress Clca2 transcription. Finally, it was observed that Clca2 over-expression attenuated whereas Clca2 knockdown enhanced FMyT. In conclusion, our data demonstrate that a Twist1-HDAC1 complex represses Clca2 transcription in cardiac fibroblasts, which may contribute to FMyT and cardiac fibrosis.

Maritime transportation is one of the vital means delivering jet fuel from refineries to end-users. The possible deterioration of fuel quality during maritime transportation directly impacts the final performance of jet fuel and, in severe cases, may even compromise aviation safety. While numerous studies have delved into the deterioration of jet fuel quality during long-term storage on land, there is a notable lack of research reporting on its quality deterioration during maritime transportation. This paper summarizes the unique conditions faced by jet fuel during maritime storage and transportation. Based on these characteristics, experimental studies were conducted to investigate the effects of storage duration, atmosphere, impurities, water content, and fuel blending on the quality deterioration process of jet fuel. The results reveal the process and underlying causes of jet fuel quality deterioration during maritime transportation.