'; ?> 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 Wed, 05 Nov 2025 20:31:45 EST Wed, 05 Nov 2025 20:31:45 EST jirtle@radonc.duke.edu james001@jirtle.com Comprehensive evaluation of diverse massively parallel reporter assays to functionally characterize human enhancers genome-wide. Zhang J, Leung AK, Zhu Y, Yao L, Willis A, Pan X, Ozer A, Zhou Z, Siklenka K, Barrera A, Liang J, Tippens ND, Reddy TE, Lis JT, Yu H
Genome Biol (Nov 2025)

Massively parallel reporter assays (MPRAs) and self-transcribing active regulatory region sequencing (STARR-seq) have revolutionized enhancer characterization by enabling high-throughput functional assessment of regulatory sequences.]]> Wed, 31 Dec 1969 19:00:00 EST Host-microbe multi-omics and succinotype profiling have prognostic value for future relapse in patients with inflammatory bowel disease. O'Sullivan J, Patel S, Leventhal GE, Fitzgerald RS, Laserna-Mendieta EJ, Huseyin CE, Konstantinidou N, Rutherford E, Lavelle A, Dabbagh K, DeSantis TZ, Shanahan F, Temko A, Iwai S, Claesson MJ
Gut Microbes (Dec 2025)

Crohn's disease (CD) and ulcerative colitis (UC) are chronic relapsing inflammatory bowel disorders (IBD), the pathogenesis of which is uncertain but includes genetic susceptibility factors, immune-mediated tissue injury and environmental influences, most of which appear to act via the gut microbiome. We hypothesized that host-microbe alterations could be used to prognostically stratify patients experiencing relapses up to four years after endoscopy. We therefore examined multiple omics data, including published and new datasets, generated from paired inflamed and non-inflamed mucosal biopsies from 142 patients with IBD (54 CD; 88 UC) and from 34 control (non-diseased) biopsies. The relapse-predictive potential of 16S rRNA gene and transcript amplicons (standing and active microbiota) were investigated along with host transcriptomics, epigenomics and genetics. While standard single-omics analysis could not distinguish between patients who relapsed and those that remained in remission within four years of colonoscopy, we did find an association between the number of flares and a patient's succinotype. Our multi-omics machine learning approach was also able to predict relapse when combining features from the microbiome and human host. Therefore multi-omics, rather than single omics, better predicts relapse within 4 years of colonoscopy, while a patient's succinotype is associated with a higher frequency of relapses.]]> Wed, 31 Dec 1969 19:00:00 EST Immunofluorescence Staining and Microscopic Imaging of Plant Nuclei for Epigenetic Modifications. Gandhivel VH, Raju S, Shivaprasad PV
Methods Mol Biol (2026)

Histone posttranslational modifications (PTMs) and DNA methylation are the predominant epigenetic modifications on the chromatin that regulate gene expression. These modifications can be spatially resolved using microscopic examination of the nuclei with the help of commercially available antibodies. Here, we describe a detailed method to obtain intact nuclei from plant tissues and reproducibly immunostain the nuclei for specific chromatin marks and microscopic examination. This method can be readily extended to multiple plant species as the antibodies are raised against conserved epigenetic marks.]]> Wed, 31 Dec 1969 19:00:00 EST PoreMeth2 for decoding the evolution of methylome alterations with nanopore sequencing. Mattei G, Baragli M, Gega B, Mingrino A, Chieca M, Ducci T, Frigè G, Mazzarella L, D'Aurizio R, De Logu F, Nassini R, Pelicci PG, Magi A
Genome Res (Nov 2025)

In epigenetic analysis, the identification of differentially methylated regions (DMRs) typically involves the detection of consecutive CpGs groups that show significant changes in their average methylation levels. However, the methylation state of a genomic region can also be characterized by a mixture of patterns (epialleles) with variable frequencies, and the relative proportions of such patterns can provide insights into its mechanisms of formation. Traditional methods based on bisulfite conversion and high-throughput sequencing, such as Illumina, owing to the read size (150 bp) allow epiallele frequency analysis only in high CpG density regions, limiting differential methylation studies to just 50% of the human methylome. Nanopore sequencing, with its long reads, enables the analysis of epiallele frequency across both high and low CpG density regions. Here, we introduce a novel computational approach, PoreMeth2, an R library that integrates epiallelic diversity and methylation frequency changes from nanopore data to identify DMRs, providing insights into their possible mechanisms of formation, and annotate them to genic and regulatory elements. We apply PoreMeth2 to cancer and glial cell data sets, providing evidence of its advance over other state-of-the-art methods and demonstrating its ability to distinguish epigenomic alterations with a strong impact on gene expression from those with weaker effects on transcriptional activity.]]> Wed, 31 Dec 1969 19:00:00 EST Using Epigenetic Data to Deconvolute Immune Cells in Cancer from Blood Samples. Boughanem H, Ouzounis S, Callari M, Sanz-Pamplona R, Macias-Gonzalez M, Katsila T
Methods Mol Biol (2026)

DNA methylation plays a crucial role in regulating gene expression and is a hallmark of epigenetic dysregulation in human tumors. High-throughput DNA methylation profiling can unravel intricate patterns in cancer. Moreover, understanding immune cell dynamics is essential for comprehending cancer progression and treatment response. Using DNA methylation data in immune cells, we can apply deconvolution algorithms estimate proportions of major immune cell types, providing insights into immune status and its implications in cancer. Functional analysis can identify specific overrepresented or underrepresented immune cell subsets, potentially uncovering novel biomarkers or therapeutic targets. This pipeline presents a detailed workflow in RStudio for DNA methylation studies and immune cell deconvolution, enhancing reproducibility and efficiency. The workflow integrates preprocessing, analysis, and visualization steps, facilitating robust inference of cell-type proportions from DNA methylation data.]]> Wed, 31 Dec 1969 19:00:00 EST Advancing epigenetic signatures as functional biomarkers in rare diseases. Ciolfi A, Ferilli M, Cappelletti C, Tartaglia M
Epigenomics (Nov 2025)

Alterations of the DNA methylation (DNAm) status of the genome underlie an increasing number of rare diseases. Recently, DNAm has also emerged as a highly informative biomarker for diagnosing rare disorders, which can be associated with distinctive genome-wide DNAm patterns (., episignatures). Indeed, episignature testing has proven to represent an effective orthogonal omics technology, providing independent functional evidence to support or prioritize specific diagnostic hypotheses for hundreds of rare diseases, and reclassify variants of uncertain significance (VUS) emerging from genomic sequencing. Furthermore, the stability and plasticity inherent in DNAm make it a promising tool for personalized medicine, including patient stratification and therapeutic monitoring. This review outlines current technologies and analytical methodologies for genome-wide DNAm profiling and explores potential avenues of research, emphasizing artificial intelligence and multiomics integration to effectively manage patients with rare and complex phenotypes. We critically assess the current limitations and future directions of genome-wide DNAm profiling to expand the implementation of DNAm signatures as functional biomarkers, highlighting their importance as supplementary tools to genomic sequencing in clinical and research settings.]]> Wed, 31 Dec 1969 19:00:00 EST Single-cell multi-omics characterize colorectal tumors, adjacent healthy tissue and matched (tumor) organoids identifying CRC-unique features. Yu Z, Derksen M, Te Pas BM, Ladstätter S, Overmeer R, Brazda P, van de Wetering M, Pourfarzad F, Vries RGJ, Megchelenbrink W, Bock C, Altucci L, Stunnenberg HG
Int J Cancer (Dec 2025)

Colorectal cancer (CRC) arises in the colorectal tissue driven by genetic disorder or the accumulation of somatic mutations, leading to abnormal epithelial cell growth. In this study, we employed single-nucleus multi-omics analysis, including single-nucleus RNA-seq and single-nucleus ATAC-seq, on over 100,000 high-quality nuclei to investigate the molecular landscape of both primary tissue and patient-derived organoids (PDOs). Our analysis showed that normal PDOs (N-PDOs) derived from tissue adjacent to tumors replicate the cellular composition and differentiation trajectory of colorectal crypts. In contrast, tumor PDOs (T-PDOs) showed patient-specific transcriptomic and epigenomic heterogeneity yet consistently maintained a stem cell-like state. T-PDOs retained the somatic mutation profile of the primary tumor while also exhibiting de novo mutations not detected in either the primary tumor or N-PDOs. Notably, inferred cell-cell interaction analysis highlighted the activin signaling pathway as a potential unique feature of fibroblast-epithelial interactions within the tumor microenvironment. This study provides a comprehensive view of the transition from normal to malignant colorectal epithelium and underscores the utility of PDOs as a faithful model for capturing both conserved and patient-specific features of colorectal cancer.]]> Wed, 31 Dec 1969 19:00:00 EST Genomic and epigenomic maps of mouse centromeres and pericentromeres. Chaudhry G, Chen J, Snipes L, Bahl S, Packiaraj J, Lin X, Thakur J
Nat Commun (Nov 2025)

Satellite DNA comprises ~11% of the mouse genome and is primarily located in centromeres and pericentromeres. We present comprehensive genomic and epigenomic maps of these regions utilizing Hifiasm assemblies, CUT&RUN-seq, DNA methylation analysis, and RNA-seq alongside recent mouse telomere-to-telomere assembly drafts. We show that 120-mer Minor satellites (MiSats) occupy core centromeres, while MiSat length variants localize at centromere-pericentric junctions. Pericentromeres contain mostly homogeneous Major satellites (MaSats), with divergent MaSats concentrated near pericentric non-satellite repeat islands and pericentric-chromosomal junctions. Most centromeres contain higher-order repeats (HORs), with shorter HORs more common. Centromeres are hypomethylated compared to pericentromeres, and transcripts are detected from a small subset of satellites with lower DNA methylation. CENP-A is highly enriched at 120-mer MiSats but reduced at MiSat length variants. Homogeneous MaSats are enriched with H3K9me3, whereas divergent MaSats are associated with H3K9me3 and H3K27me3. Finally, the density and type of satellite sequence motifs correlate with chromatin signatures.]]> Wed, 31 Dec 1969 19:00:00 EST gene and male infertility: a South Slavic case-control study and multi-omics data integration. Kunej T, Podgrajsek R, Jaklic H, Hodzic A, Stimpfel M, Miljanovic O, Ristanovic M, Novakovic I, Plaseska-Karanfilska D, Noveski P, Ostojic S, Buretic-Tomljanovic A, Grskovic A, Peterlin B
Syst Biol Reprod Med (Dec 2025)

Components of the renin-angiotensin system (RAS) are expressed in both female and male reproductive tracts, with angiotensin I converting enzyme (ACE) being an important component for male reproductive function, as shown in animal models. The most studied polymorphism is the Alu insertion-deletion (I/D), which has been proposed to have a negative effect on male fertility. Given the conflicting evidence in the literature, we conducted a multicentric case-control study to investigate the association between the Alu I/D polymorphism and impaired spermatogenesis. Using PCR amplification and agarose electrophoresis, we genotyped the gene Alu I/D polymorphism in 745 South Slavic men. The study group consisted of 457 patients with impaired spermatogenesis, 239 with non-obstructive azoospermia (NOA) and 218 with oligoasthenoteratozoospermia (OAT) and a control group of 288 fertile men. No association was found between the Alu I/D polymorphism and these semen phenotypes, suggesting that it is not associated with NOA or severe OAT in this cohort. To provide a broader regulatory context, we also developed an integrative atlas of regulatory elements by in silico multi-omics analysis using genomics databases and bioinformatics tools. Data integration revealed various regulatory mechanisms at multiple omics levels, including genomics, epigenomics, miRNAomics, transcriptomics, proteomics and epiproteomics. These include genomic variants with predicted deleterious effects, a CpG island, microRNAs (miRNAs) and post-translational modifications (PTMs). In addition, protein interaction analysis revealed that ACE is indirectly linked to several proteins previously associated with male infertility and is also targeted by miRNA previously associated with oligozoospermia. This comprehensive, multi-faceted approach, combining genetic association analysis with bioinformatics, provides insights into regulation in its broader molecular context. These results emphasize the importance of further integrative multi-omics and systems biology research to better understand the role of ACE in male reproductive function.]]> Wed, 31 Dec 1969 19:00:00 EST From renal development to pathology: An analysis of the multilevel role of insulin‑like growth factor 2 (Review). Sun Y, Hao W, Liu W, Hu W
Mol Med Rep (Jan 2026)

Insulin‑like growth factor 2 (IGF2) is a multifunctional polypeptide hormone that serves important roles in embryonic development, metabolic regulation and disease pathogenesis. IGF2 expression is tightly regulated by genomic imprinting, which restricts transcription to the paternal allele. IGF2 modulates cellular processes, including proliferation, differentiation and metabolic homeostasis, by activating downstream signaling cascades via binding to IGF1 receptor, insulin receptor isoform A and IGF2 receptor. IGF2 is important for kidney development, promoting both nephron formation, and the functional maintenance of renal tubules and glomeruli. Aberrant IGF2 expression is associated with the pathogenesis of diverse renal diseases, including acute kidney injury, chronic kidney disease, diabetic nephropathy, renal cell carcinoma and Wilms' tumor. Under pathological conditions, IGF2 promotes renal fibrosis and promotes tumor expansion and progression by activating key signaling pathways such as the PI3K/Akt and TGF‑β pathways. Due to these roles, IGF2 has attracted growing clinical interest as a potential therapeutic target. The present review presents a comprehensive analysis of the structure and function of IGF2, its roles in renal pathophysiology, and its therapeutic potential, while outlining future research directions.]]> Wed, 31 Dec 1969 19:00:00 EST Sex-stratified piRNA expression analysis reveals shared functional impacts of perinatal lead (Pb) exposure in murine hearts. Sala-Hamrick KE, Wang K, Perera BPU, Sartor MA, Svoboda LK, Dolinoy DC
Epigenetics (Dec 2025)

The landscape of PIWI-interacting RNA (piRNA) expression in the heart is poorly understood, particularly regarding sex differences. Altered piRNA expression has been reported in cardiovascular disease (CVD), and although exposure to the metal lead (Pb) is strongly associated with CVD risk, no studies have investigated Pb's effects on cardiac piRNAs. This study aimed to characterize piRNA expression in the murine heart and assess sex-specific effects of human-relevant maternal Pb exposure on adult offspring cardiac piRNA expression. piRNAs were identified from whole mouse hearts using sodium periodate exclusion of small RNA and subsequent sequencing. Control mice expressed 18,956 piRNAs in combined-sex analysis; sex-specific analyses revealed 9,231 piRNAs in female hearts and 5,972 piRNAs in male hearts. Genomic mapping showed 28-41% aligned to introns, while 12-28% mapped to exons. Comparing control and Pb-exposed hearts, we found more potential Pb-induced expression changes in females (847) compared to males (187) (p-value < 0.05 and |logFC| > 1). These piRNAs were significantly enriched near genes involved in biological processes related to heart function and CVD development, including mitochondrial function, energy metabolism, and cardiac muscle structure (FDR < 0.05). Overall, we characterized combined and sex-stratified piRNA expression in both control and Pb-exposed murine hearts. In addition to providing a foundation for sex-specific piRNA expression in the heart, these findings suggest a novel epigenetic mechanism by which developmental Pb exposure may impact CVD risk later in life. Future studies will link these sex-specific molecular changes to Pb-induced alterations in cardiac function.]]> Wed, 31 Dec 1969 19:00:00 EST Maternal hypoxia exposure perturbs imprinted gene methylation in adult sperm and induces intergenerational placental impairments in male offspring. Zhang LY, Jia GX, Tao HP, Liu KX, Luo YW, Hou YP, Yang QE
Zool Res (Nov 2025)

Hypobaric hypoxia encountered at high altitudes impairs reproductive health and fertility across species. Previous findings have demonstrated that maternal hypoxia exposure disrupts granulosa cell (GC) viability and oocyte maturation in female offspring; however, its transgenerational impact on male reproductive outcomes remains poorly elucidated. In this study, pregnant mice (F0) were subjected to hypoxic conditions, and male progeny across four generations (F1‒F4) were evaluated. Results revealed that maternal hypoxia induced mild alterations in sperm DNA methylation in F1 males but caused profound developmental defects in F2 embryos, predominantly affecting males. Following mating of F1 males with control females, a substantial proportion of male F2 fetuses were lost at embryonic day (E) 13.5, attributed to placental malformations. Integrated RNA sequencing and whole-genome bisulfite sequencing of placentas from male fetuses revealed aberrant expression of imprinted genes, including , , , and , which also exhibited differential methylation in F1 sperm. These findings demonstrate that maternal hypoxia disrupts epigenetic programming in F1 germ cells, impairing placental development and fetal viability in F2 males, thereby leading to an unbalanced sex ratio. Overall, this study elucidates the mechanisms by which environmental hypoxia influences sex ratios and offers critical insights into hypoxia-induced reproductive impairments in mammals.]]> Wed, 31 Dec 1969 19:00:00 EST and are human placenta-specific imprinted genes associated with germline-inherited maternal DNA methylation. Daskeviciute D, Sainty B, Chappell-Maor L, Bone C, Russell S, Iglesias-Platas I, Arnaud P, Monteagudo-Sánchez A, Greenberg MVC, Chen K, Manerao-Azua A, Perez de Nanclares G, Lartey J, Monk D
Epigenetics (Dec 2025)

Genomic imprinting is the parent-of-origin specific monoallelic expression of genes that result from complex epigenetic interactions. It is often achieved by monoallelic 5-methylcytosine, resulting in the formation of differentially methylated regions (DMRs). These show a bias towards oocyte-derived methylation and survive reprogramming in the pre-implantation embryo. Imprinting is widespread in the human placenta. We have recently performed whole-genome screens for novel imprinted placenta-specific germline DMRs (gDMRs) by comparing methylomes of gametes, blastocysts and various somatic tissues, including placenta. We observe that, unlike conventional imprinting, for which methylation at gDMRs is observed in all tissues, placenta-specific imprinting is associated with transient gDMRs, present only in the pre-implantation embryo and extra-embryonic lineages. To expand the list of imprinted genes subject to placenta-specific imprinting, we reinvestigated our list of candidate loci and characterized two novel imprinted genes, and , both of which display polymorphic imprinting. Interrogation of placenta single-cell RNA-seq datasets, as well as cell-type methylation profiles, revealed complex cell-type specificity. We further interrogated their methylation and expression in placental samples from complicated pregnancies, but failed to identify differences between intrauterine growth restricted or pre-eclamptic samples and controls, suggesting they are not involved in these conditions.]]> Wed, 31 Dec 1969 19:00:00 EST Epigenomics of embryogenesis in turbot. Aramburu O, Pardo BG, Jimenez-Gonzalez A, Blanco-Hortas A, Macqueen D, Bouza C, Martinez P
Genome Res (Nov 2025)

Embryogenesis is the foundational step of ontogeny, where a complex organism emerges from a single totipotent cell. This process is orchestrated by changes in transcriptional regulation, influenced by chromatin accessibility and epigenetic modifications, enabling transcription factor accessibility. Epigenomic regulation of embryogenesis has been studied in model fish, but little attention has been paid to farmed fish - where relevant traits to aquaculture rely on early developmental processes. This study reports a regulatory atlas of turbot () embryogenesis. 14,560 active genes were identified in the embryonic transcriptome with > 90% showing differential expression across consecutive stages. By integrating multi-histone ChIP-seq with ATAC-seq, we built a genome-wide chromatin state model, defining promoter and enhancer activity across stages. Diverse transcription factor binding motifs were detected within regulatory elements showing differential accessibility at distinct developmental stages. Strong shifts in chromatin accessibility across stages, notably during the transition from shield to early segmentation, suggest profound chromatin reorganization underpinning somitogenesis and early organogenesis. Regardless, most changes in chromatin accessibility did not affect promoters of differentially expressed genes, suggesting that their accessibility precedes gene transcription changes. Comparative analyses with zebrafish revealed a global transcriptomic correlation of single-copy orthologs at matched stages. While conserved expression dynamics were revealed for many orthologous genes, notable cross-species differences were identified from pre-ZGA leading up to hatching. This multi-omics investigation provides a novel atlas of noncoding regulatory elements controlling turbot development, with key applications for flatfish biology and sustainable aquaculture.]]> Wed, 31 Dec 1969 19:00:00 EST The myoblast methylome: multiple types of associations with chromatin and transcription. Sen S, Lacey M, Baribault C, Ponnaluri VKC, Esteve PO, Ehrlich KC, Meletta M, Pradhan S, Ehrlich M
Epigenetics (Dec 2025)

Epigenetic changes are implicated in development, repair, and physiology of postnatal skeletal muscle (SkM). We generated methylomes for human myoblasts (SkM progenitor cells) and determined myoblast differentially methylated regions (DMRs) for comparison to the epigenomics and transcriptomics of diverse cell types. Analyses were from global genomic and single-gene perspectives and included reporter gene assays. One atypical finding was the association of promoter-adjacent hypermethylation in myoblasts with transcription turn-on, but at downmodulated levels, for certain genes (., and ). In contrast, brain-specific was in repressed chromatin and silent in most cell types but linked to hypermethylated DMRs specifically in myoblasts. The -linked DMRs might be needed because of the overlapping or nearby binding of myogenic differentiation protein 1 (MYOD). We found genome-wide overlap of DMRs with MYOD or CCCTC-binding factor (CTCF) binding sites in myoblasts that is consistent with the importance of MYOD, as well as CTCF, in organizing myoblast transcription-enhancing chromatin interactions. We also observed some gene upregulation correlated with a special association of regional DNA hypomethylation with H3K36me3, H3K27ac, and H3K4me1 enrichment. Our study highlights unusual relationships between epigenetics and gene expression that illustrate the interplay between DNA methylation and chromatin epigenetics in the regulation of transcription.]]> Wed, 31 Dec 1969 19:00:00 EST Adaptive multi-omics integration framework for breast cancer survival analysis. Hasanzadeh E, Charkari NM
Sci Rep (Nov 2025)

Breast cancer remains a major global health issue, requiring novel strategies for prognostic evaluation and therapeutic decision-making. In this study, we leverage multi-omics data from The Cancer Genome Atlas to obtain deeper insights into breast cancer biology. By integrating genomics, transcriptomics, and epigenomics, we aim to identify complex molecular signatures that drive breast cancer progression and impact patient survival. To optimize the integration and feature selection process within the multi-omics dataset, we have employed genetic programming. Genetic programming helps us to optimize multi-omics integration, enabling the identification of robust biomarkers and more accurate survival analysis. The proposed framework consists of three key components: data preprocessing, adaptive integration and feature selection via genetic programming, and model development. The experimental results indicate that the integrated multi-omics approach yields a concordance index (C-index) of 78.31 during 5 fold cross-validation on the training set and 67.94 on the test set. In conclusion, our study demonstrates the potential of adaptive multi-omics integration in improving breast cancer survival analysis. It also highlights the importance of considering the complex interplay between different molecular layers. Furthermore, this framework provides a flexible and scalable approach that can be extended to other cancer types, offering valuable insights into oncological processes.]]> Wed, 31 Dec 1969 19:00:00 EST Differential methylation patterns in cord blood associated with prenatal exposure to neighborhood crime: an epigenome-wide association study and regional analysis. Martin CL, Chen J, D'Alessio AS, Ward-Caviness CK, Ye A, Lodge EK, Ghastine L, Dhingra R, Jima DD, Murphy SK, Hoyo C
Epigenetics (Dec 2025)

Exposure to prenatal social stressors during pregnancy is associated with adverse birth outcomes and has been linked to epigenetic changes in DNA methylation (DNAm); however, less understood is the effect of neighborhood-level stressors like crime during pregnancy on offspring DNAm. Using data from the Newborn Epigenetic Study, we conducted epigenome-wide and regional analyses of the association between exposure to neighborhood crime and DNAm in offspring cord blood using Illumina's HumanMethylation450k BeadChip among 185 mother-offspring pairs. Prenatal exposure to neighborhood crime at the census block group level was mapped to participants' residential addresses during the gestational window from the date of last menstrual period to delivery. Models for the epigenome-wide and regional analyses were adjusted for maternal age, race/ethnicity, education, smoking, cell-type composition, and offspring sex. Genetic influence and gene expression enrichment were assessed using methylation quantitative trait loci (mQTLs) and expression quantitative trait methylation (eQTMs) analyses. Functional enrichment was determined using Gene Ontology and KEGG databases. We did not find evidence of epigenome-wide associations between prenatal neighborhood crime exposure and DNAm; however, we identified nine differentially methylated regions (DMRs) comprising 51 CpG sites associated with neighborhood crime. CpG sites within significant differentially methylated regions were associated with mQTLs at birth and eQTMs upon further examination. KEGG analysis identified a significant Th1 and Th2 cell differentiation pathway. Our results suggest potential links between prenatal neighborhood crime exposure and offspring DNAm; however, additional research is needed in larger cohorts across wider geographic areas to confirm our results.]]> Wed, 31 Dec 1969 19:00:00 EST Recent advances in methodologies of epigenomics. Ohishi H, Au Yeung WK
Epigenomics (Nov 2025)

Rapid methodological breakthroughs over the past ten years have transformed epigenomics from bulk, population-averaged assays into single-cell, multi-omic, and intracellular spatial investigations. This review surveys the interconnected technology pillars that now map the epigenome with unprecedented breadth and resolution. First, advances in next-generation and long-read sequencing empower investigators to chart chromatin accessibility, histone and DNA modifications, and three-dimensional higher-order chromatin structure in thousands of individual cells while retaining allele-specific information across kilobase-long molecules. Second, live-cell fluorescence probes and multiplexed chromatin tracing enable visualizing the dynamic organization of epigenetic marks and genome architecture of intact nuclei and tissues. Third, integrative platforms merge base-level reads with their native 3D coordinates, providing a holistic view of gene regulation in physiologic context. We distill key biological insights yielded by each methodology, discuss unresolved and persistent limitations, and outline future directions toward routine, cost-effective investigations. Together, these innovations are redefining how we interrogate chromatin biology in health and disease.]]> Wed, 31 Dec 1969 19:00:00 EST use capsules, transporters, mobile genetic elements, and other evolutionary adaptations to survive antibiotics exposure in the absence of resistance genes. Mmatli M, Mbelle NM, Fourie B, Osei Sekyere J
Virulence (Dec 2025)

Whole-genome sequencing, transcriptomic profiling, and epigenomic analyses were performed. Phenotypic assays were used to evaluate the effects of various inhibitors on antibiotic susceptibility, while bioinformatic pipelines were used to characterize resistance determinants, virulence factors, and mobile genetic elements (MGEs).]]> Wed, 31 Dec 1969 19:00:00 EST Adaptation of centromeres to breakage through local genomic and epigenomic remodeling in wheat. Zhou J, Huang Y, Ma H, Chen Y, Chen C, Han F, Su H
Genome Res (Nov 2025)

Centromeres, characterized by their unique chromatin attributes, are indispensable for safeguarding genomic stability. Due to their intricate and fragile nature, centromeres are susceptible to chromosomal rearrangements. However, the mechanisms preserving their functional integrity and supporting nuclear homeostasis following breakages remain enigmatic. In this study, we use wheat ditelosomic stocks, which arise from centromere breakage, to explore the genetic and epigenetic alterations in damaged centromeres. Our investigations suggest novel chromosome end structures marked by de novo addition of telomeres, as well as localized chromosomal shattering, including segment deletions and duplications near centromere breakpoints. We reveal that the damaged centromeres possess a remarkable capacity for self-regulation, through employing structural modifications such as expansion, contraction, and neocentromere formation to maintain their functional integrity. Centromere breakage triggers nucleosome remodeling and is accompanied by local transcription changes and chromatin reorganization, and subsequently may contribute to the stabilization of broken chromosomes. Our findings highlight the resilience and adaptability of plant chromosomes in response to centromere breakage and provide valuable insights into the stability of centromeres, thereby offering promising prospects to manipulate centromeres for targeted chromosomal innovation and crop genetic improvement.]]> Wed, 31 Dec 1969 19:00:00 EST