Beyond simple tails: poly(A) tail-mediated RNA epigenetic regulation.

The poly(A) tail is an essential structural component of mRNA required for the latter's stability and translation. Recent technologies have enabled transcriptome-wide profiling of the length and composition of poly(A) tails, shedding light on their overlooked regulatory capacities. Notably, poly(A) tails contain not only adenine but also uracil, cytosine, and guanine residues. These findings strongly suggest that poly(A) tails could encode a wealth of regulatory information, similar to known reversible RNA chemical modifications. This review aims to succinctly summarize our current knowledge on the composition, dynamics, and regulatory functions of RNA poly(A) tails. Given their capacity to carry rich regulatory information beyond the genetic code, we propose the concept of 'poly(A) tail epigenetic information' as a new layer of RNA epigenetic regulation.

Chemokine signaling synchronizes angioblast proliferation and differentiation during pharyngeal arch artery vasculogenesis.

Developmentally, the great vessels of the heart originate from the pharyngeal arch arteries (PAAs). During PAA vasculogenesis, PAA precursors undergo sequential cell fate decisions that are accompanied by proliferative expansion. However, how these two processes are synchronized remains poorly understood. Here, we find that the zebrafish chemokine receptor Cxcr4a is expressed in PAA precursors, and genetic ablation of either cxcr4a or the ligand gene cxcl12b causes PAA stenosis. Cxcr4a is required for the activation of the downstream PI3K/AKT cascade, which promotes not only PAA angioblast proliferation, but also differentiation. AKT has a well-known role in accelerating cell-cycle progression through the activation of cyclin-dependent kinases. Despite this, we demonstrate that AKT phosphorylates Etv2 and Scl, the key regulators of angioblast commitment, on conserved serine residues, thereby protecting them from ubiquitin-mediated proteasomal degradation. Altogether, our study reveals a central role for chemokine signaling in PAA vasculogenesis through orchestrating angioblast proliferation and differentiation.

Defect-Rich Functional HfO2-x for Highly Reversible Zn Metal Anode.

Interface engineering attracted tremendous attention owing to its remarkable ability to impede dendrite growth and side reactions in aqueous zinc-ion batteries. Artificial interface layers composed of crystalline materials have been extensively employed to stabilize the Zn anode. However, the diffusion kinetics of Zn2+ in highly crystalline materials are hindered by steric effects from the lattice, thereby limiting the high-rate performance of the cell. Here, defect-rich HfO2-x polycrystals derived from metal-organic frameworks (MOFs) (D-HfO2-x) are developed to enhance the Zn deposition behavior. The discrepancy of dielectric constants between metallic Zn and HfO2 enables the building of an electrostatic shielding layer for uniform Zn deposition. More importantly, the oxygen vacancies in D-HfO2-x provide abundant active sites for Zn2+ adsorption, accelerating the kinetics of Zn2+ migration, which contributes to the preferential exposure of the Zn (002) plane during plating. Consequently, the D-HfO2-x-modified Zn anode delivers ultrastable durability of over 5000 h at 1 mA cm-2 and a low voltage hysteresis of 30 mV. The constructed defective coating provides a guarantee for the stable operation of Zn anodes, and the innovative approach of defective engineering also offers new ideas for the protection of other energy storage devices.

Genome-wide identification of Avicennia marina aquaporins reveals their role in adaptation to intertidal habitats and their relevance to salt secretion and vivipary.

Aquaporins (AQPs) regulate the transport of water and other substrates, aiding plants in adapting to stressful environments. However, the knowledge of AQPs in salt-secreting and viviparous Avicennia marina is limited. In this study, 46 AmAQPs were identified in A. marina genome, and their subcellular localisation and function in transporting H2 O2 and boron were assessed through bioinformatics analysis and yeast transformation. Through analysing their expression patterns via RNAseq and real-time quantitative polymerase chain reaction, we found that most AmAQPs were downregulated in response to salt and tidal flooding. AmPIP (1;1, 1;7, 2;8, 2;9) and AmTIP (1;5, 1;6) as salt-tolerant candidate genes may contribute to salt secretion together with Na+ /H+ antiporters. AmPIP2;1 and AmTIP1;5 were upregulated during tidal flooding and may be regulated by anaerobic-responsive element and ethylene-responsive element cis-elements, aiding in adaptation to tidal inundation. Additionally, we found that the loss of the seed desiccation and dormancy-related TIP3 gene, and the loss of the seed dormancy regulator DOG1 gene, or DOG1 protein lack heme-binding capacity, may be genetic factors contributing to vivipary. Our findings shed light on the role of AQPs in A. marina adaptation to intertidal environments and their relevance to salt secretion and vivipary.

Metformin Therapeutic Targets for Aortic Aneurysms: A Mendelian Randomization and Colocalization Study.

Background: Identifying effective pharmacological interventions to prevent the progressive enlargement and rupture of aortic aneurysms (AAs) is critical. Previous studies have suggested links between metformin use and a decreased incidence of AAs. In this study, we employed Mendelian randomization (MR) to investigate causal effects of metformin's targets on AA risk and to explore the underlying mechanisms underlying these effects. Methods: To examine the relationship between metformin use and AA risk, we implemented both two-sample MR and multivariable MR analyses. Utilizing genetic instrumental variables, we retrieved cis-expression quantitative trait loci (cis-eQTL) data for potential targets of metformin from the Expression Quantitative Trait Loci Genetics Consortium (eQTLGen) Consortium and Genotype-Tissue Expression (GTEx) project. Colocalization analysis was employed to ascertain the probability of shared causal genetic variants between single nucleotide polymorphisms (SNPs) associated with eQTLs and AA. Results: Our findings reveal that metformin use reduces AA risk, exhibiting a protective effect with an odds ratio (OR) of 4.88 × 10 - 3 (95% confidence interval [CI]: 7.30 × 10 - 5 -0.33, p = 0.01). Furthermore, the protective effect of type 2 diabetes on AA risk appears to be driven by metformin use ( OR MVMR = 1.34 × 10 - 4 , 95% CI: 3.97 × 10 - 8 -0.45, p = 0.03). Significant Mendelian randomization (MR) results were observed for the expression of two metformin-related genes in the bloodstream: NADH:ubiquinone oxidoreductase subunit A6 (NDUFA6) and cytochrome b5 type B (CYB5B), across two independent datasets ( OR CYB5B = 1.35, 95% CI: 1.20-1.51, p = 2.41 × 10 - 7 ; OR NDUFA6 = 1.12; 95% CI: 1.07-1.17, p = 1.69 × 10 - 6 ). The MR analysis of tissue-specific expression also demonstrated a positive correlation between increased NDUFA6 expression and heightened AA risk. Lastly, NDUFA6 exhibited evidence of colocalization with AA. Conclusions: Our study suggests that metformin may play a significant role in lowering the risk of AA. This protective effect could potentially be linked to the mitigation of mitochondrial and immune dysfunction. Overall, NDUFA6 has emerged as a potential mechanism through which metformin intervention may confer AA protection.

cGAS-STING, inflammasomes and pyroptosis: an overview of crosstalk mechanism of activation and regulation.

BACKGROUND: Intracellular DNA-sensing pathway cGAS-STING, inflammasomes and pyroptosis act as critical natural immune signaling axes for microbial infection, chronic inflammation, cancer progression and organ degeneration, but the mechanism and regulation of the crosstalk network remain unclear. Cellular stress disrupts mitochondrial homeostasis, facilitates the opening of mitochondrial permeability transition pore and the leakage of mitochondrial DNA to cell membrane, triggers inflammatory responses by activating cGAS-STING signaling, and subsequently induces inflammasomes activation and the onset of pyroptosis. Meanwhile, the inflammasome-associated protein caspase-1, Gasdermin D, the CARD domain of ASC and the potassium channel are involved in regulating cGAS-STING pathway. Importantly, this crosstalk network has a cascade amplification effect that exacerbates the immuno-inflammatory response, worsening the pathological process of inflammatory and autoimmune diseases. Given the importance of this crosstalk network of cGAS-STING, inflammasomes and pyroptosis in the regulation of innate immunity, it is emerging as a new avenue to explore the mechanisms of multiple disease pathogenesis. Therefore, efforts to define strategies to selectively modulate cGAS-STING, inflammasomes and pyroptosis in different disease settings have been or are ongoing. In this review, we will describe how this mechanistic understanding is driving possible therapeutics targeting this crosstalk network, focusing on the interacting or regulatory proteins, pathways, and a regulatory mitochondrial hub between cGAS-STING, inflammasomes, and pyroptosis. SHORT CONCLUSION: This review aims to provide insight into the critical roles and regulatory mechanisms of the crosstalk network of cGAS-STING, inflammasomes and pyroptosis, and to highlight some promising directions for future research and intervention.

Homotherapy for heteropathy: therapeutic effect of Butein in NLRP3-driven diseases.

BACKGROUND: Aberrant inflammatory responses drive the initiation and progression of various diseases, and hyperactivation of NLRP3 inflammasome is a key pathogenetic mechanism. Pharmacological inhibitors of NLRP3 represent a potential therapy for treating these diseases but are not yet clinically available. The natural product butein has excellent anti-inflammatory activity, but its potential mechanisms remain to be investigated. In this study, we aimed to evaluate the ability of butein to block NLRP3 inflammasome activation and the ameliorative effects of butein on NLRP3-driven diseases. METHODS: Lipopolysaccharide (LPS)-primed bone-marrow-derived macrophages were pretreated with butein and various inflammasome stimuli. Intracellular potassium levels, ASC oligomerization and reactive oxygen species production were also detected to evaluate the regulatory mechanisms of butein. Moreover, mouse models of LPS-induced peritonitis, dextran sodium sulfate-induced colitis, and high-fat diet-induced non-alcoholic steatohepatitis were used to test whether butein has protective effects on these NLRP3-driven diseases. RESULTS: Butein blocks NLRP3 inflammasome activation in mouse macrophages by inhibiting ASC oligomerization, suppressing reactive oxygen species production, and upregulating the expression of the antioxidant pathway nuclear factor erythroid 2-related factor 2 (Nrf2). Importantly, in vivo experiments demonstrated that butein administration has a significant protective effect on the mouse models of LPS-induced peritonitis, dextran sodium sulfate-induced colitis, and high-fat diet-induced non-alcoholic steatohepatitis. CONCLUSION: Our study illustrates the connotation of homotherapy for heteropathy, i.e., the application of butein to broaden therapeutic approaches and treat multiple inflammatory diseases driven by NLRP3.

Neg1 overexpression in Trichoderma harzianum T4 enhanced its ability to produce spores and antagonistic activity against phytopathogenic fungi.

Trichoderma harzianum T4 is a soil fungus that plays an important role in the biological control of plant diseases. The aim of this study was to functionally characterize the ß-1,6-glucanase gene Neg1 in T. harzianum T4 and to investigate the effect of its overexpression on biocontrol traits, especially antagonism against pathogenic fungi. We found that overexpression of Neg1 did not affect growth of T. harzianum but enhanced sporulation of T. harzianum T4 cultures. Generally, spores are closely related to the defense ability of defense fungi and can assist their proliferation and improve their colonization ability. Secondly, overexpression of Neg1 also increased the secretion level of various hydrolytic enzymes and enhanced the antagonistic ability against phytopathogenic fungi of Fusarium spp. The results suggest that Neg1 is a key gene for improving the biocontrol effect of T. harzianum T4, which contributes to a better understanding of the mechanism of action of T. harzianum T4 as a fungal biocontrol agent.

Latent transition of social participation and its effects on depression among older adults in China: A National Longitudinal Study.

OBJECTIVES: As populations age, the issue of social participation among older adults has gained prominence. Studies indicate variability in social participation trajectories among this demographic, yet the transition patterns and their effects on depression remain unclear. This longitudinal study aims to explore the latent classes and transition patterns in social participation among older adults and to evaluate their effects on depression. METHODS: Data from the Chinese Longitudinal Healthy Longevity Survey (CLHLS) in 2014 (T1) and 2018 (T2) were analyzed, including 2293 older adults. Latent class analysis (LCA) and latent transition analysis (LTA) were employed to identify latent classes of social participation at T1 and T2, as well as the transition probabilities between these classes. Multinomial logistic regression was used to examine predictors of transitions, and depression levels at T2 were compared across transition patterns. RESULTS: The LCA results supported a 3-class model labeled as low, moderate, and high social participation. The probabilities of remaining stable and transitioning to other classes were similar across the three classes (ranging from 0.50 to 0.54). Age, gender, and other baseline characteristics emerged as significant predictors of transition patterns. Older adults experiencing positive transitions exhibited reduced depression compared to those in their original class over time, while those with negative transitions showed increased depression. CONCLUSIONS: This research prompts a deep understanding of social participation dynamics in older adults and their effects on depression. Identifying social participation classes and transition patterns could inform interventions to enhance social participation and reduce depression among older adults.

Split Phenomenon of Fasciculation between Antagonistic Muscles in Amyotrophic Lateral Sclerosis: An Ultrasound Study.

OBJECTIVE: Paresis of muscle groups in patients with amyotrophic lateral sclerosis (ALS) tends to present split phenomena. We explored the split phenomenon of fasciculation in multiple antagonistic muscle groups in ALS patients. METHODS: One hundred and forty ALS patients and 66 non-ALS patients were included from a single ALS center. Muscle ultrasonography (MUS) was performed to detect fasciculation in elbow flexor-extensor, wrist flexor-extensor, knee flexor-extensor, and ankle flexor-extensor. Split phenomena of fasciculation between different antagonistic muscle groups were summarized, and the possible influence factors were analyzed through stratified analysis. RESULTS: The frequency of split phenomenon of fasciculation intensity was significantly higher than those of muscle strength (26.1% vs. 7.1% for elbow flexor-extensor, 38.3% vs. 5.7% for wrist flexor-extensor, 37.9% vs. 3.0% for knee extensor-flexor, and 33.6% vs. 14.4% for ankle flexor-extensor) (P < 0.01). For muscles with 0-1 level of muscle strength (the Medical Research Council, MRC, score), significance difference in mean fasciculation intensity was observed only in ankle flexor-extensor. For muscles with 2-5 level of muscle strength, significant dissociation of fasciculation grade was common, especially among patients with slow rapid progression rate and both upper and lower motor neuron (UMN and LMN) involvement. As for non-ALS patients, no significant difference was observed in fasciculation intensity between antagonistic muscles. CONCLUSION: Split phenomenon of fasciculation between antagonistic muscles was common and relatively specific in ALS patients. Muscle strength, progression rate, and UMN involvement were influence factors of the split phenomenon of fasciculation intensity.

The immun function of dendritic cells in SFTS patients.

OBJECTIVES: Severe fever with thrombocytopenia syndrome (SFTS) is a newly emerging infectious disease caused by a novel bunyavirus in which host immune system suppression is thought to be crucial in disease development. Dendritic cells (DCs) are professional antigen-presenting cells (APCs) critical for initiation and orchestration of the immune response. And it have been suggested that functionally impaired DCs may mediate the suppression of host-specific T-cell immune responses and thus facilitate viral persistence and disease progression.This study was designed to improve the in vitro culture method for DCs and investigate the different immunologic functions of DCs between SFTS patients and healthy people. METHODS: All confirmed SFTS patients (N = 10) were recruited from the Jinan Infectious Diseases Hospital in 2019; routine laboratory parameters were collected. The frequencies, phenotypes were analyzed by flow cytometry. And the levels of 8 cytokines in the cell culture supernatant were detected by flow cytometry. RESULTS: On day 8 of the incubation period, cells were harvested and analyzed by flow cytometry. There were significant differences in the rates of CD1a-, CD83-positive cells between SFTS patients and healthy people (all P < 0.05). The detection of 8 cytokines in the culture supernatant showed that the expressions of IFN-α and IFN-γ in the culture supernatant of DC cells in SFTS patients were lower than those in normal people (P < 0.05, P < 0.01). CONCLUSIONS: The present results indicate that DCs may be functionally impaired in SFTS. A decreased level of circulating mDCs was closely correlated with SFTS progression.

Latent transition analysis of instrumental activities of daily living in Chinese elderly: based on the 2014-2018 wave of the Chinese Longitudinal Healthy Longevity Survey.

BACKGROUND: The instrumental activities of daily living (IADL) among the elderly have been found to be heterogeneous, with different trajectories. However, the transition of the IADL over time remains unclear. We aimed to explore the transition probabilities and the predictors of IADL among the elderly. METHODS: Longitudinal data from the 2014 (T1) and 2018 (T2) waves of the Chinese Longitudinal Healthy Longevity Survey were extracted. A sample of 2,944 participants aged 65 years or older, with complete responses to the IADL scale, was included. Latent profile analysis (LPA) and latent transition analysis (LTA) were employed to identify latent profiles of IADL and investigate the transition probabilities between profiles from T1 to T2. The predictors of latent profiles and transition probabilities were examined using multinomial regression analysis. RESULTS: The results of LPA at both T1 and T2 supported a 4-profile model solution. They were labeled as the "Normal function profile," "Mildly impaired profile," "Moderately impaired profile," and "Highly impaired profile". The Normal function profile and Highly impaired profile were characterized by maintaining stability rather than transitioning over time, with transition probabilities of 0.71 and 0.68, respectively, for maintaining stability. The Mildly impaired profile and Moderately impaired profile were characterized by a stronger tendency towards transition rather than stability, with transition probabilities of 0.29 and 0.45, respectively, of transitioning to the Highly impaired profile. The transition probabilities from the three impaired function profiles to the Normal function profile ranged from 0.05 to 0.19. Age, gender, place of residence, and social participation were significant predictors of profile attribution at T1 and transition probabilities over time. CONCLUSIONS: This study employed the LTA to examine the transition probability of IADL among the Chinese elderly. By recognizing the different profiles of IADL and understanding the factors associated with transitions among the elderly, interventions can be tailored to improve their functional independence and successful reintegration into families and society.

A preliminary investigation of epigenome-wide DNA methylation and temperament during infancy.

This study provides preliminary evidence for an epigenetic architecture of infant temperament. At 12 months of age, blood was collected and assayed for DNA methylation and maternally reported infant temperament was assessed using the Infant Behavior Questionnaire in 67 mother-infant dyads. Epigenome-wide analyses showed that the higher order temperament dimensions Surgency and Negative Affect were associated with DNA methylation. The epigenetic signatures of Surgency and Negative Affect were situated at genes involved in synaptic signaling and plasticity. Although replication is required, these results are consistent with a biologically based model of temperament, create new avenues for hypothesis-driven research into epigenetic pathways that underlie individual differences in temperament, and demonstrate that infant temperament has a widespread epigenetic signature in the methylome.

Perceptions of Continuous Glucose Monitoring Systems in the T1D Exchange Diabetes Registry: Satisfaction, Concerns, and Areas for Future Improvement.

Manufacturers continue to improve performance and usability of continuous glucose monitoring (CGM) systems. As CGM becomes a standard of care, especially for people on insulin therapy, it is important to routinely gauge how satisfied people with diabetes are with this technology. This article describes survey feedback from a large cohort of people with diabetes using older and current CGM systems and highlights areas of current satisfaction, concern, and future system improvement.

Multi-Channel Multi-Scale Convolution Attention Variational Autoencoder (MCA-VAE): An Interpretable Anomaly Detection Algorithm Based on Variational Autoencoder.

With the rapid development of industry, the risks factories face are increasing. Therefore, the anomaly detection algorithms deployed in factories need to have high accuracy, and they need to be able to promptly discover and locate the specific equipment causing the anomaly to restore the regular operation of the abnormal equipment. However, the neural network models currently deployed in factories cannot effectively capture both temporal features within dimensions and relationship features between dimensions; some algorithms that consider both types of features lack interpretability. Therefore, we propose a high-precision, interpretable anomaly detection algorithm based on variational autoencoder (VAE). We use a multi-scale local weight-sharing convolutional neural network structure to fully extract the temporal features within each dimension of the multi-dimensional time series. Then, we model the features from various aspects through multiple attention heads, extracting the relationship features between dimensions. We map the attention output results to the latent space distribution of the VAE and propose an optimization method to improve the reconstruction performance of the VAE, detecting anomalies through reconstruction errors. Regarding anomaly interpretability, we utilize the VAE probability distribution characteristics, decompose the obtained joint probability density into conditional probabilities on each dimension, and calculate the anomaly score, which provides helpful value for technicians. Experimental results show that our algorithm performed best in terms of F1 score and AUC value. The AUC value for anomaly detection is 0.982, and the F1 score is 0.905, which is 4% higher than the best-performing baseline algorithm, Transformer with a Discriminator for Anomaly Detection (TDAD). It also provides accurate anomaly interpretation capability.

Malware Identification Method in Industrial Control Systems Based on Opcode2vec and CVAE-GAN.

Industrial Control Systems (ICSs) have faced a significant increase in malware threats since their integration with the Internet. However, existing machine learning-based malware identification methods are not specifically optimized for ICS environments, resulting in suboptimal identification performance. In this work, we propose an innovative method explicitly tailored for ICSs to enhance the performance of malware classifiers within these systems. Our method integrates the opcode2vec method based on preprocessed features with a conditional variational autoencoder-generative adversarial network, enabling classifiers based on Convolutional Neural Networks to identify malware more effectively and with some degree of increased stability and robustness. Extensive experiments validate the efficacy of our method, demonstrating the improved performance of malware classifiers in ICSs. Our method achieved an accuracy of 97.30%, precision of 92.34%, recall of 97.44%, and F1-score of 94.82%, which are the highest reported values in the experiment.

Ceramide Ehux-C22 Targets the miR-199a-3p/mTOR Signaling Pathway to Regulate Melanosomal Autophagy in Mouse B16 Cells.

Melanosomes are specialized membrane-bound organelles where melanin is synthesized and stored. The levels of melanin can be effectively reduced by inhibiting melanin synthesis or promoting melanosome degradation via autophagy. Ceramide, a key component in the metabolism of sphingolipids, is crucial for preserving the skin barrier, keeping it hydrated, and warding off the signs of aging. Our preliminary study indicated that a long-chain C22-ceramide compound (Ehux-C22) isolated from the marine microalga Emiliania huxleyi, reduced melanin levels via melanosomal autophagy in B16 cells. Recently, microRNAs (miRNAs) were shown to act as melanogenesis-regulating molecules in melanocytes. However, whether the ceramide Ehux-C22 can induce melanosome autophagy at the post-transcriptional level, and which potential autophagy-dependent mechanisms are involved, remains unknown. Here, miR-199a-3p was screened and identified as a novel upregulated miRNA in Ehux-C22-treated B16 cells. An in vitro high melanin expression model in cultured mouse melanoma cells (B16 cells) was established by using 0.2 µM alpha-melanocyte-stimulating hormone(α-MSH) and used for subsequent analyses. miR-199a-3p overexpression significantly enhanced melanin degradation, as indicated by a reduction in the melanin level and an increase in melanosome autophagy. Further investigation demonstrated that in B16 cells, Ehux-C22 activated miR-199a-3p and inhibited mammalian target of rapamycin(mTOR) level, thus activating the mTOR-ULK1 signaling pathway by promoting the expression of unc-51-like autophagy activating kinase 1 (ULK1), B-cell lymphoma-2 (Bcl-2), Beclin-1, autophagy-related gene 5 (ATG5), and microtubule-associated protein light chain 3 (LC3-II) and degrading p62. Therefore, the roles of Ehux-C22-regulated miR-199a-3p and the mTOR pathway in melanosomal autophagy were elucidated. This research may provide novel perspectives on the post-translational regulation of melanin metabolism, which involves the coordinated control of melanosomes.

DC-SIGN of Largemouth Bass (Micropterus salmoides) Mediates Immune Functions against Aeromonas hydrophila through Collaboration with the TLR Signaling Pathway.

C-type lectins in organisms play an important role in the process of innate immunity. In this study, a C-type lectin belonging to the DC-SIGN class of Micropterus salmoides was identified. MsDC-SIGN is classified as a type II transmembrane protein. The extracellular segment of MsDC-SIGN possesses a coiled-coil region and a carbohydrate recognition domain (CRD). The key amino acid motifs of the extracellular CRD of MsDC-SIGN in Ca2+-binding site 2 were EPN (Glu-Pro-Asn) and WYD (Trp-Tyr-Asp). MsDC-SIGN-CRD can bind to four pathogen-associated molecular patterns (PAMPs), including lipopolysaccharide (LPS), glucan, peptidoglycan (PGN), and mannan. Moreover, it can also bind to Gram-positive, Gram-negative bacteria, and fungi. Its CRD can agglutinate microbes and displays D-mannose and D-galactose binding specificity. MsDC-SIGN was distributed in seven tissues of the largemouth bass, among which the highest expression was observed in the liver, followed by the spleen and intestine. Additionally, MsDC-SIGN was present on the membrane of M. salmoides leukocytes, thereby augmenting the phagocytic activity against bacteria. In a subsequent investigation, the expression patterns of the MsDC-SIGN gene and key genes associated with the TLR signaling pathway (TLR4, NF-κB, and IL10) exhibited an up-regulated expression response to the stimulation of Aeromonas hydrophila. Furthermore, through RNA interference of MsDC-SIGN, the expression level of the DC-SIGN signaling pathway-related gene (RAF1) and key genes associated with the TLR signaling pathway (TLR4, NF-κB, and IL10) was decreased. Therefore, MsDC-SIGN plays a pivotal role in the immune defense against A. hydrophila by modulating the TLR signaling pathway.

In silico analysis of NAC gene family in the mangrove plant Avicennia marina provides clues for adaptation to intertidal habitats.

NAC (NAM, ATAF1/2, CUC2) transcription factors (TFs) constitute a plant-specific gene family. It is reported that NAC TFs play important roles in plant growth and developmental processes and in response to biotic/abiotic stresses. Nevertheless, little information is known about the functional and evolutionary characteristics of NAC TFs in mangrove plants, a group of species adapting coastal intertidal habitats. Thus, we conducted a comprehensive investigation for NAC TFs in Avicennia marina, one pioneer species of mangrove plants. We totally identified 142 NAC TFs from the genome of A. marina. Combined with NAC proteins having been functionally characterized in other organisms, we built a phylogenetic tree to infer the function of NAC TFs in A. marina. Gene structure and motif sequence analyses suggest the sequence conservation and transcription regulatory regions-mediated functional diversity. Whole-genome duplication serves as the driver force to the evolution of NAC gene family. Moreover, two pairs of NAC genes were identified as positively selected genes of which AmNAC010/040 may be imposed on less constraint toward neofunctionalization. Quite a few stress/hormone-related responsive elements were found in promoter regions indicating potential response to various external factors. Transcriptome data revealed some NAC TFs were involved in pneumatophore and leaf salt gland development and response to salt, flooding and Cd stresses. Gene co-expression analysis found a few NAC TFs participates in the special biological processes concerned with adaptation to intertidal environment. In summary, this study provides detailed functional and evolutionary information about NAC gene family in mangrove plant A. marina and new perspective for adaptation to intertidal habitats.

Controllable Solid Electrolyte Interphase by Ionic Environment Regulation for Stable Zn-Ion Battery.

Artificial solid electrolyte interphase in organic solutions is effective and facile for long-cycling aqueous zinc ion batteries. However, the specific effects on different ionic environments have not been thoroughly investigated. Herein, pyromellitic acid (PA) are employed as organic ligand to coordinate with Zn2+ under various ionic environments. The connection between the ionic environment and reaction spontaneity is analyzed to provide insights into the reasons behind the effectiveness of the SEI layer and to characterize its protective impact on the zinc anode. Notably, the PA solution (pH4) lacking OH- contributes to the formation of a dense and ultrathin SEI with Zn-PA coordination, preventing direct contact between the anode and electrolyte. Moreover, the presence of organic functional groups facilitates a uniform flux of Zn2+ . These advantages enable stable cycling of the PA4-Zn symmetric cell at a current density of 3 mA cm-2 for over 3500 h. The PA4-Zn//MVO full cell demonstrates excellent electrochemical reversibility. Investigating the influence of the ionic environment on SEI generation informs the development of novel SEI strategies.