'; ?> geneimprint : Hot off the Press http://www.geneimprint.com/site/hot-off-the-press Daily listing of the most recent articles in epigenetics and imprinting, collected from the PubMed database. en-us Sat, 10 Jan 2026 01:53:01 EST Sat, 10 Jan 2026 01:53:01 EST jirtle@radonc.duke.edu james001@jirtle.com A latent activated olfactory stem cell state revealed by single-cell transcriptomic and epigenomic profiling. Van den Berge K, Bakalar D, Chou HJ, Kunda D, Risso D, Street K, Purdom E, Dudoit S, Ngai J, Heavner W
Stem Cell Reports (Jan 2026)

The olfactory epithelium is one of the few regions of the nervous system that sustains neurogenesis throughout life. Its experimental accessibility makes it especially tractable for studying molecular mechanisms that drive neural regeneration in response to injury. In this study, we used single-cell sequencing to identify transcriptional and epigenetic processes involved in determining olfactory epithelial stem cell fate during injury-induced regeneration. By combining gene expression and accessible chromatin profiles of individual lineage-traced olfactory stem cells, we identified transcriptional heterogeneity among activated stem cells at a stage when cell fates are being specified. We further identified a subset of resting cells that appears poised for activation, characterized by accessible chromatin around silent genes prior to their expression in response to injury. These results provide evidence for a latent activated stem cell state in which a subset of quiescent olfactory epithelial stem cells are epigenetically primed to support injury-induced regeneration.]]> Wed, 31 Dec 1969 19:00:00 EST Cross-species prediction of histone modifications in plants via deep learning. Lv T, Han Q, Li Y, Liang C, Ruan Z, Chao H, Chen M, Chen D
Genome Biol (Jan 2026)

The regulation of gene expression in plants is governed by complex interactions between cis-regulatory elements and epigenetic modifications such as histone marks. While deep learning models have achieved success in predicting regulatory features from DNA sequence, their cross-species generalizability in plants remains largely unexplored.]]> Wed, 31 Dec 1969 19:00:00 EST CRISPR 2.0: Expanding the genome engineering Toolbox for epigenetics, RNA editing, and molecular diagnostics. Pradhan K, Anoop S
Gene (Feb 2026)

Non-canonical CRISPR systems adaptation has led to genome editing through nucleases, and the development of transcriptional and epigenetic regulation, transcriptome editing, and molecular diagnostics has resulted in a diversified set of tools-CRISPR 2.0. In this review, the author summarizes the mechanisms and recent engineering advances of (i) dCas9-based epigenetic effectors, (ii) RNA-targeting Cas13 systems and engineered RNA editors, (iii) DNA base editors and prime editors, and (iv) CRISPR-powered diagnostic platforms and their translational readiness. There is a critical comparison of the various approaches (e.g., RNAi/ASO versus Cas13-based methods; base editing versus prime editing) along with practical translational considerations such as delivery technologies, safety (off-target/edit windows, mosaicism), and regulatory pathways which are evaluated. Three concise case studies refer to map laboratory evidence to clinical or near-clinical outcomes and the ethical and governance discussion is widened to include global access, intellectual property and equity in deployment. Finally, the authors classify technologies according to their level of readiness - diagnostics and some ex-vivo therapeutic approaches are already in or very close to clinical use, chosen in-vivo editing methods are undergoing early trials, and AI-assisted nuclease design is still mostly theoretical but is getting better fast. This comprehensive viewpoint is intended to help researchers and physicians understand which CRISPR tools are most likely to be translated soon and where more validation is required.]]> Wed, 31 Dec 1969 19:00:00 EST Deciphering Sjögren's disease: New insights and perspectives extend from advanced omics approaches and immunology. Chen H, Kaneko N, Ohyama Y, Moriyama M
J Autoimmun (Jan 2026)

Sjögren's disease (SjD), formerly termed Sjögren's syndrome, is a chronic autoimmune exocrinopathy that has seen substantial advances in basic research over the past decade. Classical experimental approaches have revealed immune dysregulation encompassing aberrant activation of the adaptive immune system, activation of humoral autoimmunity against autoantigens, and upstream participation of innate immune mechanisms. In parallel, with the rapid development of sequencing and omics technologies, researchers are able to use these high-throughput methods to gain a more unbiased, sytem-wide view of disease processes and pathegenesis in SjD. Among them, numerous disease-associated traits have been revealed by genomics and epigenomics, while transcriptomics, proteomics, and immunogenomics have also depicted a more detailed landscape of phenotypes and cell states of immune cells, as well as the roles of key molecules such as Toll-like receptors (TLRs) in promoting autoimmune responses, yielding profound insights for the understanding of SjD. Meanwhile, these diverse data analysis methods offer the researchers impotant tools to further invertigate and understand SjD in the future. The convergence of these modalities supports data-driven disease prediction, refined patient stratification, and identification of therapeutic targets, thereby expanding translational opportunities. Collectively, integrating innovative omics with classical methodologies provides a coherent framework for capturing the pathogenesis of SjD, linking system-wide views to experimental validation, and accelerating the path from pathobiology to precision therapeutics. This review summarizes recent advances in the understanding of the pathogenesis of SjD, lymphomagenesis in SjD, patient stratification and promising targeted therapy, and also outlines future perspectives and challenges to be addressed.]]> Wed, 31 Dec 1969 19:00:00 EST A smoothing method for DNA methylome analysis to enhance epigenomic signature detection in epigenome-wide association studies. Oussalah A, Mousel L, Trégouët DA, Guéant JL
Methods (Feb 2026)

Epigenome-wide association studies (EWAS) are instrumental for mapping DNA methylation changes in human traits and diseases but often suffer from low statistical power and false positives, especially in small cohorts. We developed an EWAS smoothing method that exploits co-methylation of adjacent CpG probes within CpG islands via a sliding-window average and generalized it using Savitzky-Golay filtering. We applied the smoothing approach-with window widths of 1-3 CpGs and, for generalization, Savitzky-Golay filters of varying polynomial orders and window sizes-across five distinct EWAS settings. Performance was quantified by signal-to-noise ratio (SNR), noise-variance reduction, variance ratio (VR), Bayes factors, and sample-size sensitivity. In the MMACHC epimutation dataset, a 5-CpG window (width, w = 2) increased SNR by 90 %, reduced noise variance by 80 %, and elevated VR by 176 % at the target CpG island, with no genome-wide false positives. For MLH1, smoothing preserved the top association and suppressed background signals. In the aging EWAS, a "Polyepigenetic CpG aging score" was derived following smoothing. This score correlated strongly with chronological age in the discovery cohort (Spearman's ρ = 0.89; P = 3.0 × 10) and was independently validated in a separate dataset, significantly distinguishing newborns from nonagenarians (P = 3.4 × 10). Savitzky-Golay filtering of order 0 with a 5-CpG window yielded optimal SNR across bootstrap iterations, supporting this configuration as a robust choice for methylation array smoothing. As an extension of the Savitzky-Golay-based smoothing framework, reanalysis of a liver cancer dataset identified five top loci surpassing a smoothed P-value threshold of 1 × 10. Among these, MIR10A within the HOXB3 locus was the only previously reported functionally relevant site. In conclusion, the smoothing method improves EWAS performance by enhancing SNR, enabling detection of meaningful associations even in small cohorts, and offers a valuable tool for reanalyzing existing Infinium methylation array datasets to uncover previously undetected epigenomic signatures.]]> Wed, 31 Dec 1969 19:00:00 EST Bioinformatics insights into plant genomic imprinting: approaches, challenges, and future perspectives. Jing X, Su X, Zou Q, Niu M
Brief Funct Genomics (Jan 2026)

Genomic imprinting is an epigenetic occurrence that results in the expression of alleles specific to the parent of origin, plays pivotal roles in plant development, stress adaptation, and agronomic trait regulation. While imprinting has been intensively investigated in model plants (e.g. Arabidopsis, maize, and rice), its dynamic regulatory mechanisms and evolutionary implications remain enigmatic. Recent advances in bioinformatics-including single-cell omics, machine learning, and deep learning-have revolutionized the identification, functional annotation, and network modeling of imprinted genes. This review not only provides a detailed summary of the identification, functions and regulatory mechanisms of plant imprinted genes, but also systematically summarizes methodologies for studying plant genomic imprinting, highlights challenges in multi-omics data integration, and envisions artificial intelligence-driven strategies for epigenetic breeding.]]> Wed, 31 Dec 1969 19:00:00 EST TALE Homeodomain Proteins in Plant Reproductive Development and Environmental Stress Resilience. Niu X, Jiang X, Li H, Qin R, Qin Y
Plant Cell Environ (Feb 2026)

TALE (Three Amino acid Loop Extension) homeodomain transcription factors are key conserved elements in eukaryotic developmental patterning. In plants, this superclass divides into the KNOX and BELL families, which are essential for regulating meristem maintenance, organogenesis, and tissue identity. Recent advances show that TALE proteins are intricately involved in plant reproductive processes, including gametophyte differentiation, embryonic axis formation, and floral organogenesis. They function as molecular scaffolds, integrating spatiotemporal signals and hormonal signaling like auxin, cytokinin, and gibberellin to control phase transitions and reproductive cell fate determination. The lineage-specific expansions and domain rearrangements of TALE genes across bryophytes, gymnosperms, and angiosperms indicate repeated co-option and neofunctionalization throughout land plant evolution. Emerging insights from epigenomics and protein interactomes reveal that TALE complexes modulate cell type-specific transcriptional responses. This review synthesizes current understanding of TALE-mediated regulatory networks during plant reproductive development and presents a conceptual framework for investigating their roles in developmental plasticity and stress-responsive fertility. We also highlight opportunities to utilize TALE-based regulatory modules to develop climate-resilient crops through multi-omics and genome editing approaches. Decoding the reproductive logic embedded in TALE networks offers transformative potential for reprogramming plant development in an era of agricultural and ecological uncertainty.]]> Wed, 31 Dec 1969 19:00:00 EST Epigenome editing based treatment: Progresses and challenges. Yuan L, Xiong Y, Zhang Y, Gu S, Lei Y
Mol Ther (Jan 2026)

Epigenome editing is emerging as a transformative approach in clinical treatment, enabling precise modifications to gene expression without altering the underlying DNA sequence. The ongoing transition of epigenome editing techniques from foundational research to clinical applications highlights several key strategies. These include targeted DNA methylation/demethylation, histone modification, and transcriptional regulation. These approaches offer the potential for durable and reversible gene expression modulation, paving the way for precisely tailored therapies for genetic and complex diseases. Here, we review pioneering research, technological advancements, granted patents, and clinical trials that have been reported during the past decade. By synthesizing current research and development efforts, this review aims to provide insights into the promising landscape of epigenome editing and its potential to promote therapeutic interventions.]]> Wed, 31 Dec 1969 19:00:00 EST Forensic genetics in the omics era. Kayser M
Nat Rev Genet (Feb 2026)

Recent advances in forensic genetics, driven by technological innovation coupled with the use of an expanding range of nucleic acid markers, have markedly improved the scope, accuracy and reliability of evidential information obtainable from human biological traces recovered at crime scenes. The majority of these biomarkers have been identified using non-targeted omics approaches, including genomics, transcriptomics, epigenomics and microbiome profiling. Moreover, targeted massively parallel sequencing, in some cases non-targeted whole-genome sequencing, are being applied to the analyses of biological trace material. These approaches and methods are being used for the identification of perpetrators (including monozygotic twins), their relatives or victims of criminal activities; the prediction of phenotypic and behavioural traits of unknown individuals; and the determination of trace characteristics, including tissue type and time of deposition.]]> Wed, 31 Dec 1969 19:00:00 EST A cell type enrichment analysis tool for brain DNA methylation data (CEAM). Müller J, Laroche VT, Imm J, Weymouth L, Harvey J, Reijnders RA, Smith AR, van den Hove D, Lunnon K, Cavill R, Pishva E
Epigenetics (Dec 2026)

DNA methylation (DNAm) signatures are highly cell type-specific, yet most epigenome-wide association studies (EWAS) are performed on bulk tissue, potentially obscuring critical cell type-specific patterns. Existing computational tools for detecting cell type-specific DNAm changes are often limited by the accuracy of cell type deconvolution algorithms. Here, we introduce CEAM (Cell-type Enrichment Analysis for Methylation), a robust and interpretable framework for cell type enrichment analysis in DNA methylation data. CEAM applies over-representation analysis with cell type-specific CpG panels from Illumina EPIC arrays derived from nuclei-sorted cortical post-mortem brains from neurologically healthy aged individuals. The constructed CpG panels were systematically evaluated using both simulated datasets and published EWAS results from Alzheimer's disease, Lewy body disease, and multiple sclerosis. CEAM demonstrated resilience to shifts in cell type composition, a common confounder in EWAS, and remained robust across a wide range of differentially methylated positions, when upstream modeling of cell type composition was modeled with sufficient accuracy. Application to existing EWAS findings generated in neurodegenerative diseases revealed enrichment patterns concordant with established disease biology, confirming CEAM's biological relevance. The workflow is publicly available as an interactive Shiny app (https://um-dementia-systems-biology.shinyapps.io/CEAM/) enabling rapid, interpretable analysis of cell type-specific DNAm changes from bulk EWAS.]]> Wed, 31 Dec 1969 19:00:00 EST Detection of Isodisomy Utilizing SNP Microarray: Frequency, Ascertainment, and Implications. Molinari S, Williams N, Haskell G, Penton A, Arreola A, Gadi I, Phillips K, Tepperberg J, Schwartz S
Am J Med Genet A (Feb 2026)

This study investigates the frequency, ascertainment, and clinical implications of whole chromosomal isodisomy using a database of over 415,000 chromosomal microarray (CMA) tests conducted since 2008 across prenatal, postnatal, and products of conception specimens. In this cohort, 0.04% of cases exhibited the rare chromosomal phenomenon of isodisomy. Analysis of these cases revealed distinct patterns in frequency, chromosome involvement, and parent of origin related to specimen type. Isodisomy 14 was most frequent in prenatal samples, while chromosomes 6, 7, and 15 were more common in postnatal cases. The involvement of imprinted and non-imprinted chromosomes was equivalent for prenatal cases, while imprinted chromosomes consisted of two-thirds of postnatal cases, with paternal uniparental isodisomy more prevalent than maternal across all specimen types. Several cases demonstrated unmasking of pathogenic variants in recessive genes, and findings support prior studies of associations between isodisomy 11 and prenatal or neonatal lethality. These results underscore the diagnostic value of CMA and contribute to an extended understanding of isodisomy's clinical relevance.]]> Wed, 31 Dec 1969 19:00:00 EST Accelerated epigenetic age in hypertension: a systematic review and meta-analysis. Dollin C, Ward M, Stafford MYC, Krason-Kidzinska E, Crawford L, McNulty H, Barry F, Murphy M, Lees-Murdock DJ
Hypertens Res (Jan 2026)

Chronological age is a well-established risk factor for Hypertension (HTN), yet while biological ageing markers such as epigenetic age acceleration (EAA), have been associated with HTN, findings are inconsistent. This study aimed to conduct a systematic review and meta-analysis to evaluate the association between EAA, HTN and blood pressure (BP) to provide an understanding of the role of EAA in HTN development and progression. Six databases were searched, and studies which reported associations between DNA and HTN, and/or BP were included. Functional enrichment analysis was conducted using DAVID and STRING to elucidate underlying molecular pathways. From 4334 studies, 165 met the inclusion criteria. Qualitative analysis indicated that 17.0% of studies reporting global methylation and 49.1% of studies reporting gene-specific methylation demonstrated significant associations with HTN and/or BP. A random effects meta-analysis of 16,136 participants from 8 studies using three epigenetic clock algorithms demonstrated that HTN was associated with increased EAA (β: 0.29, 95%Cl: 0.15-0.43; P < 0.0001). All three individual epigenetic clocks demonstrated a positive association between clinically measured HTN and EAA (Horvath β: 0.33, 95%Cl: 0.08-0.58, P = 0.010; Hannum β: 0.64, 95%Cl: 0.09-1.20; PhenoAge β: 1.21, 95%Cl: 0.56-1.86), whereas this relationship was not clear when using self-reported HTN. This study is the first to systematically demonstrate that HTN is associated with EAA. We recommend the use of clinically measured over self-reported HTN in appropriately powered studies of epigenetic age to obtain an accurate understanding of BP regulation/HTN on the epigenome, supporting pathways to translation and development of novel therapeutic targets for HTN.]]> Wed, 31 Dec 1969 19:00:00 EST Maternal UPD(20) Leading to Mulchandani-Bhoj-Conlin Syndrome: A Rare Neonatal Case With Additional TRPS1 Deletion. Zhang J, Chen X, Chen M, Wu S, Huang F, Pan R, Chen G
Am J Med Genet A (Feb 2026)

Mulchandani-Bhoj-Conlin syndrome is an extremely rare imprinting disorder caused by maternal uniparental disomy of chromosome 20, primarily characterized by intrauterine growth restriction, severe postnatal growth failure, and feeding difficulties. Here, we report a neonate diagnosed with Mulchandani-Bhoj-Conlin syndrome via whole exome sequencing and copy number variation analysis, which also identified a 0.26 Mb deletion on chromosome 8q23.3 affecting the TRPS1 gene, associated with Trichorhinophalangeal syndrome. We describe the clinical features and genetic findings of this infant, with the aim of contributing to a better understanding of these two rare diseases.]]> Wed, 31 Dec 1969 19:00:00 EST Advances in the application of spatial transcriptomics in understanding development and disease. Li Y, Zheng QW, Li M, Chen J, Zhao LY
Mol Cell Biochem (Jan 2026)

Spatial transcriptomics (In this review, 'spatial transcriptomics' (ST) is employed as a overarching term, encompassing two distinct concepts. Firstly, 'tissue-level ST' refers to the capture of tissue samples at a resolution of 10-100 μm, encompassing 1-20 cells. Secondly, 'spatially resolved single-cell transcriptomics' (sc-ST) involves the analysis of individual cells or nuclei, with each sequencing unit measuring ≤ 2 μm) fuses high-throughput sequencing with positional information to map gene expression within intact tissues. By preserving spatial context, the technology uncovers cell types, signaling circuits and regulatory networks that drive organogenesis, differentiation and disease. Here we synthesize recent methodological advances and their application to developmental and clinical questions. The term "Spatial Transcriptomics" as used in this paper comprehensively encompasses all sequencing technologies that preserve spatial coordinates, including multimodal data such as transcriptomics (RNA), genomics (DNA), epigenomics (ATAC, CUT&Tag), and translationalomics (Ribo-seq).]]> Wed, 31 Dec 1969 19:00:00 EST Comprehensive epigenomic and transcriptomic analysis identifies FABP7 and CLIC6 as methylation-driven prognostic biomarker for a novel breast cancer subtype. Fahima K, Hosen MR, Mahmud Z
Comput Biol Med (Jan 2026)

Breast cancer (BRCA) is the most prevalent malignancy among women and exhibits significant molecular and clinical heterogeneity. To improve risk stratification and identify novel molecular subtypes, we employed integrative analysis on DNA CpG methylation and transcriptomic data to construct a methylation-driven prognostic model for BRCA. Using LASSO, we identified a 10-gene prognostic signature that effectively stratified patients into two groups designated as high-risk and low-risk groups. Kaplan-Mayer survival analysis revealed worse overall survival of the high-risk patients in the TCGA cohort (p < 0.0001). The risk model was independently validated in two external GEO datasets GSE86166 (p = 0.00011) and GSE42568 (p = 0.00013) demonstrating its resilience and clinical relevance. In addition, the risk groups were not associated with any canonical molecular subtypes of breast cancer. Among the 10 genes, FABP7 and CLIC6 were differentially expressed between the risk groups. FABP7 had the highest negative LASSO coefficients followed by CLIC6. In further analysis, FABP7 (R = 0.42, p = 3e-04) and CLIC6 (R = 0.48, P < 0.001) both showed a strong inverse correlation between CpG methylation and expression, with more than two-fold higher expression in low-risk group and linked to improved survival in all three independent cohort. Functional enrichment analysis identified that genes overexpressed in the low-risk subtype were significantly enriched in immune-related pathways. Immunological analysis indicated a more immunogenic tumor microenvironment in the FABP7 and CLIC6 positive, low-risk group, with significantly higher infiltration of CD8 T cells (p = 0.047) and resting NK cells (p = 0.0391), while FABP7 and CLIC6 negative, high-risk tumors had increased M2 macrophages (p = 9.19 × 10) and Tregs (p = 0.0122). To summarize, this integrative model identified a novel methylation-based risk classifier/molecular subtype for BRCA, highlighting FABP7 and CLIC6 as a key prognostic biomarker with potential utility for risk stratification for strategic treatment. These findings require further validation through wet-lab experiments and prospective clinical studies to support clinical translation.]]> Wed, 31 Dec 1969 19:00:00 EST From 2D to 4D: a containerized workflow and browser to explore dynamic chromatin architecture. Rogers DH, Roth C, Tauxe C, Lee JT, Steadman CR, Sanbonmatsu KY, Lappala A, Starkenburg SR
BMC Bioinformatics (Jan 2026)

]]> Wed, 31 Dec 1969 19:00:00 EST Epigenomics-guided precision oncology: Chromatin variants in prostate tumor evolution. Furlano K, Keshavarzian T, Biernath N, Fendler A, de Santis M, Weischenfeldt J, Lupien M
Int J Cancer (Jan 2026)

Prostate cancer is a common malignancy that in 5%-30% leads to treatment-resistant and highly aggressive disease. Metastasis-potential and treatment-resistance is thought to rely on increased plasticity of the cancer cells-a mechanism whereby cancer cells alter their identity to adapt to changing environments or therapeutic pressures to create cellular heterogeneity. To understand the molecular basis of this plasticity, genomic studies have uncovered genetic variants to capture clonal heterogeneity of primary tumors and metastases. As cellular plasticity is largely driven by non-genetic events, complementary studies in cancer epigenomics are now being conducted to identify chromatin variants. These variants, defined as genomic loci in cancer cells that show changes in chromatin state due to the loss or gain of epigenomic marks, inclusive of histone post-translational modifications, DNA methylation and histone variants, are considered the fundamental units of epigenomic heterogeneity. In prostate cancer chromatin variants hold the promise of guiding the new era of precision oncology. In this review, we explore the role of epigenomic heterogeneity in prostate cancer, focusing on how chromatin variants contribute to tumor evolution and therapy resistance. We therefore discuss their impact on cellular plasticity and stochastic events, highlighting the value of single-cell sequencing and liquid biopsy epigenomic assays to uncover new therapeutic targets and biomarkers. Ultimately, this review aims to support a new era of precision oncology, utilizing insights from epigenomics to improve prostate cancer patient outcomes.]]> Wed, 31 Dec 1969 19:00:00 EST Toxicoepigenomics: Epigenetic disruption by environmental exposures and implications for biomarker development. Kim JY, Kim JW
J Hazard Mater (Jan 2026)

Environmental exposures are increasingly recognized as key modulators of the epigenome, contributing to both immediate and long-term disease risk. The field of toxicoepigenomics, which investigates how environmental toxicants alter epigenetic regulation, has demonstrated that exposures to endocrine-disrupting chemicals, heavy metals, polycyclic aromatic hydrocarbons (PAHs), and air pollutants can disrupt gene expression through changes in DNA methylation, histone modifications, non-coding RNA expression, and higher-order chromatin structure. Additionally, lifestyle factors-including diet, physical activity, stress, and sleep-interact with these exposures to shape individual epigenetic profiles and influence health trajectories across the lifespan. This review synthesizes current evidence across major pollutant classes and molecular pathways, emphasizing both well-characterized and emerging mechanisms. Retained introns represent post-transcriptional consequences of chromatin-based epigenetic regulation and serve as sensitive indicators of environmentally induced disruptions in transcriptional elongation and splicing fidelity. We also highlight recent advances in high-throughput technologies, including whole-genome bisulfite sequencing, single-cell epigenomics, and epigenetic clock models, which are rapidly enhancing biomarker discovery and mechanistic understanding. By integrating multilayered epigenetic insights across diverse exposure contexts, this review advances the field of toxicoepigenomics and lays the groundwork for developing robust, exposure-responsive biomarkers of environmental disease. These insights offer significant promise for guiding mechanistic research, improving exposure surveillance, and informing the design of precision strategies in environmental health.]]> Wed, 31 Dec 1969 19:00:00 EST A hitchhiker's guide to single-cell epigenomics: Methods and applications for cancer research. Moreno-Gonzalez M, Sierra I, Kind J
Int J Cancer (Jan 2026)

Genetic mutations are well known to influence tumorigenesis, tumor progression, treatment response and relapse, but the role of epigenetic variation in cancer progression is still largely unexplored. The lack of epigenetic understanding in cancer evolution is in part due to the limited availability of methods to examine such a heterogeneous disease. However, in the last decade the development of several single-cell methods to profile diverse chromatin features (chromatin accessibility, histone modifications, DNA methylation, etc.) has propelled the study of cancer epigenomics. In this review, we detail the current landscape of single-omic and multi-omic single-cell methods with a particular focus on the examination of histone modifications. Furthermore, we provide recommendations on both the application of these methods to cancer research and how to perform initial computational analyses. Together, this review serves as a referential framework for incorporating single-cell methods as an important tool for tumor biology.]]> Wed, 31 Dec 1969 19:00:00 EST Comparative characterization of chromatin-targeting mechanisms across seven H3K4 methyltransferases in Arabidopsis. Oya S, Uehara S, Watabe H, Juliarni , Kodama Y, Mori S, Osakabe A, Tanaka N, Noyori T, Takahashi M, Nomoto M, Tada Y, Kakutani T, Inagaki S
Plant Commun (Jan 2026)

Methylation of histone H3 at lysine 4 (H3K4me) marks transcribed elements of the eukaryotic genome, and its distribution dynamically changes through developmental stages and in response to environmental factors. These dynamic regulatory changes are achieved by the combinatorial action of H3K4me methyltransferases, with multi-cellular organisms carrying multiple copies of these enzymes. The model plant Arabidopsis has at least seven H3K4 methyltransferase genes. Here, we comparatively analyze the seven H3K4 methyltransferases using epigenomics and biochemical approaches to better understand the mechanisms underlying their target specificity. Our findings, in combination with previous work, show that ATX1 to ATX5 (Trx/Trr-type methyltransferases) localize to loci with distinct sets of chromatin modifications and DNA motifs, which differ among the various ATX proteins. Notably, ATX3 localizes to the binding motifs of ASR3 and RAP2.11 transcriptional factors and directly interacts with these TFs. ATXR7 (Set1-type) and ATXR3 (non-canonical H3K4 methyltransferase) co-localize with the transcriptional machinery, suggesting co-transcriptional mechanisms of action for these enzymes. Interestingly, ATXR3, the major H3K4me3 methyltransferase in Arabidopsis, appears to form a protein complex independent of COMPASS, indicating that the regulatory mechanisms of H3K4me3 have diverged between plants and animals. Our work provides a foundation for understanding the chromatin targeting of H3K4 methyltransferases in plants and highlights significant differences in H3K4me3 regulation between plants and other eukaryotes.]]> Wed, 31 Dec 1969 19:00:00 EST