SEARCH · PubMed Health

Search PubMed Health

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 793 records · Page 44Linked to original sources

PubMed2026

Asparagine Synthetase Deficiency: Neuropathological Evidence of Disrupted Cortical Development.

Asparagine synthetase deficiency (ASNSD) is a rare metabolic disease causing congenital microcephaly, severe developmental delay, and spastic quadriplegia. Although the central nervous system is severely affected, other organ systems appear unaffected by asparagine deficiency. We present an infant homozygous for the mutation c.904-1G>A in the ASNS gene, whose clinical presentation and radiological findings were typical for ASNSD. Following the patient's death at the age of 6 months, histological and immunohistochemical examination of the telencephalon revealed a vast disturbance of migration of neuronal subpopulations, consequently severe disorganization of cortical layers, and thinning of the cerebral cortex. These findings provide novel insights into disease pathogenesis and may explain the hallmark features of ASNSD, including microcephaly and epilepsy.

ASNS gene↗

PubMed2026

Genome-wide identification of the Glutathione Peroxidase (GPX) gene family in Taxodium distichum and functional characterization of TdGPX9 in enhancing salt tolerance.

This study systematically identified 10 TdGPX genes in Taxodium distichum, demonstrating that the nucleocytoplasmic-localized TdGPX9 plays a pivotal role in salt stress response. Overexpression of TdGPX9 significantly enhances salt tolerance by strengthening the antioxidant defense system and improving root system plasticity under stress. Taxodium distichum is a premier coniferous species renowned for its exceptional waterlogging and salinity tolerance, serving as a vital forest resource for coastal afforestation and wetland ecological restoration. Within the physiological framework of plant stress resistance, the glutathione peroxidase (GPX) family represents a cornerstone of the antioxidant enzymatic system, playing a critical role in scavenging reactive oxygen species and maintaining cellular redox homeostasis. In this study, 10 TdGPX genes were identified via a comprehensive genome-wide analysis and mapped across eight chromosomes. These genes possess a highly conserved Thioredoxin_like domain, with structural and motif analyses revealing a well-maintained arrangement of conserved motifs within each subgroup. The promoter analysis identified a sophisticated regulatory network enriched with cis-acting elements responsive to light, phytohormones, and abiotic stresses, suggesting their integration into diverse signaling pathways. Expression profiling across various tissues and embryonic developmental stages further highlighted the versatile roles of TdGPX members in plant growth and organogenesis. Notably, qRT-PCR analysis identified the nucleocytoplasmic-localized TdGPX9 as a primary respondent to salinity. Functional validation demonstrated that TdGPX9 overexpression significantly enhances salt tolerance in transgenic Arabidopsis and T. distichum callus by strengthening the antioxidant defense system. Furthermore, TdGPX9 promoted root system plasticity under stress, as evidenced by increased lateral root density. These findings provide a systematic basis for understanding the redox-regulatory mechanisms in baldcypress and offer vital genetic resources for improving forest resilience in coastal wetland ecosystems.

Salt Tolerance↗

PubMed2026

Nipah virus in the era of global connectivity: molecular evolution, transmission risk, and preparedness strategies.

Nipah virus (NiV) is a highly pathogenic zoonotic RNA virus belonging to the genus Henipavirus within the family Paramyxoviridae, representing a continuing global health concern due to its high case fatality rate and potential for epidemic expansion in the era of increasing international connectivity. The virus demonstrates strong evolutionary adaptability driven by the absence of proofreading mechanisms during RNA replication, enabling genetic diversification that may influence host range, virulence, and transmission dynamics. Molecular pathogenesis of NiV is primarily mediated through interaction of viral glycoproteins with ephrin-B2 and ephrin-B3 receptors, facilitating host cell entry, endothelial damage, and neuroinvasion. Immune evasion facilitated by the action of accessory proteins encoded by the P gene (P, V, W, and C) acts to suppress innate antiviral immunity through the inhibition of interferon induction and JAK/STAT signaling. Human-to-human transmission of Nipah virus remains limited, with epidemiological evidence indicating basic reproduction numbers generally below unity; however, respiratory involvement and healthcare-associated exposure may enhance cluster outbreaks. Global travel, ecological disruption, and fragmented surveillance systems contribute to spillover risk, particularly in South and Southeast Asia where fruit bats of the genus Pteropus serve as natural reservoirs. Despite advances in vaccine technology, including subunit, viral vector, mRNA-based platforms, and monoclonal antibody therapies, no licensed prophylactic or therapeutic agent is currently available for human use. Global preparedness remains challenged by the scarcity of high-containment biosafety facilities, limited research funding, and absence of integrated One Health surveillance networks. Ethical considerations surrounding wildlife population control further complicate disease mitigation strategies. Emerging genomic surveillance, artificial intelligence-assisted predictive modeling, and regional data-sharing frameworks are essential for early detection and response. Strengthening molecular research on viral-host interactions and transmission determinants will be critical for preventing future Nipah virus outbreaks in an increasingly interconnected world.

Genomic surveillance↗

PubMed2026

Key enzyme optimization and multi-node metabolic flux regulation drive l-arginine production in Escherichia coli.

Microbial production of l-arginine is often constrained by tight metabolic regulation and insufficient precursor supply. Here a plasmid-free, non-auxotrophic Escherichia coli strain for high-level production of l-arginine was rationally engineered, based on our previous constructed strain G0 with 12.4 g/L l-arginine production in flask. Glucose metabolism and glutamate/aspartate uptake were initially enhanced, with subsequent semi-rational engineering of key enzymes, ornithine acetyltransferase (OAT) and argininosuccinate synthase (ASS), to promote ATP synthesis. OAT was firstly rational engineered by introducing amide group for the residues near substrate-binding pocket to stabilize oxyanion transition states, with achieving that variant Y386Q showed Km/kcat at 6.58 mM-1 min-1, 2 times higher than that of wild type. Variant Y332L of ASS was novelty fused with argininosuccinate lyase via GGGGS linker for ASS activity measurement, which helped improve l-arginine titer to 17.5 g/L. With further studies by screening of rate-limiting nodes on the genome-scale level based on sRNA strategy, aspartate and glutamate pathways were synergistically enhanced, along with utilizing carbon dioxide recycling for carbamoyl phosphate synthesis to drive ammonia donor supply. The obtained final plasmid-free and non-auxotrophic strain G16 produced 21.1 g/L l-arginine in flask, 76.6% higher than that of original strain G0. In 5 L fermenter, 125.6 g/L l-arginine was produced by fed-batch fermentation, with a yield of 0.53 g/g glucose. This study underscores that the convergence of mechanistic enzyme redesign and systems-level pathway optimization is critical to unlocking high-efficient amino acid production, offering a transferable blueprint for rational strain engineering in industrial biotechnology.

Argininosuccinate synthase↗

PubMed2026

From dysbiosis to resilience: Microbiome engineering for sustainable shrimp aquaculture.

The intensification of shrimp aquaculture has increased exposure to disease, environmental perturbations, and antimicrobial pressure, making microbial stability increasingly relevant to sustainable production. Microbiome stability-encompassing resistance to disturbance and resilience of functional recovery-provides an ecological framework for understanding how shrimp and culture-environment microbial communities respond to intensive farming. This review examines the transition from microbial homeostasis to dysbiosis and evaluates how microbiome engineering could redirect disrupted communities towards resilient states. Evidence is integrated across the intestine, hepatopancreas, rearing water, sediment and biofloc to assess how host genetics, ontogeny, diet, culture conditions, antibiotics and pollutants shape microbiome assembly and destabilization. Disease-associated changes in acute hepatopancreatic necrosis disease, white faeces syndrome, Enterocytozoon hepatopenaei infection, and white spot syndrome virus infection are critically evaluated, with explicit separation of associations, pathogen-induced dysbiosis, and community-level causality. Established and emerging interventions-including probiotics, prebiotics, synbiotics, functional diets, biofloc management, phages, postbiotics, microbiota transplantation and synthetic microbial communities-are assessed according to their capacity to modify microbial function, persistence and recovery rather than taxonomic change alone. We further examine how multi-omics, microbiome-informed breeding, and environmental monitoring could support biomarker development, predictive decision support and context-specific intervention. We argue that progress requires a shift from taxonomic description to function-guided engineering, from endpoint comparisons to direct measurement of resilience, and from laboratory efficacy to reproducible farm-scale validation. Overall, microbiome management may contribute to more disease-resilient and sustainable shrimp production, provided that its effectiveness can be validated under commercial farming conditions.

Dysbiosis↗

PubMed2026

Differential DNA damage vulnerability in human neuropathies.

The maintenance of genomic integrity is a fundamental prerequisite for tissue homeostasis, which is critical for central nervous system (CNS) function. During neurogenesis, the transition from rapidly proliferating neuroprogenitors to post-mitotic neurons entails a fundamental shift in genotoxic threats, which must be addressed by the robust DNA damage response (DDR) network. The spatiotemporal utilisation of distinct DDR pathways in different neural cell types establishes heterogeneous vulnerabilities in specific brain regions to pathological processes. While the cerebrum exhibits varying or negligible degrees of sensitivity to DDR defects, cerebellar atrophy and degeneration are common hallmarks of various human genomic instability syndromes (GIS). Biomedical and cellular studies of human GIS and the corresponding mouse models have shed light on the aetiology of the associated neuropathies; however, cerebellar vulnerability to DDR defects remains poorly understood. Here, we review the cell type- and species-specific divergences in DDR reliance in different brain regions, along with the corresponding DDR pathways underpinning the distinct susceptibility of neuropathological manifestations.

Animal model↗

PubMed2026

Multi-omics and spatial transcriptomics reveal that S100A10 drives CD8+ T-cell exhaustion and immune evasion in hepatocellular carcinoma through cPLA2-5-LOX-mediated arachidonic acid metabolism and ferroptosis.

Immune evasion in hepatocellular carcinoma (HCC) represents a major biological barrier limiting the efficacy of immunotherapy, yet its molecular basis remains incompletely understood. Increasing evidence indicates that tumor metabolic reprogramming and ferroptosis-related signaling play critical roles in shaping an immunosuppressive tumor microenvironment (TME); however, the specific regulatory factors involved remain unclear. This study aims to systematically elucidate the functional role of S100 calcium-binding protein A10 (S100A10) in immune evasion in HCC, with a particular focus on the molecular mechanisms by which S100A10 regulates CD8+ T-cell exhaustion through arachidonic acid (AA) metabolism and ferroptosis, as well as its potential therapeutic implications. To this end, data from The Cancer Genome Atlas Liver Hepatocellular Carcinoma (TCGA-LIHC) cohort are integrated to analyze the expression patterns of S100A10, its prognostic value, and its association with the immune microenvironment. S100A10 overexpression and knockout models are established in HCCLM3 and MHCC97L cell lines, and S100A10-mediated metabolic pathway reprogramming is characterized using transcriptomic profiling, untargeted metabolomics, and ferroptosis-related functional assays. In parallel, single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics are employed to delineate the cell-type specificity and spatial distribution of S100A10. Furthermore, human CD8+ T-cell co-culture systems and orthotopic mouse HCC models are used to evaluate the impact of S100A10 on immune function and responsiveness to anti-programmed cell death protein 1 (anti-PD-1) therapy. The results demonstrate that S100A10 is significantly upregulated in HCC and is closely associated with poor prognosis and an immunosuppressive state. Mechanistically, S100A10 activates cytosolic phospholipase A2-arachidonate 5-lipoxygenase (cPLA2-5-LOX)-mediated AA oxidative metabolism, leading to the accumulation of lipid peroxidation products and ferroptosis-associated signals, thereby driving CD8+ T-cell exhaustion and promoting immune evasion. Significantly, inhibition of S100A10 reshapes the tumor immune microenvironment (TIME) and enhances the therapeutic efficacy of anti-PD-1 treatment. Collectively, these findings identify S100A10 as a critical regulator of metabolic-immune coupling in HCC and provide a theoretical basis for combinatorial strategies targeting metabolism and immunotherapy.

Arachidonic acid metabolism↗

PubMed2026

Remission status in persistent depressive disorder following acute treatment with psychotherapy plus medication or medication alone: A 2-year naturalistic follow-up.

OBJECTIVE: Long-term benefits of acute-phase treatments for persistent depressive disorder (PDD) are unclear. Treatment guidelines disagree on the efficacy of cognitive behavioral analysis system of psychotherapy (CBASP). We examined whether acute CBASP protected against recurrence in PDD patients over two years of naturalistic follow-up. METHODS: An observational study evaluated major depressive episode (MDE) recurrences in patients completing the Research Evaluating the Value of Augmenting Medication with Psychotherapy (REVAMP) trial. Enrollees 18-75 years had PDD: current chronic MDE, recurrent MDEs with incomplete recovery, or double depression. All received open-label antidepressant medication (ADM) for 12 weeks. Non-remitters, continuing on ADM, were randomized (2:2:1) to 12 weeks of 1) CBASP, 2) brief supportive therapy (BSP), or 3) ADM alone (MEDS). Patients completing this 12-week randomized phase were offered two-year follow-up. Blinded raters assessed the primary outcome, remission status, using the Longitudinal Interval Follow-up Evaluation and Hamilton Depression Rating Scale at 3-month intervals. Analyses evaluated group differences and non-specific predictors of remission status. RESULTS: Of 323 participants entering follow-up, 203 (62.8%) met current MDE criteria during follow-up, without between-group differences: BSP: 83 (65.3%), CBASP: 85 (60.2%), MEDS: 35 (63.6%), Chi-square = 0.75; p = 0.69. Remission after acute treatment, lack of comorbid anxiety disorder, and female gender were significantly associated with lower recurrence risk. CONCLUSION: Similar to the acute phase outcomes, no group differences emerged over the 2-year follow-up, suggesting no long-term benefit of a 12-week CBASP treatment with ADM over other PDD treatments. Findings underscore the difficulty of PDD treatment and the importance of acute treatment remission. TRIAL REGISTRATION: ClinicalTrials.gov identifier: NCT00057551.

Antidepressant↗

PubMed2026

Light-activated CRISPR/dCas9 nanomedicine for programmable control of renal fibrosis.

Renal fibrosis is the final common pathway of progressive chronic kidney disease and is maintained by spatially heterogeneous interactions among injured epithelial cells, activated fibroblasts, immune cells, extracellular matrix remodeling, metabolic stress, and persistent profibrotic transcriptional programs. Current therapies slow renal functional decline but do not directly control the regulatory circuits that stabilize maladaptive repair. Photoresponsive renal nanomedicine offers a potential strategy to add external control to anti-fibrotic intervention by combining kidney-directed delivery with light-gated release or activation of molecular payloads. This review examines the emerging interface between photoresponsive nanomaterials and CRISPR/dCas9-based gene regulation for renal fibrosis, with emphasis on upconversion nanoparticles, photoresponsive polymers, ROS- and pH-responsive matrices, optogenetic switches, and renal-compartment-directed carrier design. We argue that the most defensible therapeutic objective is not permanent genome editing or autonomous organ regeneration, but spatially confined, temporally limited, and reversible regulation of validated fibrotic or protective gene programs using CRISPRa, CRISPRi, or dCas9-based epigenome editors. The review therefore evaluates material requirements, optical-dosimetry constraints, payload architecture, renal biodistribution, target-selection logic, safety risks, and preclinical validation criteria. By defining the engineering and biological conditions required for controlled anti-fibrotic regulation, this framework positions photoresponsive renal nanomedicine as a translationally testable route toward localized modulation of fibrotic cell states rather than an overextended claim of kidney regeneration.

Anti-fibrotic gene regulation↗

PubMed2026

Molecular subgroups of human malignant peripheral nerve sheath tumors are conserved in canines.

Malignant peripheral nerve sheath tumors (MPNST) are aggressive sarcomas of Schwann cell lineage with poor prognosis in both humans and dogs. While rare in humans, MPNSTs occur more frequently in dogs and share histomorphological and clinical features. Recent methylome and transcriptome analyses have identified two molecular subgroups of human MPNST with distinct oncogenic signaling pathways and prognostic implications; however, it remains unclear if these subgroups also exist in canines. Given their higher incidence and biological similarities to human disease, canine MPNSTs represent a promising comparative model to investigate molecular subtypes and evaluate novel therapeutic strategies. To characterize canine MPNST and assess molecular parallels with the human subgroups, we applied laser-capture microdissection (LCM) followed by RNAsequencing to analyze tumor tissue from 20 canine MPNST. Principle component and differential gene expression analyses identified two clearly distinct transcriptional clusters corresponding to spindle cell and epithelioid MPNST variants, respectively. Unsupervised cross-species comparison aligned the two canine clusters with the human G1 and G2 subgroups. Accordingly, one cluster was characterized by SHH pathway activation and increased cell cycle activity, while the other showed non-canonical WNT pathway, Schwann cell-like features and marked macrophage infiltration. Immunohistochemistry further demonstrated loss of H3K27me3, p-ERK activation and β-catenin signaling by IHC in a subset of tumors. These findings support the value of canine MPNST as clinically amenable model for structured assessment of novel therapeutic approaches to benefit patients of both species.

Canine cancer model↗

PubMed2026

FGF19 as a site-specific candidate biomarker in colorectal neuroendocrine carcinomas.

PURPOSE: Gastrointestinal neuroendocrine carcinomas (GI-NECs) are aggressive tumors with marked site-specific heterogeneity, yet molecular markers for colorectal origin are lacking. This study characterized genomic and protein expression profiles to identify origin-specific biomarkers. METHODS: Nineteen GI-NECs (7 esophageal, 6 gastric, 6 colorectal) were analyzed by targeted next-generation sequencing (NGS) of 425 genes and immunohistochemistry (IHC). Genetic variations across primary sites were compared, and associations between FGF19 expression, clinicopathological features, microsatellite (MS) status, and tumor mutational burden (TMB) were assessed. FGF19 transcriptional expression was further examined in The Cancer Genome Atlas (TCGA) colorectal cohort using the UALCAN platform. RESULTS: A total of 163 genomic alterations were identified. FGF19 was the only gene showing site-specific alterations, being exclusively mutated or amplified in colorectal NECs (50%, 95% CI: 11.8-88.2%) with significantly elevated protein expression (83.3%, 95% CI: 35.9-99.6%) compared with other sites. A microsatellite instability-high (MSI-H) subgroup (10.5%, 95% CI: 1.3-33.1%) exhibited markedly higher TMB. TCGA data confirmed upregulated FGF19 in colorectal tumors but showed no survival association, consistent with the prognostic neutrality in our cohort. CONCLUSIONS: FGF19 may act as a site-specific candidate biomarker for colorectal NECs, with 83.3% protein positivity and exclusive site-specific alterations in 50% of cases. Detection of MSI-H suggests that mismatch repair (MMR) testing may be considered in selected patients with suggestive clinical or family histories to inform immunotherapy decisions.

FGF19↗

PubMed2026

Functional characterization of lncIMF_17214 in regulating intramuscular fat deposition of yellow-feathered broilers.

Intramuscular fat (IMF) content and lipid composition are key determinants of both the nutritional value and sensory attributes of poultry meat, yet the underlying regulatory mechanisms remain insufficiently elucidated. In this study, triglyceride (TG) content was employed as a quantitative phenotypic proxy to dissect the molecular basis of IMF deposition in yellow-feathered broilers. By integrating TG phenotypic data from 315 individuals with transcriptomic profiles and whole-genome resequencing datasets, a TG-associated long noncoding RNA (lncRNA), lncIMF_17214, was identified. Functional characterization revealed that lncIMF_17214 functions as a negative regulator of lipid deposition. Specifically, its knockdown led to significant increases in TG and total cholesterol concentrations, promoted lipid droplet accumulation, and decreased shear force in breast muscle, whereas its overexpression elicited the opposite effects. Mechanistically, lncIMF_17214 interacts with the RNA-binding protein CNBP, forming a regulatory complex that inhibits lipid accumulation. Furthermore, liver-directed overexpression increased the abundance of lncIMF_17214 in plasma exosomes, while liver-directed manipulation was associated with changes in hepatic and breast-muscle lipid deposition; direct exosome-mediated transfer to intramuscular adipocytes remains to be established. Transcriptomic profiling coupled with pathway enrichment analyses demonstrated that lncIMF_17214 predominantly influences steroid biosynthesis, unsaturated fatty acid metabolism, and peroxisome proliferator-activated receptor (PPAR) signaling pathways. This suggests that it may be involved in the regulation of these pathways, although the underlying molecular mechanisms remain to be further elucidated. Collectively, these findings define a lncIMF_17214-centered regulatory axis linking intracellular and systemic lipid metabolism and provide a robust molecular framework for the targeted improvement of meat quality traits in yellow-feathered broilers.

Breast muscle↗

PubMed2026

A chromosome-level genome assembly and developmental transcriptome profiling reveal stage-specific remodeling of the molecular chaperone system in Helicoverpa armigera.

Helicoverpa armigera is one of the most destructive lepidopteran pests worldwide owing to its remarkable polyphagy, long-distance migration, and rapid adaptation to insecticides. Here, we present a chromosome-level genome assembly of H. armigera generated from a field-collected individual in southwestern China, providing a valuable resource for future population genomic and pangenome studies. Developmental transcriptome analyses of first-instar larvae, fifth-instar larvae, and adults identified 6817, 3519, and 5518 differentially expressed genes, respectively, including 797 shared among all developmental transitions. Functional enrichment and co-expression network analyses revealed extensive transcriptional reprogramming, characterized by coordinated regulation of glycolysis, the tricarboxylic acid (TCA) cycle, and fatty acid β-oxidation, indicating dynamic metabolic remodeling during development. Genome-wide analysis identified 77 heat shock protein (HSP) genes belonging to six subfamilies. These genes were unevenly distributed across chromosomes, with HSP20 members exhibiting extensive tandem duplication. Expression profiling revealed pronounced stage specificity, suggesting progressive remodeling of molecular chaperone networks during development. Early larvae primarily relied on HSP40/HSP60/HSP70 and HSP10/HSP60 chaperone systems; fifth-instar larvae exhibited HSP20-centered proteostasis; and adults predominantly expressed HSP40 together with multiple HSP70 members, accompanied by enrichment of stress response and metamorphosis-related functions. This study provides new insights into developmental transcriptional regulation, metabolic remodeling, and stage-specific specialization of molecular chaperone networks in H. armigera, establishing a foundation for future studies of stress adaptation, population genomic variation, and developmental mechanisms.

Cotton bollworm↗

PubMed2026

Nuclear single-copy orthologous genes as phylogenomic markers for resolving the closely related firefly genera Pteroptyx, Medeopteryx, and Trisinuata (Coleoptera: Lampyridae: Luciolinae).

Fireflies (Lampyridae) are bioluminescent beetles with broad ecological roles across temperate and tropical ecosystems, occupying diverse habitats including forests, wetlands, grasslands, mangroves, and riverine systems. The subfamily Luciolinae is primarily distributed across Asia and the Indo-Pacific. Phylogenetic relationships among three closely related Luciolinae genera - Medeopteryx, Pteroptyx, and Trisinuata - remain unresolved using mitochondrial genome data alone. This study used nuclear genome data to resolve relationships among these genera and identify a lighter-weight nuclear marker panel for expanding taxon sampling. Draft genomes were reconstructed for fifteen firefly species, eight from the focal genera, and analyzed with five published firefly genomes. Using BUSCO and OrthoFinder, 1,011 nuclear single-copy orthologs (SCOs) were identified for phylogenomic inference. Discordance between concatenation- and coalescence-based phylogenies indicated incomplete lineage sorting (ILS). The coalescence-based phylogeny recoveredPteroptyxas monophyletic and sister to a (Medeopteryx,Trisinuata) clade, with Trisinuata nested within a non-monophyletic Medeopteryx; however, quartet support at the base of Pteroptyx, particularly at Pt. valida, was low.Filtering for compositional homogeneity, clock-likeness, and species-tree concordance yielded 103 SCOs with a significantly higher proportion of parsimony-informative sites than non-selected loci, retaining the backbone topology with higher gene concordance support at scored clades, while ILS-driven discordance at Pt. valida persists - confirming that the reduced panel retains phylogenetic resolving power for future taxon sampling. These findings demonstrate a practical framework for using nuclear SCOs to resolve close phylogenetic relationships within Luciolinae. Future work should expand taxon sampling - especially forTrisinuata - alongside long-read assemblies, for a more robust phylogenomic framework.

Fireflies↗

PubMed2026

Large-Scale Genomic Analysis of Stripe Rust Resistance in Chinese Wheat Germplasm Using Multi-Environment Trial Data.

Wheat stripe rust, caused by Puccinia striiformis f. sp. tritici (Pst), is a significant disease affecting global wheat crops and causing substantial economic losses. This study aimed to identify effective resistance genes by evaluating 120 common wheat accessions from diverse regions in China. These samples were tested with three Pst races at the seedling stage and with natural Pst inoculum at four field locations in three crop seasons. Genotypic data were collected through a Wheat55K iSelect single-nucleotide polymorphism array. The genome-wide association study identified 17 distinct loci linked to stripe rust response, accounting for 1.07 to 30.58% of the phenotypic variation across trials. These loci were distributed among three wheat genome groups: 2 in Group A, 10 in Group B, and 5 in Group D. Among these, eight loci overlapped with the reported stripe rust resistance genes or quantitative trait loci, while nine loci were novel and mainly distributed on chromosomes 2A, 6B, and 7D. This research enhances the understanding of genetic mechanisms underlying wheat stripe rust resistance and provides valuable germplasm resources for breeding new cultivars with enhanced disease resilience.

Puccinia striiformis f. sp. tritici↗

PubMed2026

Rhizosphere Dialogue: Microorganisms Mediated by Root Exudates Alleviate Drought Stress in Grasses.

Drought stress threatens the ecological functions and economic value of grasses, posing a major challenge to their sustainable production. Plants co-evolve with rhizosphere microbial communities, sometimes described as the plant's second genome, that can contribute to drought adaptation. Drought alters root architecture, hormonal and redox regulation and belowground carbon allocation, thereby modifying the quantity and composition of root exudation and reshaping the rhizosphere environment. This review uses the rhizosphere dialogue as an integrative framework to link these plant responses with microbial recruitment and subsequent feedback to the host. We summarise three linked stages of this dialogue: drought-induced changes in root exudation; microbial recruitment and colonisation through chemotaxis, attachment, biofilm formation, and root colonisation; and microbiome-mediated feedback that improves plant water relations, hormonal and redox homoeostasis, nutrient acquisition, and root function. We highlight microbial extracellular polymeric substances, 1-aminocyclopropane-1-carboxylate deaminase, and microbial volatile organic compounds as key mediators of drought alleviation. We then discuss how this framework may inform rational synthetic microbial community (SynCom) design, microbiome-informed breeding, artificial intelligence and machine-learning assisted strain prioritisation, rhizosphere legacy effects, and real-time monitoring. Future work should distinguish active exudate-mediated recruitment from drought-driven environmental filtering and integrate multi-omics, plant genetics, functional validation, and multi-location field trials to determine whether rhizosphere dialogue can become a predictive framework for climate-resilient grass production.

drought stress↗

PubMed2026

The Wild Soybean C3HC4-Type RING Zinc-Finger Protein ZFP4 Enhances Resistance to Soybean Mosaic Virus.

Soybean [Glycine max (L.) Merr.] is a globally important source of protein and edible oil, but is severely threatened by soybean mosaic virus (SMV). Wild soybean [Glycine soja Sieb. & Zucc.], the wild ancestor of cultivated soybean, exhibits high genetic diversity and strong resistance to pathogens. In this study, we identified a novel SMV resistance locus RSC7-4 and its candidate gene ZFP4 from wild soybean, encoding a C3HC4-type RING zinc-finger protein. The knockout mutants of ZFP4 showed enhanced susceptibility to SMV strains SC7 and SC3, while its overexpressing lines conferred resistance without yield penalty; ZFP4 mediates resistance by inhibiting GSTT1 to increase glutathione and reduce excessive reactive oxygen species accumulation. Domestication analysis revealed reduced genetic diversity of ZFP4 in cultivated soybean, with the resistant ZFP4Hap1 underutilized in breeding. In summary, this study provides not only excellent genetic resources for SMV-resistant soybean breeding but also new insights into the regulatory mechanisms of soybean resistance to SMV.

ZFP4↗

PubMed2026

Clonotypic characterization defines B-cell drivers of clonal expansion and intratumor heterogeneity in IgM monoclonal gammopathies.

Waldenström macroglobulinemia (WM) and IgM monoclonal gammopathy of undetermined significance (MGUS) share the same cell of origin but differ in clonal size. Compared with other B-cell neoplasms, the lymphoplasmacytic clone in WM can be rather small, limiting our understanding of clonal expansion. We applied an integrative approach using single-cell RNA with B-cell receptor (BCR) sequencing, the assay for transposase-accessible chromatin, and whole-genome sequencing to characterize the tumor clone in patients with IgM MGUS, smoldering WM (SWM), and symptomatic WM (WM). IgM MGUS and low- or intermediate-risk SWM harbored multiple B-cell clones compared to WM. CD9, JCHAIN, RASSF6, and DUSP22 were the main markers of the dominant B-cell clone at gene expression and chromatin activity levels, with CD9 preferentially expressed in plasma cell-like tumor cells. POU2F2 had high activity in the tumor clone and was linked to CD9 regulatory regions. MYD88 and IGLL5 mutations, mainly associated with the mutational signature SBS5, were present in minor clones, whereas the MYD88 mutation was also detected in nonexpanded B-cells. The 6q deletion was present in tumor cells from high-risk patients, which harbored fitness advantage over copy-neutral tumor cells. Coding mutations clustered tumor and minor clones from oligoclonal patients and were associated with abnormal transcriptional programs. The B-cell clones also showed enriched predicted interactions with monocytes. Our integrative single-cell approach reveals the importance of clone size in IgM gammopathy and identifies key markers promoting clonal expansion.

Journal Article↗