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PubMed2026

A CqbZIP55-CqPIF3 regulatory module associated with light-responsive flavonoid biosynthesis during quinoa seedling de-etiolation.

Quinoa (Chenopodium quinoa) is an emerging leafy vegetable and microgreen crop rich in health-promoting flavonoids, yet the regulatory mechanisms linking light perception to early metabolic adaptation remain unclear. Here, we integrated phenotypic, transcriptomic, metabolomic, and molecular analyses to investigate early de-etiolation responses in quinoa seedlings. Short-term light exposure rapidly promoted seedling establishment and induced transcriptional programs associated with photosynthesis, carbon metabolism, hormone signaling, and flavonoid biosynthetic gene expression, whereas metabolite changes were more limited, indicating temporal uncoupling between transcriptional activation and metabolic accumulation. Genome-wide bZIP analysis identified CqbZIP55 as a light-responsive regulator that directly binds and activates the CqCHS promoter. CqPIF3 also bound the CqCHS promoter and showed stronger transactivation activity than CqbZIP55 in transient reporter assays. Protein interaction and dual-luciferase assays showed that CqbZIP55 physically interacts with CqPIF3 and modulates CqPIF3-associated promoter activity. Exogenous quercetin upregulated CqbZIP55 and prolonged CqCHS expression, suggesting a candidate metabolite-associated reinforcement mechanism. Together, these findings support functional interplay between CqbZIP55 and CqPIF3 in light-responsive regulation of flavonoid biosynthetic gene expression in quinoa seedlings, while further quinoa-based perturbation and in vivo promoter-occupancy assays are required to establish their physiological role in planta. This study provides a framework for further investigation of photoprotective metabolic regulation in quinoa.

Chenopodium quinoa↗

PubMed2025

How to analyze and understand the human immune system.

To enhance our understanding of the pathogenesis of diseases, including rheumatic diseases, and to improve disease control, it is essential to attain a thorough understanding of the human immune system, alongside mouse immunology. Historically, the investigation of the human immune system has posed significant challenges due to methodological limitations. Nonetheless, recent advancements in genomic studies of multifactorial diseases have elucidated that numerous risk-associated genetic variants affecting quantitative differences in cell-specific gene expression. In light of these findings, we are currently examining individual genetic variations in both healthy individuals and patients, as well as categorizing cells into distinct subsets in order to construct a comprehensive dataset concerning the human immune system. This is accomplished by combining data on gene expression, factors influencing the expression mechanisms, protein expression, metabolomics, and environmental variables pertinent to immune functionality-such as gut microbiota. These datasets will facilitate the comprehensive characterization of the human immune system. Using these datasets and through the integrative analyses of data related to risk genetic variations and gene expression profiles of each disease and individual, we anticipate uncovering novel insights into the human immune system, the heterogeneity of diseases, immune function mechanisms, and their regulatory strategies that may not be achievable through murine models.

Humans↗

PubMed2026

A stem-like chromatin program in small-cell lung cancer is associated with poor outcomes after chemoimmunotherapy.

Small-cell lung cancer (SCLC) is an aggressive malignancy with substantial tumor heterogeneity and limited clinically actionable biomarkers beyond established features such as liver metastases. We profile tumor-intrinsic chromatin accessibility in a patient-derived xenograft biobank and identify three recurrent chromatin programs: neuroendocrine, marked by ASCL1/NEUROD1 activity; immunogenic, marked by IRF-associated activity; and stem-like, marked by TEAD/OCT activity. These programs are reproduced at the cohort level across bulk and single-cell transcriptomic datasets comprising more than 800 tumors, including 300 extensive-stage samples. In patients treated with chemoimmunotherapy, the stem-like program is associated with inferior survival, including a median overall survival of 7.41 months versus 15.9 and 12.6 months for immunogenic and neuroendocrine groups, respectively. This association remains significant after adjustment for liver metastases, brain metastases, and elevated lactate dehydrogenase. These findings support a high-risk stem-like SCLC chromatin program for prospective biomarker refinement and therapeutic investigation.

ATAC-seq↗

PubMed2024

Genetics of Latin American Diversity Project: Insights into population genetics and association studies in admixed groups in the Americas.

Latin Americans are underrepresented in genetic studies, increasing disparities in personalized genomic medicine. Despite available genetic data from thousands of Latin Americans, accessing and navigating the bureaucratic hurdles for consent or access remains challenging. To address this, we introduce the Genetics of Latin American Diversity (GLAD) Project, compiling genome-wide information from 53,738 Latin Americans across 39 studies representing 46 geographical regions. Through GLAD, we identified heterogeneous ancestry composition and recent gene flow across the Americas. Additionally, we developed GLAD-match, a simulated annealing-based algorithm, to match the genetic background of external samples to our database, sharing summary statistics (i.e., allele and haplotype frequencies) without transferring individual-level genotypes. Finally, we demonstrate the potential of GLAD as a critical resource for evaluating statistical genetic software in the presence of admixture. By providing this resource, we promote genomic research in Latin Americans and contribute to the promises of personalized medicine to more people.

Humans↗

PubMed2025

Admixture-mapping analysis reveals genetic determinants of the human plasma proteome.

Protein profiling and genetic findings can be integrated to define the genetic architecture of the circulating proteome in chronic diseases. Most self-identified African American (AA) individuals have both African and European genetic ancestry. Admixture mapping can detect genomic association regions in which causal variants exist with substantial differences in allele frequency or effect sizes between genetic ancestries. We performed admixture mapping of the circulating proteome in 1,989 participants from the Jackson Heart Study (JHS), investigating the relation of local African ancestry within genomic regions with levels of circulating proteins. We conditioned protein-local ancestry association models on variants previously found to be associated with those proteins in genome-wide association studies (GWASs). We replicated findings in 196 AA participants from the Multi-Ethnic Study of Atherosclerosis (MESA). 62 proteins were associated with local African ancestry. 21 of 62 remained statistically significant after conditioning on protein-associated variants observed in previous GWASs. 48 of 54 available protein-local ancestry associations were replicated in the MESA. Proteins associated with local African ancestry included chemokines, factors associated with vascular biology and inflammation, and other biologically interesting proteins. Admixture associations unexplained by previously reported protein-associated variants in conditional analysis suggest the existence of causal variants missed by standard GWAS techniques.

Aged↗

PubMed2026

Integrated transcriptomic and metabolomic analyses reveal key regulators associated with lipid metabolic differences between subcutaneous and visceral adipose tissues in sheep.

The location of fat deposition has a significant impact on meat quality and body health, and different adipose tissues exhibit significant differences in lipid metabolism and immune regulation. This study aimed to systematically compare the phenotypic characteristics, transcriptome, and metabolome of subcutaneous adipose tissue (SAT) and two types of visceral adipose tissue (VAT) in sheep, in order to reveal the metabolic differences between SAT and VAT and their potential regulatory mechanisms. The results showed that compared with VAT, SAT had stronger triglyceride deposition ability and obvious cellular hypertrophy. Through integrative analysis, 15 key lipid metabolism genes and 12 differential metabolites were identified. Among them, ACACA, FASN, ELOVL6, SCD, as well as metabolites palmitic acid and glycerol-3-phosphate, may play a central role in SAT lipid synthesis and storage; whereas IGFBP2, ADRB3, LTA4H, and metabolites arachidonic acid and leukotriene B4 may be involved in the lipolysis regulation and inflammatory response of VAT. These findings may provide deeper insights into the regulatory mechanisms of fat deposition in sheep.

Animals↗

PubMed2026

Mechanistic analysis of rice caryopsis morphogenesis regulated by exogenous hormones and related precursor substances under blue light conditions.

Rice caryopsis morphogenesis is regulated by light signals and hormonal networks. However, the mechanism by which exogenous hormones and related precursor substances modulate rice caryopsis morphogenesis under blue light remains elusive. In the present study, we aimed to elucidate the molecular mechanisms underlying the regulatory effects of exogenous phytohormones and related precursor substances on caryopsis development at 10 days after pollination (10 DAP) in the japonica rice cultivar 'Chujing 27' under blue light conditions. Results showed that tryptamine treatment increased caryopsis cell volume, thereby significantly driving caryopsis expansion; meanwhile, it markedly enhanced the activities of TDC and TAA, the key rate-limiting enzymes mediating the conversion of tryptophan to auxin, leading to a significant elevation in endogenous auxin content (P < 0.05). In comparison, exogenous auxin treatment significantly boosted carbohydrate accumulation and the activities of associated metabolic enzymes (P < 0.05). Integrated transcriptomic and metabolomic analyses revealed that tryptamine treatment led to significant enrichment of the starch and sucrose metabolic pathway, and drove the coordinated enhancement of carbon metabolic flux and auxin biosynthesis by upregulating key auxin biosynthetic genes (e.g., TAA1) and repressing auxin oxidative degradation. Genes Os04g0531100, Os03g0266100 and Os11g0221200 identified by weighted gene co-expression network analysis (WGCNA) may serve as important candidate targets regulating rice caryopsis morphology and physiological traits under blue light conditions. This study first uncovers the critical function of the "tryptamine-auxin axis" in regulating rice caryopsis development under blue light, laying a theoretical foundation for regulating caryopsis morphogenesis via exogenous hormones and their precursors.

Oryza↗

PubMed2024

Whole-genome sequencing in 333,100 individuals reveals rare non-coding single variant and aggregate associations with height.

The role of rare non-coding variation in complex human phenotypes is still largely unknown. To elucidate the impact of rare variants in regulatory elements, we performed a whole-genome sequencing association analysis for height using 333,100 individuals from three datasets: UK Biobank (N = 200,003), TOPMed (N = 87,652) and All of Us (N = 45,445). We performed rare ( < 0.1% minor-allele-frequency) single-variant and aggregate testing of non-coding variants in regulatory regions based on proximal-regulatory, intergenic-regulatory and deep-intronic annotation. We observed 29 independent variants associated with height at P < after conditioning on previously reported variants, with effect sizes ranging from -7cm to +4.7 cm. We also identified and replicated non-coding aggregate-based associations proximal to HMGA1 containing variants associated with a 5 cm taller height and of highly-conserved variants in MIR497HG on chromosome 17. We have developed an approach for identifying non-coding rare variants in regulatory regions with large effects from whole-genome sequencing data associated with complex traits.

Humans↗

PubMed2024

Rare variant contribution to the heritability of coronary artery disease.

Whole genome sequences (WGS) enable discovery of rare variants which may contribute to missing heritability of coronary artery disease (CAD). To measure their contribution, we apply the GREML-LDMS-I approach to WGS of 4949 cases and 17,494 controls of European ancestry from the NHLBI TOPMed program. We estimate CAD heritability at 34.3% assuming a prevalence of 8.2%. Ultra-rare (minor allele frequency ≤ 0.1%) variants with low linkage disequilibrium (LD) score contribute ~50% of the heritability. We also investigate CAD heritability enrichment using a diverse set of functional annotations: i) constraint; ii) predicted protein-altering impact; iii) cis-regulatory elements from a cell-specific chromatin atlas of the human coronary; and iv) annotation principal components representing a wide range of functional processes. We observe marked enrichment of CAD heritability for most functional annotations. These results reveal the predominant role of ultra-rare variants in low LD on the heritability of CAD. Moreover, they highlight several functional processes including cell type-specific regulatory mechanisms as key drivers of CAD genetic risk.

Humans↗

PubMed2026

In silico analysis of SH3BP2 genomic alterations and expression profiles in CRC.

AIM: Colorectal cancer (CRC) is a widespread health issue that attains high mortality. The adaptor protein SH3BP2 amplification results in metabolic changes, oxidative stress, NK cell activity, and inflammation. The NK cells are capable of destroying tumor cells without prior activation, help prevent metastasis, and have prognostic value. Targeting SH3BP2 to regulate NK cell activity in the TME could enhance CRC-based immunotherapy. MATERIALS AND METHODS: The cancer hallmark tool helps in understanding SH3BP2 hallmark annotation. Utilizing the STRING tool and the KEGG pathway, protein functional enrichment and PPI networking were analyzed. TIMER 2.0 was used for immune cell infiltration correlation analysis, and UALCAN was used for CPTAC-based protein expression profiling. RESULTS AND CONCLUSIONS: The GEO (GSE9348) dataset showed SH3BP2 is upregulated in CRC (log2 fold change = 1.18). GEO, TCGA, and cBioPortal revealed SH3BP2 alterations in CRC cases, potentially aiding immune evasion. Mutations in SH3BP2 influence cancer growth, suppressing tumors or promoting them by activating NF-κB and affecting immune responses through WNT/β-catenin, PI3K, MAPK, and JAK-STAT pathways. Overall, SH3BP2 plays a key role in cancer growth and immune regulation, making it a promising target for CRC therapy. Further experimental validation is needed to demonstrate its diagnostic and therapeutic potency.

Humans↗

PubMed2024

Stroke genetics and how it Informs novel drug discovery.

INTRODUCTION: Stroke is one of the main causes of death and disability worldwide. Nevertheless, despite the global burden of this disease, our understanding is limited and there is still a lack of highly efficient etiopathology-based treatment. It is partly due to the complexity and heterogenicity of the disease. It is estimated that around one-third of ischemic stroke is heritable, emphasizing the importance of genetic factors identification and targeting for therapeutic purposes. AREAS COVERED: In this review, the authors provide an overview of the current knowledge of stroke genetics and its value in diagnostics, personalized treatment, and prognostication. EXPERT OPINION: As the scale of genetic testing increases and the cost decreases, integration of genetic data into clinical practice is inevitable, enabling assessing individual risk, providing personalized prognostic models and identifying new therapeutic targets and biomarkers. Although expanding stroke genetics data provides different diagnostics and treatment perspectives, there are some limitations and challenges to face. One of them is the threat of health disparities as non-European populations are underrepresented in genetic datasets. Finally, a deeper understanding of underlying mechanisms of potential targets is still lacking, delaying the application of novel therapies into routine clinical practice.

Humans↗

PubMed2026

Changes of DNA methylation and gene expression profile in placental villi and chorioamniotic membranes under preeclampsia.

BACKGROUND: Preeclampsia (PE) is a serious pregnancy complication with elusive pathogenesis. Although epigenetic dysregulation is implicated, its layer-specific placental roles are poorly defined. This study aimed to identify shared and layer-specific epigenetic alterations in PE by profiling DNA methylation and gene expression in placental villi (PV) and chorioamniotic membranes (CAM). RESEARCH DESIGN AND METHODS: PV and CAM samples were collected from 7 normal and 8 PE pregnancies, and three public DNA methylation datasets (GSE98224, GSE44667, GSE75196) were integrated. Differentially methylated genes (DMGs) and differentially expressed genes (DEGs) were identified based on whole-genome methylation and transcriptome sequencing. Layer-specific and shared gene sets were identified by cross-analysis, with functional annotation using Gene Ontology (GO). RESULTS: EM-seq revealed a hypermethylation-dominant, tissue-specific methylation landscape in PE placentas. Cross-tissue comparison identified shared DMGs between the two layers, including nine key genes consistently altered in public datasets. Integrated analysis in PV further identified 22 co-dysregulated genes, enriched in thermoregulation, maternal-fetal immunity, signal transduction, and cell differentiation. CONCLUSIONS: This study elucidates the shared and layer-specific dysregulation of gene networks at methylomic and transcriptomic levels in PE placenta. Comparing PV and CAM highlights placental epigenetic heterogeneity and dysfunction, offering novel clues for mechanistic research and layer-targeted therapies.

Humans↗

PubMed2025

Study research protocol for Phenome India-CSIR Health Cohort Knowledgebase: A prospective multi-modal follow-up study on a nationwide employee cohort.

Predicting individual health trajectories based on risk scores can help formulate effective preventive strategies for diseases and their complications. Currently, most risk prediction algorithms rely on epidemiological data from the Caucasian population, which often do not translate well to the Indian population due to ethnic diversity, differing dietary and lifestyle habits, and unique risk profiles. In this multi-center prospective longitudinal study conducted across India, we aim to address these challenges by developing clinically relevant risk prediction scores for cardio-metabolic diseases specifically tailored to the Indian population. India, which accounts for nearly 18% of the global population, also has a significant diaspora worldwide. This program targets longitudinal collection and bio-banking of samples from over 10 000 employees both working and retirees of the Council of Scientific and Industrial Research and their spouses, with baseline sample collection already completed. During the baseline collection, we gathered multi-parametric data including clinical questionnaires, lifestyle and dietary habits, anthropometric parameters, lung function assessments, liver elastography by Fibroscan, electrocardiogram readings, biochemical data, and molecular assays, including but not limited to genomics, plasma proteomics, metabolomics, and fecal microbiome analysis. In addition to exploring associations between these parameters and their cardio-metabolic outcomes, we plan to employ artificial intelligence algorithms to develop predictive models for phenotypic conditions. This study could pave the way for precision medicine tailored to the Indian population, particularly for the middle-income strata, and help refine the normative values for health and disease indicators in India.

cardio-metabolic↗

PubMed2026

De novo chromatin remodelling variants in sporadic Chiari 1 malformation.

Chiari 1 malformation (CM1) is the most common congenital malformation of the human hindbrain. Although prior studies have implicated chromatin-remodeling genes in CM1, the de novo genetic architecture and underlying neurodevelopmental mechanisms remain incompletely defined. To investigate the molecular genetics of a novel familial form of CM1 linked with syringomyelia and tethered cord and determine whether rare, damaging de novo variants (DNVs) contribute to sporadic CM1 risk with gene- and pathway-level resolution, we performed whole-exome sequencing in an ultra-rare multigenerational family with CM1 and associated spinal pathology, and in the largest assembled trio-based cohort to date, comprising 1,585 proband-parent trios with sporadic, idiopathic CM1 (2017-2025). The comparison cohort included 1,798 unaffected control siblings. Clinical phenotyping was by systematic medical record review. Structural domain mapping, in silico modeling, and integration with single-cell transcriptomic data from developing human cerebellum was conducted to assess biological plausibility. A heterozygous loss-of-function variant in CHD3 segregated with CM1 and syringomyelia in a multigenerational family. In the trio-based cohort, rare protein-altering DNVs were significantly enriched across multiple chromodomain helicase DNA-binding (CHD) genes, including CHD1, CHD3, CHD4, and CHD8, exceeding gene-specific mutation expectations (protein-damaging variants: P = 1.3 × 10-9; predicted loss-of-function variants: P = 8.6 × 10-5). CHD1 contained two pathogenic DNVs (p.A999D and p.E984K). CHD4 (p.D744N, p.T1813P, and p.I1102T) and CHD8 (p.R1402X, p.R1472X, and p.R2035X) each contained three new DNVs. Variants clustered within conserved ATPase, helicase, and chromodomain regions essential for chromatin remodeling, and these patients frequently had comorbid developmental delay and related neurodevelopmental features. Single-cell transcriptomic analyses demonstrated enrichment in Purkinje cells and inhibitory neurons of midgestational cerebellum, where CHD gene products form a coherent chromatin-regulatory network. Rare, large-effect DNVs that disrupt chromatin-remodeling programs contribute to sporadic CM1, implicating genetically encoded dysregulation of cerebellar development as a central disease mechanism. Exome sequencing may complement surgical evaluation of children with sporadic CM1, particularly when accompanied by neurodevelopmental concerns, informing prognosis and family counseling.

de novo variants↗

PubMed2025

Quorum sensing in Saccharomyces cerevisiae brewing strains: effects of 2-phenylethanol on proteomic, lipidomic, and metabolomic profile.

Quorum sensing (QS) is a known mechanism by which microbial populations adjust gene expression and coordinate community-wide social behaviors based on the proximate population density. This regulatory system has garnered significant interest in both scientific research and the food industry. However, a central question remains whether industrial strains of Saccharomyces cerevisiae, the yeast species predominantly utilized in brewing, employ quorum signalling mechanisms similar to those observed in laboratory strains and other fungi. Despite the potential relevance of microbial social behavior regulators to brewing practices, studies examining QS in Saccharomyces spp. are limited. In this investigation, three industrial brewing strains of S. cerevisiae were cultivated on SLAD (nitrogen-restrictive) and SHAD (nitrogen-sufficient) agar media supplemented with 200 μM of the aromatic alcohol 2-phenylethanol (2-PE) over 72 h at 24°C. Subsequent analyses of the harvested biomass included proteomic, lipidomic, and metabolomic assessments. Results indicated that two of the industrial strains showed minimal differences in their profiles upon exposure to 2-PE, while the third strain exhibited significant differences. These findings imply that the impact of the QS molecule 2-PE on the proteome, lipidome, and metabolome of industrial S. cerevisiae may be strain-specific rather than universally applicable to the species.

Quorum Sensing↗

PubMed2025

Integrative Genomic, Transcriptomic and Epigenomic Analysis Reveals cis-regulatory Contributions to High-altitude Adaptation in Tibetan Pigs.

The Qinghai-Tibet Plateau, characterized by its extreme environmental conditions, presents significant challenges to life, making it an ideal region for studying adaptation and evolution. Tibetan pigs, known for their high genetic diversity and exceptional adaptability to high altitudes, serve as excellent models for investigating high-altitude adaptation. While previous studies have extensively identified genetic determinants associated with high-altitude adaptation, the molecular mechanisms, particularly cis-regulatory patterns, remain poorly understood. Here, we conducted a selective sweep analysis using 484 genomes from Chinese and Western pig breeds across various altitudes, revealing 38.56 Mb of genomic regions under selection in Tibetan pigs. Enrichment analysis identified the lung as the primary functional tissue involved in high-altitude adaptation, supported by tissue-specific transcriptional and regulatory patterns observed between Tibetan and Meishan pigs (low altitude). By integrating genomic, RNA-seq, ATAC-seq, and H3K27ac HiChIP data, we constructed comprehensive enhancer-promoter regulatory maps of candidate genes and pinpointed promising genetic determinants associated with high-altitude adaptation, including SNPs in EPAS1, KLF13, SPRED1, and CFD. These loci were predicted to influence chromatin accessibility and the interactions of regulatory elements, with altered binding strength of relevant transcription factors. Further in vitro experiments confirmed that these loci function as allele-specific enhancers, modulating the expression of target genes. Our findings elucidate the regulatory basis of high-altitude adaptation in Tibetan pigs and provide valuable insights for exploring hypoxia-related diseases in livestock and humans.

Animals↗

PubMed2026

Perineuronal net degradation in aggressive glioblastomas with KANK1::NTRK2 fusions.

BACKGROUND: Approximately 10% of glioblastomas harbor targetable genomic fusions. NTRK2 participates in a variety of fusion events that drive tumorigenesis. Two previous reports have described KANK1::NTRK2 fusions in adult glioblastoma patients with poor survival. METHODS: We performed a retrospective analysis of glioblastoma patients treated at Dartmouth-Hitchcock Medical Center (DHMC) from 2020 to 2025 to identify cases harboring KANK1::NTRK2 fusions. Clinical presentation, treatment, histopathologic features, and outcomes were reviewed. In addition, we conducted GeoMx whole-transcriptome and high-plex proteomic digital spatial profiling of a KANK1::NTRK2-positive glioblastoma and a comparator tumor from a long-term survivor. Candidate biomarkers were orthogonally validated using immunohistochemistry and/or immunofluorescence. RESULTS: Two patients with KANK1::NTRK2 fusion glioblastoma were identified, both demonstrating rapid progression, therapeutic resistance, and survival of less than 7 months. Proteomic profiling showed increased expression and activation of canonical NTRK2 downstream signaling pathways, particularly MEK1/2 and ERK1/2. This was accompanied by upregulation of extracellular matrix remodeling enzymes, including MMP3, MMP14, and ADAM15, along with reduced expression of extracellular matrix-associated transcripts and perineuronal net components in particular compared to a non-fusion glioblastoma. CONCLUSIONS: These limited, hypothesis-generating findings suggest constitutive NTRK2 signaling may promote coordinated extracellular matrix degradation and remodeling, potentially facilitating rapid and aggressive tumor growth and invasion in a subset of glioblastomas.

NTRK gene fusion↗

PubMed2026

Sympatric European white oaks species display contrasting epigenetic response to soil water availability.

In the context of climate change plants have to cope with adverse conditions, among which water scarcity is a major threat for their survival. They have developed diverse regulatory processes to face drought that may differ depending on their ecological niche. The two sympatric oaks species (Quercus robur L. and Quercus petraea (Matt.). Liebl) have different levels of drought tolerance. We have investigated their strategies to face drought stress by analysing the transcriptome, small RNAome and methylome dynamics of young plants grown under control and drought stress conditions. Data indicate that cell wall remodeling is most likely involved in the better tolerance Q. petraea than of Q. robur. Furthermore, major methylation differences were identified between both oak species that were in part associated to their difference in drought stress responses. Integration of the three datasets revealed genomic co-locations of potential importance for forest tree adaptation to drought stress. Our data are consistent with species-specific molecular responses of oak to drought stress related to their ecological niches.

Forest trees- Omics- ecological niche↗