Search Results (3,039)

Leaf rust, a devastating fungal disease caused by Puccinia triticina (Pt), severely impacts wheat quality and yield. Identifying genetic loci for wheat leaf rust resistance, developing molecular markers, and breeding resistant varieties is the most environmentally friendly and economical strategy for disease control. This study utilized a recombinant inbred line (RIL) population of Doumai and Shi4185, combined with the wheat 90 K single nucleotide polymorphisms (SNPs) chip data and maximum disease severity (MDS) of leaf rust from four environments, to identify adult plant resistance (APR) loci through linkage mapping. Additionally, kompetitive allele-specific PCR (KASP) markers suitable for breeding were developed, and genetic effects were validated in a natural population. In this study, 5 quantitative trait loci (QTL) on chromosomes 1B (2), 2A and 7B (2) were identified through inclusive composite interval mapping, and named as QLr.lfnu-1BL1, QLr.lfnu-1BL2, QLr.lfnu-2AL, QLr.lfnu-7BL1 and QLr.lfnu-7BL2, respectively, explaining 4.54–8.91% of the phenotypic variances. The resistance alleles of QLr.lfnu-1BL1 and QLr.lfnu-1BL2 originated from Doumai, while the resistance alleles of QLr.lfnu-2AL, QLr.lfnu-7BL1 and QLr.lfnu-7BL2 came from Shi4185. Among these, QLr.lfnu-1BL2, QLr.lfnu-7BL1 and QLr.lfnu-7BL2 overlapped with previously reported loci, whereas QLr.lfnu-1BL1 and QLr.lfnu-2AL are likely to be novel. Two KASP markers, QLr.lfnu-2AL and QLr.lfnu-7BL, were significantly associated with leaf rust resistance in a diverse panel of 150 wheat varieties mainly from China. Totally, 34 potential candidate genes encoded the NLR proteins, receptor-like kinases, signaling kinases and transcription factors were selected as candidate genes for the resistance loci. These findings will provide stable QTL, available breeding KASP markers and candidate genes, and will accelerate the progresses of wheat leaf rust resistance improvement through marker-assisted selection breeding. Full article

Nontuberculous mycobacteria are opportunistic pathogens increasingly associated with human disease. Within this group, the Mycobacterium avium complex (MAC), which includes M. avium, M. intracellulare and M. intracellulare subsp. chimaera, is the most frequent cause of infection. The increase in MAC cases worldwide has made it crucial to understand their population structure, clinical relevance and resistance mechanisms. Recent advances in whole-genome sequencing (WGS) and molecular approaches have improved the knowledge of taxonomy, population structure and genetic diversity, while also enabling the investigation of transmission and epidemiology. Clinically, MAC most often causes chronic pulmonary disease, but extrapulmonary forms, including disseminated disease, also occur. Presentation can vary by infecting species, while host factors such as pre-existing lung disease or immunosuppression further increase the risk. Treatment outcomes remain less favourable than desired, in part due to antimicrobial resistance involving de novo-acquired mutations. Pathogenesis is also influenced by interactions between MAC and host cells, including mechanisms of immune evasion and inflammatory modulation. In addition, emerging evidence suggests that gut–lung axis dysbiosis may influence susceptibility to MAC infection. This review outlines current knowledge on the population structure, clinical significance, resistance and host–pathogen interactions of MAC. Full article

Background: Intracranial aneurysm (IA) rupture is a life-threatening cerebrovascular event with a mortality rate of up to 40%, affecting approximately 500,000 people globally each year. Although environmental pollutants such as 2,2′,4,4′-tetrabromodiphenyl ether (PBDE-47) have been implicated in the pathogenesis of IA, the causal relationship and underlying mechanisms remain unclear. This study aims to systematically explore the potential causal role of PBDE-47 in the development of IA by integrating multi-omics approaches. Methods: We utilized the UK Biobank Drug Proteomics Project (UKB-PPP) genome-wide association study (GWAS) data, including 2940 plasma proteins and 1400 metabolites, along with IA genetic data from 456,348 individuals, to perform a two-sample Mendelian randomization (MR) analysis. Instrumental variables were selected based on genome-wide significance (p < 5 × 10⁻⁸) or suggestive thresholds (p < 5 × 10⁻⁵). Analytical methods included inverse variance weighting (IVW), MR-Egger, weighted median, MR-PRESSO, and Steiger filtering for sensitivity analysis. Molecular docking and 100-nanosecond molecular dynamics simulations were used to evaluate interactions between PBDE-47 and proteins. Mediation analysis assessed the roles of plasma metabolites and miRNAs, and SMR-HEIDI tests were used to verify causal relationships. Results: MR analysis identified 93 plasma proteins potentially causally associated with IA, including 53 protective factors and 40 risk factors. By integrating PBDE-47 targets, IA-related genes, and metabolite-related genes, we identified 15 hub genes. Molecular docking revealed potential binding between PBDE-47 and F2R (binding energy: −5.516 kcal/mol), and SMR-HEIDI testing supported F2R as a potential causal risk factor for IA. Molecular dynamics simulations indicated the stability of the complex structure. Mediation analysis suggested that F2R may influence IA risk through eight plasma metabolites, and miR-130b-3p may indirectly promote IA development by upregulating F2R. Conclusions: Our findings suggest that exposure to PBDE-47 may have a potential causal relationship with IA risk, potentially mediated through the “PBDE–47–F2R–metabolite–miRNA” regulatory axis. These results provide preliminary evidence for early diagnostic biomarkers and targeted interventions for IA. The multi-omics analytical framework established in this study offers new insights into environmental determinants of neurovascular diseases, although further validation is needed to address potential limitations. Full article

Chrysanthemum morifolium Ramat. is a major ornamental crop that suffers from diverse fungal, bacterial, viral, and insect pests, causing significant yield and quality losses. Between 2015 and 2025, rapid progress in molecular biology, genomics, and ecological regulation has advanced both fundamental research and applied control strategies. Multi-locus sequencing, multiplex PCR, and next-generation sequencing refined the identification of fungal and bacterial pathogens, while functional studies of WRKY, MYB, and NAC transcription factors revealed key resistance modules. Hormone-mediated signaling pathways, particularly those of salicylic acid, jasmonic acid, and abscisic acid, were shown to play central roles in host defense. Despite these advances, durable genetic resistance against bacterial pathogens and broad-spectrum defense against viruses remains limited. Novel technologies, including virus-free propagation, RNA interference, and spray-induced gene silencing, have shown promising outcomes. For insect pests, studies clarified the damage and virus-vectoring roles of aphids and thrips, and resistance traits linked to trichomes, terpenoids, and lignin have been identified. Biocontrol agents such as Trichoderma spp., Bacillus spp., predatory mites, and entomopathogenic fungi have also demonstrated efficacy. Future efforts should integrate molecular breeding, genome editing, RNA-based tools, and microbiome management to achieve sustainable chrysanthemum protection. Full article

Blue fescue (Festuca glauca) is a widely used ornamental grass worldwide. Drought is an important limiting factor for the growth and development of blue fescue; therefore, cultivating new strains of blue fescue with a strong drought tolerance is of great significance for its production practice. To investigate the drought tolerance mechanism of ds-1, this study subjected both ds-1 and “Festina” to a natural drought treatment and measured their physiological and biochemical indicators. A transcriptomic analysis was also conducted to explore the underlying molecular mechanisms. The results showed that, after the drought treatment, the relative water content (RWC), water use efficiency (WUE), and photosynthetic rate (Pn) of ds-1 leaves were significantly higher than those of “Festina”; in addition, the contents of H₂O₂ and O₂⁻, the relative electrical conductivity (REC), the malondialdehyde (MDA) content, the gas conductance (Gs), and the transpiration rate (Tr) were significantly lower than those of “Festina”. The peroxidase (POD) activity of ds-1 was significantly higher than that of “Festina”, while the superoxide dismutase (SOD) activity of ds-1 was significantly lower than that of “Festina”. The transcriptome data analysis showed that there were a total of 9475 differentially expressed genes (DEGs) between ds-1 and “Festina”. A Venn plot analysis showed 692 DEGs between ds-1—8d vs. “Festina”—8d and ds-1—16d vs. “Festina”—16d. A KEGG enrichment analysis showed that these 692 genes were mainly enriched in 86 pathways, including those related to the photosynthesis antenna protein, plant hormone signal transduction, MAPK signaling, starch and sucrose metabolism, and arginine and proline metabolism. Further screening identified genes that may be associated with drought stress, including PYL, PP2C, SnRK2, ABF, BRI1, JAZ, MYC2, Lhc, and MPK6. The qRT-PCR results indicated that the expression trends of the DEGs were consistent with the transcriptome sequencing results. Our research results can provide a basis for exploring candidate genes for drought tolerance in blue fescue. In addition, our research results provide valuable genetic resources for the development of drought-resistant ornamental grass varieties, which can help reduce water consumption in cities and decrease labor and capital investment. Full article

Background/Objectives: Transforming growth factor-beta (TGF-β) is a multifunctional cytokine involved in immune regulation, extracellular matrix turnover, and tissue repair. Its role in periodontitis remains controversial due to conflicting human studies. This systematic review addressed the PICO-based question: in adults with periodontitis (population), how does the expression and regulation of TGF-β isoforms (intervention/exposure) compare with healthy or post-treatment states (comparator) regarding clinical outcomes (outcomes)? Methods: A systematic search of PubMed and Scopus was conducted on 1 July 2025 for human studies published in English between 2010 and 2025. Eligible studies investigated TGF-β expression, function, or genetic regulation in periodontal tissues or biological fluids. Screening and quality appraisal were performed according to PRISMA guidelines, using design-specific risk-of-bias tools. The review protocol was prospectively registered in PROSPERO (CRD420251138456). Results: Fifteen studies met inclusion criteria. TGF-β1 was the most frequently analyzed isoform and was consistently elevated in diseased gingival tissue and gingival crevicular fluid, correlating with probing depth and attachment loss. Several studies reported post-treatment reductions in TGF-β, supporting its value as a dynamic biomarker. Additional findings linked TGF-β signaling to immune modulation, fibrosis, bone turnover, and systemic comorbidities. Evidence for TGF-β2 and TGF-β3 was limited but suggested isoform-specific roles in epithelial–mesenchymal signaling and scar-free repair. Conclusions: Current evidence supports TGF-β, particularly TGF-β1, as a central mediator of periodontal inflammation and repair, with promise as both a biomarker and therapeutic target. Standardized, isoform-specific, and longitudinal studies are needed to clarify its diagnostic and translational utility. Full article

Background/Objectives: Gastric cancer (GC) remains a leading cause of cancer mortality worldwide. While most cases are sporadic, approximately 10% show familial clustering with only a minority explained by known hereditary syndromes. The remaining, termed familial non-hereditary gastric cancer (FNHGC), lack a defined high-penetrance germline mutation. This review aims to summarize current knowledge regarding the diagnosis, risk factors, molecular characteristics and management of FNHGC. Methods: A comprehensive narrative review of the literature was conducted focusing on epidemiologic, molecular and clinical studies addressing families with multiple GC cases but no identified germline mutation. Results: The etiology of FNHGC is multifactorial, and H. pylori, with its related chronic gastritis, is probably the key driver. Familial clustering likely occurs when combined with other elements such as genetic polymorphisms, shared exposures to risk factors or even epigenetic phenomena. Molecular profiling reveals distinct patterns in familial tumors such as more frequent microsatellite instability; somatic CDH1 promoter hypermethylation; and recurrent somatic mutations in TP53, RHOA and DNA repair genes. Current management focuses on genetic testing to rule out hereditary syndromes, endoscopic surveillance and mitigation of risk factors, with eradication of H. pylori paramount. Conclusions: FNHGC represents a distinct subgroup of GC characterized by a multifactorial etiology related to exposure to risk factors and genetic susceptibility although significant gaps remain in fully explaining the condition. Ongoing research holds promise to provide tools for better detection and prevention in order to reduce the burden of GC in familial settings. Full article

Background: attention-deficit/hyperactivity disorder (ADHD) and Alzheimer’s disease (AD) are distinct neurological conditions that may share genetic and molecular underpinnings. ADHD, a neurodevelopmental disorder, affects approximately 5% of children and 3% of adults globally, while AD, a neurodegenerative disorder, is the leading cause of dementia in older adults. Emerging evidence suggests potential overlapping contributors, including pathways related to synaptic plasticity, neuroinflammation, and oxidative stress. Methods: this systematic review investigated potential genetic predispositions linking Attention-Deficit/Hyperactivity Disorder (ADHD) and Alzheimer’s Disease (AD). Following PRISMA guidelines, a search was conducted in Web of Science, Embase, PsycINFO, and PubMed using keywords related to ADHD, AD, and genetic factors. Studies included were original human studies utilizing genetic analyses and ADHD polygenic risk scores (PRS), with AD confirmed using established diagnostic criteria. Exclusion criteria comprised non-original studies, animal research, and articles not addressing genetic links between ADHD and AD. Screening was conducted with Rayyan software, assessing relevance based on titles, abstracts, and full texts. Results:. The search identified 1450 records, of which 1092 were screened after duplicates were removed. Following exclusions, two studies met inclusion criteria. One study analyzed ADHD-PRS in 212 cognitively unimpaired older adults using amyloid-beta (Aβ) PET imaging and tau biomarkers. The findings revealed that ADHD-PRS was associated with progressive cognitive decline, increased tau pathology, and frontoparietal atrophy in Aβ-positive individuals, suggesting that ADHD genetic liability may exacerbate AD pathology. Another study assessed ADHD-PRS in a cohort of 10,645 Swedish twins, examining its association with 16 somatic conditions. The results showed modest risk increases for cardiometabolic, autoimmune, and neurological conditions, with mediation effects through BMI, education, tobacco use, and alcohol misuse, but no direct link between ADHD-PRS and dementia. Discussion and conclusion: this review highlights preliminary but conflicting evidence for a genetic intersection between ADHD and AD. One study suggests that ADHD genetic liability may exacerbate AD-related pathology in Aβ-positive individuals, whereas another large registry-based study finds no direct link to dementia, with associations largely mediated by lifestyle factors. The potential ADHD–AD relationship is likely complex and context-dependent, influenced by biomarker status and environmental confounders. Longitudinal studies integrating genetics, biomarkers, and detailed lifestyle data are needed to clarify this relationship. Full article

TCP transcription factors represent a crucial family of plant regulators that contribute significantly to growth and developmental processes. Although the TCP gene family has been extensively studied in various plant species, research on Chimonanthus praecox (wintersweet) remains limited. Here, we performed genome-wide identification and analysis of the TCP gene family in C. praecox and identified 22 CpTCP genes. We further systematically examined the associated physicochemical properties, evolutionary relationships, gene structures, and regulatory features. Analysis revealed that all CpTCP proteins possess a conserved TCP domain, and subcellular localization prediction indicated their localization in the nucleus. Promoter analysis revealed that multiple cis-elements are associated with abiotic stress responses and plant growth regulation. Further analysis revealed high CpTCP2 expression in the leaves and stamen, with significantly increased levels during flower senescence. CpTCP2 expression was upregulated in response to methyl jasmonate (MeJA), salicylic acid, abscisic acid, and shade. CpTCP2 overexpression in Arabidopsis thaliana resulted in a reduced leaf area, delayed flowering, and increased rosette leaf numbers. Moreover, MeJA treatment accelerated leaf senescence in CpTCP2 transgenic Arabidopsis. These findings provide insights into the evolutionary characteristics of the TCP family in C. praecox, highlighting the functional role of CpTCP2 in regulating leaf development and flowering time in Arabidopsis, thereby offering valuable genetic resources for wintersweet molecular breeding. Full article

Antimicrobial resistance (AMR) is traditionally discussed in the context of horizontally acquired resistance genes and point mutations at target loci. However, this gene-centred model fails to account for a large number of clinically important modalities of resistance. There is now substantial evidence implicating bacteria in the ability to escape the effects of antibiotics in a variety of non-canonical ways, which are not considered in traditional diagnostic and surveillance pipelines. Among these factors, we can list those arising from global regulatory networks, phase variability, epigenetic tuning, small RNAs, genome structural variability, and phenotypic states like tolerance and persistence. This review will blend the current knowledge on these alternative pathways of resistance and underscore how they intersect with canonical genetic determinants. We will highlight cases where resistance emerges in the absence of known resistance genes, analyse the role of regulatory plasticity in efflux pump expression and membrane remodelling, and examine the contributions of bacterial stress responses and post-transcriptional control. Additionally, we will address methodological gaps in the detection of these mechanisms and their implications for clinical treatment failure, resistance surveillance, and drug development. By integrating insights from molecular microbiology, systems biology, and genomics, this review aims to offer a framework for understanding AMR as a multifaceted, context-dependent phenotype, not merely a genotype. We conclude by identifying knowledge gaps and suggesting priorities for research and diagnostic innovation in this evolving field. Full article

Neurodegeneration is intrinsically linked to aging through processes such as oxidative stress, mitochondrial dysfunction, and chronic inflammation. Nuclear factor erythroid 2-related factor 2 (Nrf2) emerges as a central transcription factor regulating these molecular events and promoting cytoprotective responses. In neurodegenerative diseases, notably, frontotemporal dementia (FTD) and Parkinson’s disease (PD), genetic mutations—including MAPT, LRRK2, PINK1, PRKN, and SNCA—have been reported to alter Nrf2 signaling, both in vitro and in vivo. Melatonin, a neurohormone widely known for its strong antioxidant and mitochondria-stabilizing properties, has been shown to activate Nrf2 and restore redox balance in several experimental models of neurodegeneration. Its effects include a reduction in tau hyperphosphorylation, α-synuclein aggregation, and neuroinflammation. While most data are derived from sporadic models of Alzheimer’s disease and PD, emerging evidence supports a role for melatonin in familial forms of FTD and PD as well. Thus, targeting Nrf2 through melatonin may offer a promising approach to mitigating neurodegeneration, especially in the context of mutation-driven pathologies. Further investigation is warranted to explore mutation-specific responses and optimize the therapeutic strategies. Full article

The rising prevalence of food allergies, particularly to peanuts and tree nuts, poses significant challenges for pediatric health worldwide. These allergens are among the leading causes of severe allergic reactions, including anaphylaxis, often manifesting in early life. This review synthesizes the current knowledge on the immune mechanisms underlying these allergies, emphasizing the interplay between genetic, immunologic, and environmental factors in shaping allergic sensitization. Advances in prevention strategies, including early allergen introduction, have been critically evaluated. Predictive and diagnostic methodologies, from traditional IgE evaluation to cutting-edge proteomics and metabolomics approaches, have been explored to identify biomarkers that predict allergy onset and severity. By unraveling early immunological and molecular signatures, this study aimed to summarize the early prediction, prevention, diagnosis, and treatment of peanut and tree nut allergies, ultimately contributing to more effective interventions and a better quality of life for affected children. Full article

Background: High-temperature stress is one of the major abiotic stresses limiting cotton production. Identifying genetic loci and genes for heat tolerance is crucial for breeding heat-tolerant varieties. Methods: Given the complexity of heat tolerance phenotypes in cotton, this study, which focused on resource materials, identified an A/C SNP mutation at position 5486185 on chromosome D06 within the heat tolerance interval through genome-wide association studies (GWAS) of natural Gossypium hirsutum populations. Results: A total of 308 resource materials were identified and evaluated for their heat tolerance phenotypes over two years of field research. Kompetitive allele-specific PCR (KASP) molecular markers were developed on the basis of the D06-5486185 SNP to characterize the heat tolerance phenotypes of these 308 resource materials. Genotyping for heat tolerance-related traits and agronomic traits was also performed. Materials with the C/C haplotype at position D06-5486185 presented increased heat tolerance (higher pollen viability (PV), leaf area (LA), chlorophyll (Chl) and number of bolls on the third fruit branch (FB3) and a lower number of dry buds (DBs) and drop rate (DR)) without negatively impacting key yield traits. This locus is located in the intergenic region of two adjacent bZIP transcription factor genes (GH_D06G0408 and GH_D06G0409). Expression analysis revealed that the expression levels of these two genes were significantly greater in heat-tolerant accessions (C/C type) than in sensitive accessions and that their expression levels were significantly correlated with multiple heat-tolerant phenotypes. Conclusions: In summary, this study developed a Kompetitive Allele Specific PCR (KASP) marker associated with heat tolerance in G. hirsutum and identified two key heat tolerance candidate genes. These results provide an efficient marker selection tool and important genetic resources for the molecular breeding of heat-tolerant G. hirsutum, laying an important foundation for further establishing a molecular marker-assisted breeding system for heat tolerance in G. hirsutum. Full article

Base editing represents a major breakthrough in the field of genome editing in recent years. By fusing deaminases with the CRISPR/Cas system, it enables precise single-base modifications of DNA. This review systematically summarizes the development of base editing technologies, including cytosine base editors (CBEs), adenine base editors (ABEs), and glycosylase base editors (GBEs), with a particular focus on their applications in crop improvement as well as future trends and prospects. We highlight advances in the creation of novel germplasm with enhanced stress resistance and desirable agronomic traits through base editing in rice, wheat, maize, potato, and other crops, particularly for improving herbicide resistance, disease resistance, and grain quality. Furthermore, we analyze factors that influence base editing efficiency, noting that challenges remain, such as PAM sequence constraints, limited base conversion types, off-target effects, narrow editing windows, and efficiency variation. Future efforts should aim to optimize deaminase activity, expand PAM compatibility, and develop versatile tools to facilitate the broad application of base editing in molecular breeding. This review provides a timely reference for researchers and breeders, offering theoretical guidance and practical insights into harnessing base editing for crop genetic improvement. Full article

Lycoris longituba produces a single flower bearing six tepals. The double-petaled phenotype of L. longituba has gained significant interest in China due to its ornamental and commercial value in tourism industries. This double-petal phenotype, characterized by stamen petalization, shows improved esthetic characteristics compared with conventional single-petal form. However, the molecular mechanisms underlying this floral trait remain largely undefined. In this study, RNA-based comparative transcriptomic analysis was performed between single- and double-petaled flowers of L. longituba at the fully opened flower stage. Approximately 13,848 differentially expressed genes (DEGs) were identified (6528 upregulated and 7320 downregulated genes). Functional annotation through Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses revealed several DEGs potentially involved in double-petal development. Six candidate genes, including the hub genes LlbHLH49, LlNAC1, LlSEP, LlTIFY, and LlAGL11, were identified based on DEG functional annotation and weighted gene co-expression network analysis (WGCNA). Transcription factors responsive to phytohormonal signaling were found to play a pivotal role in modulating double-petal development. Specifically, 123 DEGs were involved in phytohormone biosynthesis and signal transduction pathways, including those associated with auxin, cytokinin, gibberellin, ethylene, brassinosteroid, and jasmonic acid. Moreover, 521 transcription factors (TFs) were identified, including members of the MYB, WRKY, AP2/ERF, and MADS-box families. These results improve the current understanding of the genetic regulation of the double tepal trait in L. longituba and offer a base for future molecular breeding strategies to enhance ornamental characteristics. Full article