'; ?> 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 Thu, 02 Jul 2026 16:28:30 EDT Thu, 02 Jul 2026 16:28:30 EDT jirtle@radonc.duke.edu james001@jirtle.com Neuronutrition in ASD: Involvement of gut microbiota, oxidative stress and inflammatory markers. Avolio E, Olivito I, Minervini D, Soda T, De Bartolo A, Rocca C, Alò R, Facciolo RM
Neurosci Biobehav Rev (Aug 2026)

Autism spectrum disorder (ASD) is a neurodevelopmental disorder displaying altered human behaviors, such as social interaction impairments, stereotypical/repetitive activities and emotional dysregulation. Children with ASD are often affected by gastrointestinal problems and gut microbiota dysbiosis. Inflammation and immune dysfunction are key contributors to ASD, as shown by high proinflammatory cytokines and oxidative stress. Indeed, notable implication of the nuclear factor kappa B in the severity of ASD derives from its ability to amplify neuroinflammation. This narrative review focused attention on neuronutrition and gut microbiota manipulation for mitigation of ASD symptoms, including neuroinflammation and oxidative stress. Studies in both rodents and humans with ASD have revealed that both pure and mixed Lactobacillus and Bifidobacterium were effective in ameliorating behavioral symptoms and GABA/glutamate imbalance. Often, the combined use of probiotics and prebiotics can have greater health benefits in ASD. Additionally, dietary interventions and microbiota transfer therapies along with low-to-moderate-intensity exercise have been proposed to improve gastrointestinal and behavioral symptoms. However, despite some encouraging results, biases in the neuronutrition/microbiota literature still exist. Indeed, many studies rely on small sample sizes, cross-sectional designs, and heterogeneous populations that differ in diet, medications, and comorbidities. In this context, the development of a precision diet tailored to individual gut microbiome profiles will allow for a broader understanding of the microbial ecosystem and relative therapeutical applications. Hence, by integrating metagenomics, metabolomics, epigenomics, with evaluation of environmental and nutritional factors, it will be possible to significantly improve the quality of life for people with ASD and their families.]]> Wed, 31 Dec 1969 19:00:00 EST Integrative MeRIP-seq and RNA-seq analysis reveals mA-mediated epigenetic regulation of host-virus interactions during HSV-2 infection. Li J, Lin D, Xie J, Zhang Z, Qian Y, Xu S, Xu J, Hu Y, Shi J
Virology (Sep 2026)

Herpes simplex virus type 2 (HSV-2), a highly prevalent pathogen responsible for genital herpes, is characterized by neurotropism and the ability to establish lifelong latent infection. N6-methyladenosine (mA) is a widespread epitranscriptomic modification that plays a critical role in regulating RNA metabolism and gene expression. In this study, we used methylated RNA immunoprecipitation sequencing (MeRIP-seq) and RNA sequencing (RNA-seq) to profile mA modifications and transcriptomic changes in human foreskin fibroblasts (HFF-1) infected with HSV-2. We identified 9477 common mA peaks and 15,842 differentially methylated peaks, with a predominant localization within coding sequences. Analysis of mA modification sites on HSV-2 gene transcripts from MeRIP-seq data identified a total of 145 mA sites across 63 viral genes. Functional enrichment analysis revealed that differentially mA-modified genes are involved in key biological processes, including gene expression, neural signaling, and immune responses. Pathway analysis highlighted significant enrichment in the NOD-like receptor signaling pathway, Rap1 signaling, endocytosis, and adherens junction pathways. RNA-seq analysis identified 6172 differentially expressed genes, of which 3181 were upregulated and 2991 were downregulated. Integrative analysis of the two datasets revealed that genes exhibiting both altered mA methylation and differential expression were significantly enriched in pathways including TNF signaling and the NOD-like receptor pathway. This study provides the first comprehensive landscape of mA epitranscriptomic modifications and their association with transcriptomic reprogramming during HSV-2 infection, offering new insights into the epigenetic mechanisms of virus-host interactions.]]> Wed, 31 Dec 1969 19:00:00 EST Evaluating ancestry adjustment in multi-ancestry epigenome-wide analysis. Liu Y, Kuang A, Hivert MF, Lowe WL, Josefson JL, Scholtens DM
Epigenetics (Dec 2026)

Proper adjustment for population substructure is essential in epigenome-wide association studies (EWAS), particularly in cohorts with diverse ancestries. EPISTRUCTURE offers a genotype-free approach to ancestry inference, originally developed using a European reference population from the Cooperative Health Research in the Region of Augsburg (KORA) study. However, its effectiveness in genetically diverse, multi-ancestry cohorts remains insufficiently evaluated. For EWAS using cord-blood samples from the Hyperglycemia and Adverse Pregnancy Outcome (HAPO) study, we systematically assessed the ancestry adjustment performance of EPISTRUCTURE principal components (PCs) derived from the widely used KORA-based reference set versus new reference sets generated from genotyping data of the multi-ancestry HAPO cohort. HAPO-based reference sets were defined by varying SNP - CpG thresholds (e.g. RS30: ) to identify ancestry-informative CpGs. We applied these reference sets for population substructure adjustment in EWAS of three newborn adiposity traits, birthweight, cord C-peptide, and sum of skinfolds, to evaluate their impact on association detection and biological interpretation. Compared to the KORA reference, the HAPO RS30 reference consistently produced lower genomic inflation and identified more biologically relevant associations for birthweight and cord blood C-peptide in EWAS of HAPO cord blood samples ( = 3,116). Pathway enrichment analyses revealed strong immune and metabolic signals, including pathways uniquely captured by EWAS when using the HAPO-derived reference for ancestry adjustment. Trait enrichment using the EWAS Catalog further confirmed associations with fetal growth, maternal metabolic traits, and glucose regulation. Our findings demonstrate that reference sets derived from multi-ancestry cohorts like HAPO better capture underlying population substructure and improve ancestry adjustment in diverse EWAS settings.]]> Wed, 31 Dec 1969 19:00:00 EST Population Epigenetics: Deciphering DNA Methylation Diversity and its Implications for Health, Disease, and Evolution. Cheng S, Xu S
Mol Biol Evol (Jul 2026)

Population epigenetics investigates the distribution, determinants, and evolutionary significance of epigenetic variation, particularly DNA methylation (DNAm), within and among human populations. In this review, we synthesize recent advances in population epigenetics with an explicit evolutionary perspective, focusing on three interconnected dimensions. First, we outline patterns of DNAm variation, including tissue- and cell-, and developmental-stage specificity. Second, we examine the sources of DNAm variation, highlighting population-specific methylation quantitative trait loci, ancestry-related genetic architecture, and environmental modulators such as diet, climate, pollution, and lifestyle. Third, we explore evolutionary and clinical implications, linking DNAm variation to phenotypic plasticity, disease susceptibility, and adaptive processes shaped by natural selection. Comparative population studies demonstrate that genetic ancestry accounts for a substantial proportion of DNAm differentiation, reflecting the joint effects of allele-frequency divergence, linkage disequilibrium structure, and demographic history. At the same time, environmentally induced methylation changes introduce a dynamic and rapidly responsive layer of molecular diversity that can mediate short-term adaptation to local environments. Despite rapid progress, key challenges remain, including disentangling genetic, environmental, and technical confounders, assessing the stability and heritability of population-specific DNAm patterns, and establishing causal links between methylation, fitness-related traits, and selection. Looking ahead, advances in large-scale multi-ancestry cohorts, single-cell and long-read epigenomics, and integrative multi-omics will enable high-resolution mapping of epigenetic variation across populations. By bridging evolutionary theory, epigenetic epidemiology, and functional genomics, population epigenetics offers a powerful framework for understanding human adaptation, health disparities, and precision medicine in an evolutionary context.]]> Wed, 31 Dec 1969 19:00:00 EST Global analyses of genomic and epigenomic influences on gene expression reveal as a major regulator of cardiac gene expression in response to catecholamine challenge during heart failure. Lahue C, Ravindran S, Dalal A, Avetisyan R, Rau CD
Epigenetics (Dec 2026)

Heart failure arises from maladaptive remodelling driven by genetic and epigenetic networks. Using a systems genetics framework, we mapped how DNA variants and CpG methylation shape cardiac transcriptomes during beta adrenergic stress in the Hybrid Mouse Diversity Panel, a cohort of over 100 fully inbred mouse strains. Expression QTLs (eQTLs), methylation QTLs (mQTLs) and methylation-driven eQTLs (emQTLs) were generated from over 13k expressed genes and 200k hypervariable CpGs in left ventricles. We discovered hundreds of regulatory 'hotspots' that control large portions of the genome, including several that regulate over 10% of the transcriptome and/or methylome. Approximately 16% of these hotspots overlapped with prior GWAS or EWAS signals. We focus on a hotspot on chromosome 12 and identify the serpine peptidase inhibitor , as the most likely driver gene in this hotspot. Experimental knockdown of in neonatal rat ventricular cardiomyocytes blunted hypertrophy induced by a variety of hypertrophic signals, while altering predicted target expression and modulating the activity of and . Together, these findings position as a major regulator of stress-responsive cardiac gene programs, highlighting how integration of genetic and epigenetic signals can pinpoint key drivers of heart failure.]]> Wed, 31 Dec 1969 19:00:00 EST RNA methylation in kidney disorders: Insights into molecular machinery and therapeutic opportunities. Li Z, Chen Y, Zhang X, Lv J, Chen J, Chen D, Yao Q
Cell Signal (Sep 2026)

Kidney disorders, including acute kidney injury (AKI), chronic kidney disease (CKD), diabetic nephropathy (DN), and clear cell renal cell carcinoma (ccRCC), represent major causes of morbidity and mortality worldwide and remain significant challenges in clinical management because of their complex pathogenesis and limited therapeutic options. Recent advances in epitranscriptomics have highlighted RNA methylation as an important post-transcriptional regulatory mechanism involved in renal physiology and disease development. Diverse RNA modifications, including N6-methyladenosine (m6A), 5-methylcytosine (m5C), N1-methyladenosine (m1A), N7-methylguanosine (m7G), and 3-methylcytidine (m3C), dynamically regulate RNA metabolism by affecting transcript stability, translation, splicing, and degradation. Increasing evidence demonstrates that RNA methylation regulators, including methyltransferases such as METTL3 and METTL14, demethylases such as FTO and ALKBH5, and reader proteins such as YTH domain-containing family members, participate in multiple pathogenic processes, including inflammation, fibrosis, oxidative stress, metabolic dysregulation, and tumor progression in renal disorders. Aberrant expression of these regulators has been closely associated with disease severity and progression. In this review, we summarize current knowledge regarding major RNA methylation modifications and their regulatory machinery in a spectrum of kidney diseases, with particular emphasis on the molecular mechanisms through which RNA methylation influences renal injury and repair. We further discuss the emerging value of RNA methylation-related molecules as potential biomarkers and therapeutic targets, aiming to provide new insights into epitranscriptomic regulation in kidney disease and its translational potential.]]> Wed, 31 Dec 1969 19:00:00 EST The role of RNA modifications in cancer translational control. Joy M, Cleynen A, Shirokikh NE
RNA Biol (Dec 2026)

RNA modifications have emerged as central regulators of cancer translational control. Unlike transcriptional reprogramming, which unfolds over hours, modification-dependent translational rewiring enables rapid proteomic adaptation to the nutrient-deprived, hypoxic, and immunologically hostile tumour microenvironment. Yet most existing reviews organize epitranscriptomic mechanisms by modification type or cancer hallmark, obscuring the mechanistic logic by which chemical marks collectively reshape the translational apparatus. This review adopts a translation-centric framework, examining how the most abundant modifications on mRNAs, tRNAs, and rRNAs regulate each stage of protein synthesis in malignant cells. We survey the epitranscriptomic toolkit, including modification chemistries, enzymatic writers, readers, and erasers, and detection technologies including nanopore direct RNA sequencing. We then trace how modifications control initiation (m6A-driven mRNA circularization, cap-independent translation eIF3 and eIF4G2, rRNA 2'-O-methylation-directed cap-to-IRES switching), elongation (m6A-induced ribosome stalling coupled to mRNA decay, tRNA mcm5s2U-mediated codon-biased translation, YTHDF1-dependent elongation factor recruitment), and termination (pseudouridine-mediated stop codon readthrough, NMD evasion). Crucially, we show that mRNA, tRNA, and rRNA modifications do not act in isolation but form integrated networks. For example, mRNA m6A and tRNA mcm5s2U operate on opposing arms of the same regulatory axis, with direct implications for therapeutic design. We assess the expanding drug pipeline, from the METTL3 inhibitor STC-15 now in Phase 1b/2 trials and METTL3-targeting PROTACs to FTO and ADAR1 inhibitors, and argue that biology-informed combination strategies targeting multiple modification axes will be essential for durable clinical responses.]]> Wed, 31 Dec 1969 19:00:00 EST Bridging the gaps in Alzheimer's disease biomarker research: From multi-omics integration to point-of-care diagnostics, a comprehensive review. Khasanov S, Tolibov M, Daminova N
Clin Chim Acta (Jul 2026)

Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder, yet its early and definitive diagnosis remains a formidable clinical challenge. Over the past decade, substantial progress has been made in the identification and validation of AD biomarkers across cerebrospinal fluid (CSF), blood, and emerging non-invasive biofluids. The core CSF biomarkers-amyloid-β (Aβ42), total tau (t-tau), and phosphorylated tau (p-tau)-have been integrated into revised diagnostic criteria, while blood-based biomarkers such as plasma p-tau217 and the Aβ42/Aβ40 ratio are approaching clinical readiness. Simultaneously, electrochemical biosensor technologies have demonstrated remarkable detection sensitivity at the femtomolar level, and multi-omics approaches combining metabolomics, lipidomics, proteomics, and epigenomics are revealing new molecular signatures of early AD. Despite these advances, several critical research questions remain unanswered, including how to optimally combine biomarkers across biofluids, how to translate biosensor technology from the laboratory to the clinic, how to integrate multi-omics data into practical diagnostic frameworks, how to validate non-invasive biofluid markers at clinical scale, and how to harmonize blood-based assays for global implementation. This review systematically examines the current state of AD biomarker science, identifies key unresolved challenges, evaluates the most promising existing approaches, and proposes specific methodological strategies to advance the field from discovery to clinical practice.]]> Wed, 31 Dec 1969 19:00:00 EST Interactions between nutrition and the epigenome: how can it be harnessed for public health? Anastasopoulou M, Dereki I, Sgourou A, Lagoumintzis G
Future Sci OA (Dec 2026)

A substantial body of evidence shows that dietary habits influence gene expression and epigenetic processes, holding significant implications for public health policies. Epigenetic modifications are increasingly associated with metabolic state, disease risk, and biological aging. Translating mechanistic results into scalable, efficient nutritional epigenetics treatments is difficult.]]> Wed, 31 Dec 1969 19:00:00 EST M6A-dependent regulation of microRNAs from CKD stage 5 patients: insights from epigenetic modification analysis. Yang Z, Liu F, Ye M, Yan Q, Zeng Z, Ma J, Li H, Ma H, Zhang X, Zhu X, Dai Y, Tang D
Epigenetics (Dec 2026)

Chronic kidney disease (CKD) stage 5 is frequently accompanied by systemic inflammation, and peripheral blood mononuclear cells (PBMCs) play an important role. To define the epitranscriptomic features of PBMC small RNAs in CKD stage 5, we profiled N6-methyladenosine (m6A) using small RNA modification microarrays. A total of 158 miRNAs, 149 pre-miRNAs, and 197 tsRNAs showed differential m6A modification. Enrichment analysis implicated PI3K-Akt, p53 signalling, and leukocyte transendothelial migration. Integrating target prediction with GEO transcriptomic datasets identified IRF1 and RUNX2 as key targets. MeRIP confirmed reduced m6A in miR-205-3p and miR-93-5p, accompanied by upregulation of RUNX2 and downregulation of IRF1 by qPCR. These results define an altered m6A-modification profile of PBMC small RNAs in CKD stage 5 and highlight miRNA-target gene axes with potential biomarker utility.]]> Wed, 31 Dec 1969 19:00:00 EST Advanced deep learning strategies in nanopore RNA sequencing. Ling C, Lebeau B, Keong KC, Fullwood M
RNA Biol (Dec 2026)

The epitranscriptome comprises chemical modifications found on RNA molecules that play essential roles in co- and post-transcriptional gene regulation. Dysregulation of these modifications has been implicated in various diseases, fuelling interest in evaluating them as emerging biomarkers and therapeutic targets. Nanopore direct RNA sequencing provides a powerful platform for profiling diverse RNA modifications at single-molecule resolution, but the complexity of the signals requires advanced computational approaches for interpretation. Artificial intelligence, particularly deep learning (DL), has become central to this effort. While classical DL architectures such as convolutional and recurrent neural networks have been widely applied, more recent approaches employ specialized learning frameworks and ensemble strategies to address challenges of data scarcity, noise, and biological variability while providing higher resolution output. In this review, we summarize these developments and highlight future multidisciplinary opportunities at the intersection of artificial intelligence and biology for characterizing the epitranscriptome obtained with direct RNA nanopore sequencing.]]> Wed, 31 Dec 1969 19:00:00 EST mA-Mediated epitranscriptomic control of mitochondrial dysfunction in neurodegeneration. Jauhari A
Mitochondrion (Sep 2026)

Mitochondrial dysfunction is a common pathology of neurodegenerative diseases, which contributes to neuronal vulnerability via excessive oxidative stress, impaired bioenergetics, and dysregulated apoptosis. Emerging studies highlighted the critical role of epitranscriptomic RNA modifications, particularly N-methyladenosine (mA), in mitochondrial gene expression regulation and cellular stress responses. mA modifications are installed by methyltransferases ("writers," METTL3/METTL14), recognized by reader proteins (YTH domain family proteins, IGF2BPs), and removed by demethylases ("erasers," FTO, ALKBH5), collectively orchestrating mRNA splicing, localization, stability, and translation. Recent evidence demonstrates that mA modifications modulate both nuclear-encoded and mitochondrially encoded transcripts and regulate key mitochondrial processes, including fission/fusion dynamics, oxidative phosphorylation, mitophagy, and apoptosis. Dysregulation of mA machinery disrupts mitochondrial homeostasis, exacerbates oxidative stress and neuroinflammation, and promotes neuronal loss. Importantly, pharmacological or genetic modulation of mA regulators can restore mitochondrial function, inhibit caspase activation, and dampen pro-inflammatory signaling, underscoring their therapeutic potential. This review consolidates current insights into mitochondrial epitranscriptomics, emphasizing how mA modifications act as central regulators of mitochondrial stress responses and neurodegeneration.]]> Wed, 31 Dec 1969 19:00:00 EST Melatonin-enabled omics: understanding plant responses to single and combined abiotic stresses for climate-smart agriculture. Raza A, Li Y, Charagh S, Guo C, Zhao M, Hu Z
GM Crops Food (Dec 2026)

Climate change-driven single and combined abiotic stresses pose escalating threats to sustainable, climate-smart agriculture and global food security. Melatonin (MLT, a powerful plant biostimulant) has established noteworthy potential in improving stress tolerance by regulating diverse physiological, biochemical, and molecular responses. Therefore, this review delivers a comprehensive synopsis of MLT-enabled omics responses across genomics, transcriptomics, proteomics, metabolomics, miRNAomics, epigenomics, phenomics, ionomics, and microbiomics levels that collectively regulate plant adaptation to multiple abiotic stresses. We also highlight the crosstalk between these omics layers and the power of integrated multi-omics (panomics) approaches to harness the complex regulatory networks underlying MLT-enabled stress tolerance. Lastly, we argue for translating these omics insights into actionable strategies through advanced genetic engineering and synthetic biology platforms to develop MLT-enabled, stress-smart crop plants.]]> Wed, 31 Dec 1969 19:00:00 EST The role of RNA modifications in the pathological mechanisms and therapeutic targeting of multiple myeloma. Chen H, Ren H, Wang X, Liu C, Jiang L, Zang S, Liu T, Wang S, Huang W, Zhou L
Mol Cell Probes (Aug 2026)

Multiple myeloma (MM) remains largely incurable despite major therapeutic advances, underscoring the need to define novel pathogenic mechanisms and druggable targets. Epitranscriptomic dysregulation, encompassing reversible chemical modifications on RNA, has emerged as a post-transcriptional regulatory layer that may contribute to MM biology. This focused review discusses the emerging roles of major RNA modifications and their regulators in MM pathogenesis, bone disease, drug resistance, and immune escape. We summarize representative experimental and translational studies on RNA-modifying enzymes, non-coding RNAs, and the bone marrow microenvironment, with emphasis on mechanisms directly validated in MM. Evidence derived from AML, solid tumors, or pan-cancer analyses is discussed as hypothesis-generating and requiring MM-specific validation. We summarize MM-supported evidence that m6A demethylases such as FTO and ALKBH5, as well as writers such as METTL3 and NSUN2, may regulate the stability and translation of disease-relevant transcripts. We also discuss emerging cross-cancer data on the m7G writer METTL1 as a hypothesis-generating framework that requires MM-specific validation. We delineate how RNA modification-dependent non-coding RNA networks and extracellular vesicle cargo remodel osteoclast and osteoblast function, linking the epitranscriptome to osteolytic bone disease. We further describe RNA modification-driven drug resistance circuits and immune escape pathways involving FTO, METTL3, H19, MALAT1, YTHDF1, and m5C-defined molecular subtypes. Finally, we summarize current epitranscriptomic therapeutic strategies, including small molecule inhibitors of writers, erasers, and readers, RNA-based therapeutics targeting pathogenic non-coding RNAs, and RNA modification-derived prognostic signatures for risk stratification. Collectively, this review discusses RNA-modification machinery as a potentially actionable regulatory layer in MM and outlines key challenges for clinical translation.]]> 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 Dissecting Allele-Specific Expression (ASE) in Landrace × Meishan Cross Pig Fetal-Placental Tissues: Distribution, Functional Split, and Mechanisms. Zhang J, Xu S, Wu W, Zhang L, Jiang A, Shen M, Tao J, Liu H, Pan Z
FASEB J (Jul 2026)

Allele-specific expression (ASE) is a key regulatory mechanism linking genetic variation to phenotypic diversity. This study conducted a genome-wide ASE analysis in embryonic (brain, kidney, liver) and extraembryonic (chorion) tissues of Landrace × Meishan crossbred pigs. By integrating DNA sequencing of parental and F1 hybrids and RNA-sequencing of F1 tissues, a high-resolution ASE landscape was built via strict allele-specific SNP identification. Genomically, ASE genes (ASEG) were enriched on chromosomes 6, 7, 12, X and sparse on chromosome 11, and can be classified into extreme/moderate types by expression pattern and parental bias. Paternal ASEGs had higher expression levels, while maternal ones had higher abundance. Functionally, tissue-concordant ASEGs supported embryo/placenta basal development, tissue-specific ones matched organ core functions; maternal ASEGs were enriched in mitochondrial pathways, paternal ones in cell motility and RNA transcription. Besides, chorion had more allele-specific methylated regions than embryonic tissues, with opposite ASE directions. We proposed "orthogonal dual regulatory dimensions" for the relationship between ASE and tissue-specific expression. We also proposed regulatory models of extreme and moderate ASEGs, functional division modes between embryo and extraembryonic tissues, and between paternal and maternal alleles. This study clarifies tissue-specific ASE patterns and mechanisms, providing a framework for future ASE research.]]> Wed, 31 Dec 1969 19:00:00 EST Roles of mA erasers FTO and ALKBH5 in drug resistance of hepatocellular carcinoma: mechanisms and clinical implications. Wen Q, Liu C, Li C, Yuan X
Gene (Oct 2026)

Hepatocellular carcinoma (HCC) is a highly lethal malignant tumor with substantial heterogeneity, posing formidable challenges to overcoming drug resistance. Accumulating evidence highlights the pivotal role of epitranscriptomic regulation, particularly N6-methyladenosine (mA) modification, in reshaping tumor drug resistance. This review elaborates on the dual functions and mechanisms of mA erasers FTO and ALKBH5 in HCC drug resistance. In cancer cells, these erasers post-transcriptionally regulate key transcripts to orchestrate metabolic reprogramming, enhance anti-apoptotic signaling, and sustain cancer stem cell properties. In the tumor microenvironment, they facilitate immune suppression by modulating chemokines and immune checkpoint molecules, driving the transition from immune-active to immune-suppressive tumors. Translational studies show FTO and ALKBH5 are promising dynamic biomarkers for predicting treatment responses and monitoring drug resistance. Small-molecule inhibitors targeting these erasers offer a potential strategy to surmount HCC drug resistance. Finally, we emphasize single-cell transcriptomics to dissect mA heterogeneity in "resistance niches," constructing a comprehensive epitranscriptomic landscape for precise personalized HCC treatment.]]> Wed, 31 Dec 1969 19:00:00 EST Recent Advances in Epigenetic Signatures of Nanomaterial Exposure Linked to Neurotoxicity. Liu K, Wu T
J Appl Toxicol (Jul 2026)

Nanomaterials are used in medical, industrial, and consumer settings, but their effects on the nervous system remain difficult to interpret because different materials vary widely in composition, size, surface chemistry, and exposure behavior. Epigenetic regulation provides a possible link between these material-dependent exposures and changes in neural function. This review critically discusses evidence that nanomaterials may alter DNA methylation, histone modifications, noncoding RNA expression, RNA modifications, chromatin organization, and genomic imprinting in models relevant to neurotoxicity. Rather than considering nanomaterials as a uniform class, we emphasize how epigenetic responses differ according to material properties, exposure route, dose, exposure duration, developmental stage, and biological model. These changes have been associated with oxidative stress, neuroinflammation, glial activation, blood-brain barrier dysfunction, impaired synaptic signaling, neuronal injury, and altered neurodevelopment. Evidence from gut-brain, lung-brain, and liver-brain interactions further suggests that peripheral tissues may shape the timing and regional pattern of nanomaterial-related neural injury. However, many reported epigenetic changes remain correlative, and findings from nonneural cells or high-dose short-term exposure models should not be directly generalized to the central nervous system. Future work should improve exposure characterization, distinguish direct neural evidence from indirect mechanistic evidence, and test whether specific epigenetic changes have predictive or causal value in nanomaterial-induced neurotoxicity through longitudinal, dose-responsive, and functional perturbation studies.]]> Wed, 31 Dec 1969 19:00:00 EST Differential A-to-I editing of SINE B2 RNAs unveils an epitranscriptome response to Aβ neurotoxicity. Mitchell L, Saville L, Gollen B, Haight T, Roy R, Turner C, Cheng Y, Kovalchuk I, Mohajerani MH, Zovoilis A
Life Sci Alliance (Sep 2026)

Adenosine-to-inosine (A-to-I) RNA editing is a major epitranscriptomic mechanism, yet its contribution to non-coding RNA regulation during neurodegeneration is largely unknown. SINE B2 RNAs represent the dominant editing substrates in mice and have been shown to regulate gene expression. Here, we introduce and validate a repeat-aware bioinformatics framework that enables position-specific quantification of A-to-I editing within SINE RNAs, which has been challenging using standard genome-based pipelines. Applying this approach, we identify discrete editing hotspots in mouse SINE B2 RNAs that are selectively increased during early amyloid beta pathology in independent mouse models and in hippocampal neurons exposed to amyloid beta toxicity. Functional perturbation of ADAR activity alters both B2 RNA editing levels and the expression of B2 RNA-regulated genes, directly linking RNA editing to SINE-mediated transcriptional control. Nanopore sequencing confirmed increased RNA modification signals at these regions. Together, our findings establish a previously unrecognized epitranscriptomic response to amyloid beta neurotoxicity mediated by site-specific A-to-I editing of SINE RNAs.]]> Wed, 31 Dec 1969 19:00:00 EST Genomic Imprinting: Common Threads Uniting Diverse Biological Systems. Emmerson RA, Mosher RA
Annu Rev Genet (Jul 2026)

Genomic imprinting is an epigenetic phenomenon in which chromosome behavior or gene expression depends on whether an allele was paternally or maternally inherited. Imprinting is commonly associated with a placenta or an analogous organ during embryo development; however, imprinting occurs in diverse species across animal and plant life, including those that lack a placenta. Common epigenetic modifications are associated with genome imprinting across these groups, although the exact mechanisms vary across taxa. There are also commonalities surrounding the evolutionary selection for imprinting. The most well-known hypothesis is parental conflict theory, which proposes that imprinting resolves conflict over the maternal allocation of resources to the developing embryo. Shared mechanisms and functions of imprinting across diverse groups suggest that parental epigenetic asymmetries may be an inherent characteristic of sexual reproduction in species where the sperm and egg differ in size and form.]]> Wed, 31 Dec 1969 19:00:00 EST