Abscisic acid root-to-shoot translocation by transporter AtABCG25 mediates stomatal movements in Arabidopsis.

The phytohormone abscisic acid (ABA) plays a central role in regulating stomatal movements under drought conditions. The root-derived peptide CLAVATA3/EMBRYO SURROUNDING REGION-RELATED 25 (CLE25) moves from the root to shoot for activating ABA biosynthesis under drought conditions. However, the root-to-shoot translocation of root-derived ABA and its regulation of stomatal movements in the shoot remain to be clarified. Here, we reveal that the ABA transporter ATP-binding cassette subfamily G member 25 (AtABCG25) mediates root-to-shoot translocation of ABA and ABA-glucosyl ester (ABA-GE) in Arabidopsis (Arabidopsis thaliana). Isotope-labeled ABA tracer experiments and hormone quantification in xylem sap showed that the root-to-shoot translocation of ABA and ABA-GE was substantially impaired in the atabcg25 mutant under nondrought and drought conditions. However, the contents of ABA and ABA-GE in the leaves were lower in the atabcg25 mutant than in the wild type (WT) under nondrought but similar under drought conditions. Consistently, the stomatal closure was suppressed in the atabcg25 mutant under nondrought but not under drought conditions. The transporter activity assays showed that AtABCG25 directly exported ABA and ABA-GE in planta and in yeast (Saccharomyces cerevisiae) cells. Thus, we proposed a working model in which root-derived ABA transported by AtABCG25 via xylem mediates stomatal movements in the shoot under nondrought conditions but might exhibit little effect on stomatal movements under drought conditions. These findings extend the functions of AtABCG25 and provide insights into the long-distance translocation of ABA and its role in stomatal movements.

Revealing the Complete Bispecific Phosphatase Genes (DUSPs) across the Genome and Investigating the Expression Patterns of GH_A11G3500 Resistance against Verticillium wilt.

DUSPs, a diverse group of protein phosphatases, play a pivotal role in orchestrating cellular growth and development through intricate signaling pathways. Notably, they actively participate in the MAPK pathway, which governs crucial aspects of plant physiology, including growth regulation, disease resistance, pest resistance, and stress response. DUSP is a key enzyme, and it is the enzyme that limits the rate of cell metabolism. At present, complete understanding of the DUSP gene family in cotton and its specific roles in resistance to Verticillium wilt (VW) remains elusive. To address this knowledge gap, we conducted a comprehensive identification and analysis of four key cotton species: Gossypium arboreum, Gossypium barbadense, Gossypium hirsutum, and Gossypium raimondii. The results revealed the identification of a total of 120 DUSP genes in the four cotton varieties, which were categorized into six subgroups and randomly distributed at both ends of 26 chromosomes, predominantly localized within the nucleus. Our analysis demonstrated that closely related DUSP genes exhibited similarities in terms of the conserved motif composition and gene structure. A promoter analysis performed on the GhDUSP gene promoter revealed the presence of several cis-acting elements, which are associated with abiotic and biotic stress responses, as well as hormone signaling. A tissue expression pattern analysis demonstrated significant variations in GhDUSP gene expression under different stress conditions, with roots exhibiting the highest levels, followed by stems and leaves. In terms of tissue-specific detection, petals, leaves, stems, stamens, and receptacles exhibited higher expression levels of the GhDUSP gene. The gene expression analysis results for GhDUSPs under stress suggest that DUSP genes may have a crucial role in the cotton response to stress in cotton. Through Virus-Induced Gene Silencing (VIGS) experiments, the silencing of the target gene significantly reduced the resistance efficiency of disease-resistant varieties against Verticillium wilt (VW). Consequently, we conclude that GH_A11G3500-mediated bispecific phosphorylated genes may serve as key regulators in the resistance of G. hirsutum to Verticillium wilt (VW). This study presents a comprehensive structure designed to provide an in-depth understanding of the potential biological functions of cotton, providing a strong foundation for further research into molecular breeding and resistance to plant pathogens.

Sunflower-like missing-linker covalent organic framework for efficient extraction of non-steroidal anti-inflammatory drugs.

As excellent crystalline materials, covalent organic frameworks (COFs) are widely used in drug adsorption. In this work, a defective engineering strategy was proposed for designing and preparing the functionalized end-capping monomer and missing-linker COFs. The missing-linker COF 2,4,6-trihydroxybenzene-1,3,5-tricarbaldehyde compound with glycidyltrimethyl ammonium chloride modified benzene-1,4-diamine (TpPa-GTA) was synthesized through Schiff base reaction with wide pore size distribution for adsorption of four nonsteroidal anti-inflammatory drugs (NSAIDs). The adsorption process follows pseudo-second-order kinetics, and the four drugs reached adsorption equilibrium within 10 min. The sunflower-like structure helps to promote intraparticle diffusion during the adsorption process, thereby realizing the rapid adsorption of TpPa-GTA. The equilibrium isotherms fit well with both the Freundlich and Langmuir models, with a maximum adsorption capacity of 83.3-315 mg g-1 calculated from the Langmuir model. Based on the detection results of Zeta potential and XPS, the adsorption mechanism was inferred, and the rapid capture of NSAIDs in the wide pH range of 4.0 to 7.5 was realized under electrostatic interaction, hydrogen bonding, and π-π interaction. The detection of lake and river samples using the missing adapter TpPa-GTA has a recovery rate of 84.2-117%, which provides a new approach to the adsorption of pollutants with COFs.

Exploring the genetic and socioeconomic interplay between ADHD and anxiety disorders using Mendelian randomization.

Background: ADHD and anxiety disorders often co-occur, sharing symptoms and dysfunctions, yet the underlying mechanisms remain elusive. Methods: To explore the shared and distinct genetic variations between ADHD and anxiety disorders, we applied Mendelian randomization (MR) analysis to ADHD, anxiety disorders, and three socioeconomic factors: income, educational attainment (EA), and intelligence. MR analysis utilized genome-wide association study summary datasets (anxiety disorder: 7,016 cases and 14,745 controls; ADHD: 38,691 cases and 275,986 controls; EA: 766,345 participants; intelligence: 146,808 participants; household income: 392,422 participants), with inverse-variance weighting as the primary method. Results: Our MR analysis revealed no discernible genetic-level causal effect between ADHD and anxiety disorders (p > 0.77). Additionally, the independent variables for ADHD (25 SNPs) and anxiety disorders (18 SNPs) did not overlap, highlighting the genetic distinction between the two conditions. Higher income (p < 0.002) and EA (p < 0.005) were found to serve as protective factors for both ADHD and anxiety disorders. Genetic predisposition to higher income (86 SNPs) and EA (457 SNPs) were identified as a potential common protective factors for both conditions. Lastly, genetic predisposition to higher intelligence was found to potentially guard against ADHD (p < 0.001) but not against anxiety disorders (p > 0.55). Conclusion: Our findings indicate that the shared symptoms observed between ADHD and anxiety disorders are more likely influenced by genetic predispositions related to socioeconomic factors rather than by the genetic predispositions specific to the disorders themselves.

Adverse childhood experiences and cognitive function in later life: the sequential mediating roles of education level and adult loneliness.

Background: This study assesses the impact of adverse childhood experiences (ACEs) on the cognitive function of older adults. Furthermore, it examines the potential underlying mechanism involving education level and the subjective "feeling of loneliness" (FOL). Methods: Analyzing a population-based cohort sample from the China Health and Retirement Longitudinal Study database, 8,365 subjects aged 45 or older were interviewed in 2018. Ten ACEs indicators were measured using life history questionnaires assessed at 2014. FOL was assessed using a single item from 10-item Center for Epidemiological Studies Depression Scale (CESD-10). Cognitive function was assessed using a structured questionnaire comprising four dimensions: memory, orientation, computation, and visuospatial abilities. Results: In the fully adjusted model, which accounted for age, gender, marital status, smoke, drink, rural residence, and education levels of both mothers and fathers, the linear regression analysis indicated that ACEs were inversely associated the lower education level (B = -0.058, 95% CI = -0.090, -0.026, p < 0.001), and ACEs were found to be linked to an elevated risk of FOL (B = 0.072, 95% CI = 0.056, 0.089, p < 0.001). In addition, ACEs was not significantly associated with cognitive function (B = -0.047, 95% CI = -0.108, 0.015, p = 0.136), but FOL was significantly associated with cognitive function (B = -0.483, 95% CI = -0.561, -0.404, p < 0.001). Mediation analysis revealed that education level and FOL sequentially and partially mediated the association between ACEs and the total cognitive score, with a proportion mediated of 52.58%. Limitations: The evaluation of ACEs exposure was based on binary response options. This method limited our ability to explore various dimensions of adversity, such as ages of occurrence, severity, frequency, duration, and the extent of psychological effects at the time. Furthermore, the assessment of loneliness relied on a single item from the CESD-10, introducing a potential source of measurement error. Conclusion: Our study unveils a substantial association between ACEs and education level, as well as with FOL and cognitive function in the older adults. Moreover, education level and FOL serve as sequential mediating factors in the relationship between ACEs and cognitive function.

Hemophagocytic lymphohistiocytosis associated with brucellosis.

Hemophagocytic lymphohistiocytosis (HLH) is a life-threatening immune disorder categorized as familial HLH or secondary HLH. Our case report describes a 63-year-old woman with epilepsy whose clinical signs were unremitting fever and altered consciousness. Primary abnormalities consisted of fever, splenomegaly, cytopenia, hypertriglyceridemia, hyperferritinemia and hemophagocytosis in the bone marrow. Results of blood next generation sequencing and blood culture confirmed Brucella infection. This report illustrates a sHLH case caused by Brucella melitensis infection. Here, we review the classification, clinical features, diagnostic methods, treatment regimens, differential diagnosis, and prognosis of HLH and brucellosis.

Lactic acid bacteria modulate the CncC pathway to enhance resistance to ß-cypermethrin in the oriental fruit fly.

The gut microbiota of insects has been shown to regulate host detoxification enzymes. However, the potential regulatory mechanisms involved remain unknown. Here, we report that gut bacteria increase insecticide resistance by activating the cap "n" collar isoform-C (CncC) pathway through enzymatically generated reactive oxygen species (ROS) in Bactrocera dorsalis. We demonstrated that Enterococcus casseliflavus and Lactococcus lactis, two lactic acid-producing bacteria, increase the resistance of B. dorsalis to ß-cypermethrin by regulating cytochrome P450 (P450) enzymes and α-glutathione S-transferase (GST) activities. These gut symbionts also induced the expression of CncC and muscle aponeurosis fibromatosis. BdCncC knockdown led to a decrease in resistance caused by gut bacteria. Ingestion of the ROS scavenger vitamin C in resistant strain affected the expression of BdCncC/BdKeap1/BdMafK, resulting in reduced P450 and GST activity. Furthermore, feeding with E. casseliflavus or L. lactis showed that BdNOX5 increased ROS production, and BdNOX5 knockdown affected the expression of the BdCncC/BdMafK pathway and detoxification genes. Moreover, lactic acid feeding activated the ROS-associated regulation of P450 and GST activity. Collectively, our findings indicate that symbiotic gut bacteria modulate intestinal detoxification pathways by affecting physiological biochemistry, thus providing new insights into the involvement of insect gut microbes in the development of insecticide resistance.

Maintaining Toll signaling in Drosophila brain is required to sustain autophagy for dopamine neuron survival.

Macroautophagy/autophagy is a conserved process in eukaryotic cells to degrade and recycle damaged intracellular components. Higher level of autophagy in the brain has been observed, and autophagy dysfunction has an impact on neuronal health, but the molecular mechanism is unclear. In this study, we showed that overexpression of Toll-1 and Toll-7 receptors, as well as active Spätzle proteins in Drosophila S2 cells enhanced autophagy, and Toll-1/Toll-7 activated autophagy was dependent on Tube-Pelle-PP2A. Interestingly, Toll-1 but not Toll-7 mediated autophagy was dMyd88 dependent. Importantly, we observed that loss of functions in Toll-1 and Toll-7 receptors and PP2A activity in flies decreased autophagy level, resulting in the loss of dopamine (DA) neurons and reduced fly motion. Our results indicated that proper activation of Toll-1 and Toll-7 pathways and PP2A activity in the brain are necessary to sustain autophagy level for DA neuron survival.

SHMT2 Mediates Small-Molecule-Induced Alleviation of Alzheimer Pathology Via the 5'UTR-dependent ADAM10 Translation Initiation.

It is long been suggested that one-carbon metabolism (OCM) is associated with Alzheimer's disease (AD), whereas the potential mechanisms remain poorly understood. Taking advantage of chemical biology, that mitochondrial serine hydroxymethyltransferase (SHMT2) directly regulated the translation of ADAM metallopeptidase domain 10 (ADAM10), a therapeutic target for AD is reported. That the small-molecule kenpaullone (KEN) promoted ADAM10 translation via the 5' untranslated region (5'UTR) and improved cognitive functions in APP/PS1 mice is found. SHMT2, which is identified as a target gene of KEN and the 5'UTR-interacting RNA binding protein (RBP), mediated KEN-induced ADAM10 translation in vitro and in vivo. SHMT2 controls AD signaling pathways through binding to a large number of RNAs and enhances the 5'UTR activity of ADAM10 by direct interaction with GAGGG motif, whereas this motif affected ribosomal scanning of eukaryotic initiation factor 2 (eIF2) in the 5'UTR. Together, KEN exhibits therapeutic potential for AD by linking OCM with RNA processing, in which the metabolic enzyme SHMT2 "moonlighted" as RBP by binding to GAGGG motif and promoting the 5'UTR-dependent ADAM10 translation initiation.