'; ?> 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, 22 Jan 2020 03:05:08 EST Wed, 22 Jan 2020 03:05:08 EST jirtle@radonc.duke.edu james001@jirtle.com Short AIP1 (ASK1-Interacting Protein-1) Isoform Localizes to the Mitochondria and Promotes Vascular Dysfunction. Li Z, Li L, Zhang H, Zhou HJ, Ji W, Min W
Arterioscler Thromb Vasc Biol (Jan 2020)

Vascular endothelial cells (ECs) normally maintain vascular homeostasis and are regulated by proinflammatory cytokines and reactive oxygen species. A human genome-wide association study identified that (ASK1 [apoptosis signal-regulating kinase 1]-interacting protein-1; also identified as ) gene variants confer susceptibility to cardiovascular disease, but the underlying mechanism is unknown. Approach and Results: We detected a normal AIP1 form (named AIP1A) in the healthy aorta, but a shorter form of AIP1 (named AIP1B) was found in diseased aortae that contained atherosclerotic plaques and graft arteriosclerosis. AIP1B transcription in resting ECs was suppressed through epigenetic inhibition by RIF1 (Rap1 [ras-related protein 1]-interacting factor 1)/H3K9 (histone H3 lysine 9) methyltransferase-mediated H3K9 trimethylation, and this inhibition was released by proinflammatory cytokines. AIP1A, but not AIP1B, was downregulated by proteolytic degradation through a Smurf1 (SMAD [suppressor of mothers against decapentaplegic miscellaneous] ubiquitylation regulatory factor 1)-dependent pathway in ECs under inflammation. Therefore, AIP1B was the major form present during inflammatory conditions. AIP1B, which lacks the N-terminal pleckstrin homology domain of AIP1A, localized to the mitochondria and augmented TNFα (tumor necrosis factor alpha)-induced mitochondrial reactive oxygen species generation and EC activation. AIP1B-ECTG (EC-specific AIP1B transgenic) mice exhibited augmented reactive oxygen species production, EC activation, and neointima formation in vascular remodeling models.]]> Wed, 31 Dec 1969 19:00:00 EST Genome-wide analysis of epigenetic and transcriptional changes associated with heterosis in pigeonpea. Sinha P, Singh VK, Saxena RK, Kale SM, Li Y, Garg V, Tang M, Khan AW, Kim KD, Chitikineni A, Saxena KB, Sameer Kumar CV, Liu X, Xu X, Jackson S, Powell W, Nevo E, Searle IR, Lodha M, Varshney RK
Plant Biotechnol J (Jan 2020)

Hybrids are extensively used in agriculture to deliver an increase in yield, yet the molecular basis of heterosis is not well understood. Global DNA methylation analysis, transcriptome analysis and small RNA profiling were aimed to understand the epigenetic effect of the changes in gene expression level in the two hybrids and their parental lines. Increased DNA methylation was observed in both the hybrids as compared to their parents. This increase DNA methylation in hybrids showed that majority of the 24-nt sRNA clusters had higher expression in hybrids than the parents. Transcriptome analysis revealed that various phytohormones (auxin and salicylic acid) responsive hybrid-MPV DEGs were significantly altered in both the hybrids in comparison to MPV. DEGs associated with plant immunity and growth were overexpressed whereas DEGs associated with basal defense level were repressed. This antagonistic patterns of gene expression might contribute to the greater growth of the hybrids. It was also noticed that some common as well as unique changes in regulatory pathways associated with heterotic growth in both the hybrids. Approximately 70% and 67% of down-regulated hybrid-MPV DEGs were found to be differentially methylated in ICPH 2671 and ICPH 2740 hybrid, respectively. This reflected the association of epigenetic regulation in altered gene expressions. Our findings also revealed that miRNAs might play important roles in hybrid vigor in both the hybrids by regulating their target genes, especially in controlling plant growth and development, defense and stress response pathways. The above finding provides an insight into the molecular mechanism of pigeonpea heterosis.]]> Wed, 31 Dec 1969 19:00:00 EST Epigenetics/epigenomics and prevention by curcumin of early stages of inflammatory-driven colon cancer. Wu R, Wang L, Yin R, Hudlikar R, Li S, Kuo HD, Peter R, Sargsyan D, Guo Y, Liu X, Kong AT
Mol Carcinog (Feb 2020)

Colorectal cancer (CRC) is associated with significant morbidity and mortality in the US and worldwide. CRC is the second most common cancer-related death in both men and women globally. Chronic inflammation has been identified as one of the major risk factors of CRC. It may drive genetic and epigenetic/epigenomic alterations, such as DNA methylation, histone modification, and non-coding RNA regulation. Current prevention modalities for CRC are limited and some treatment regimens such as use the nonsteroidal anti-inflammatory drug aspirin may have severe side effects, namely gastrointestinal ulceration and bleeding. Therefore, there is an urgent need of developing alternative strategies. Recently, increasing evidence suggests that several dietary cancer chemopreventive phytochemicals possess anti-inflammation and antioxidative stress activities, and may prevent cancers including CRC. Curcumin (CUR) is the yellow pigment that is found in the rhizomes of turmeric (Curcuma longa). Many studies have demonstrated that CUR exhibit strong anticancer, antioxidative stress, and anti-inflammatory activities by regulating signaling pathways, such as nuclear factor erythroid-2-related factor 2, nuclear factor-κB, and epigenetics/epigenomics pathways of histones modifications, and DNA methylation. In this review, we will discuss the latest evidence in epigenetics/epigenomics alterations by CUR in CRC and their potential contribution in the prevention of CRC.]]> Wed, 31 Dec 1969 19:00:00 EST The role of environmental exposures and the epigenome in health and disease. Perera BPU, Faulk C, Svoboda LK, Goodrich JM, Dolinoy DC
Environ Mol Mutagen (Jan 2020)

The genetic material of every organism exists within the context of regulatory networks that govern gene expression, collectively called the epigenome. Epigenetics has taken center stage in the study of diseases such as cancer and diabetes, but its integration into the field of environmental health is still emerging. As the Environmental Mutagenesis and Genomics Society (EMGS) celebrates its 50th Anniversary this year, we have come together to review and summarize the seminal advances in the field of environmental epigenomics. Specifically, we focus on the role epigenetics may play in multigenerational and transgenerational transmission of environmentally induced health effects. We also summarize state of the art techniques for evaluating the epigenome, environmental epigenetic analysis, and the emerging field of epigenome editing. Finally, we evaluate transposon epigenetics as they relate to environmental exposures and explore the role of noncoding RNA as biomarkers of environmental exposures. Although the field has advanced over the past several decades, including being recognized by EMGS with its own Special Interest Group, recently renamed Epigenomics, we are excited about the opportunities for environmental epigenetic science in the next 50 years. Environ. Mol. Mutagen. 61:176-192, 2020. © 2019 Wiley Periodicals, Inc.]]> Wed, 31 Dec 1969 19:00:00 EST A road map for understanding molecular and genetic determinants of osteoporosis. Yang TL, Shen H, Liu A, Dong SS, Zhang L, Deng FY, Zhao Q, Deng HW
Nat Rev Endocrinol (Feb 2020)

Osteoporosis is a highly prevalent disorder characterized by low bone mineral density and an increased risk of fracture, termed osteoporotic fracture. Notably, bone mineral density, osteoporosis and osteoporotic fracture are highly heritable; however, determining the genetic architecture, and especially the underlying genomic and molecular mechanisms, of osteoporosis in vivo in humans is still challenging. In addition to susceptibility loci identified in genome-wide association studies, advances in various omics technologies, including genomics, transcriptomics, epigenomics, proteomics and metabolomics, have all been applied to dissect the pathogenesis of osteoporosis. However, each technology individually cannot capture the entire view of the disease pathology and thus fails to comprehensively identify the underlying pathological molecular mechanisms, especially the regulatory and signalling mechanisms. A change to the status quo calls for integrative multi-omics and inter-omics analyses with approaches in 'systems genetics and genomics'. In this Review, we highlight findings from genome-wide association studies and studies using various omics technologies individually to identify mechanisms of osteoporosis. Furthermore, we summarize current studies of data integration to understand, diagnose and inform the treatment of osteoporosis. The integration of multiple technologies will provide a road map to illuminate the complex pathogenesis of osteoporosis, especially from molecular functional aspects, in vivo in humans.]]> Wed, 31 Dec 1969 19:00:00 EST Targeting epigenetic regulators in the treatment of T-cell lymphoma. Ahmed N, Feldman AL
Expert Rev Hematol (Jan 2020)

: T-cell lymphomas represent a broad group of malignant T-cell neoplasms with marked molecular, clinical, and biologic heterogeneity. Survival rates after conventional chemotherapy regimens are poor for most subtypes and new therapies are needed. Rapidly expanding knowledge in the field of epigenomics and the development of an increasing number of epigenetic modifying agents have created new opportunities for epigenetic therapies for patients with this complex group of diseases.: The present review summarizes current knowledge on epigenetic alterations in T-cell lymphomas, availability and mechanisms of action of epigenetic modifying agents, results of clinical trials of epigenetic therapies in T-cell lymphomas, status of FDA approval, and biomarker approaches to guide therapy. Promising future directions are discussed.: Mutations in epigenetic modifying genes are among the most common genetic alterations in T-cell lymphomas, highlighting the potential for epigenetic therapies to improve management of this group of diseases. Single-agent efficacy is well documented, leading to FDA approval for several indications, but overall response rates and durability of responses remain modest. Critical next steps for the field include optimizing combination therapies that incorporate epigenetic modifying agents and developing predictive biomarkers that help guide patient and drug selection.]]> Wed, 31 Dec 1969 19:00:00 EST Epigenetic reprogramming in periodontal disease: Dynamic crosstalk with potential impact in oncogenesis. Barros SP, Fahimipour F, Tarran R, Kim S, Scarel-Caminaga RM, Justice A, North K
Periodontol 2000 (Feb 2020)

Periodontitis is a chronic multifactorial inflammatory disease associated with microbial dysbiosis and characterized by progressive destruction of the periodontal tissues. Such chronic infectious inflammatory disease is recognized as a major public health problem worldwide with measurable impact in systemic health. It has become evident that the periodontal disease phenotypes are not only determined by the microbiome effect, but the extent of the tissue response is also driven by the host genome and epigenome patterns responding to various environmental exposures. More recently there is mounting evidence indicating that epigenetic reprogramming in response to combined intrinsic and environmental exposures, might be particularly relevant due its plasticity and potential application towards precision health. The complex epigenetic crosstalk is reflected in the prognosis and progress of periodontal diseases and may also lead to a favorable landscape for cancer development. This review discusses epigenomics modifications focusing on the role of DNA methylation and pathways linking microbial infection and inflammatory pathways, which are also associated with carcinogenesis. There is a more clear vision whereas 'omics' technologies applied to unveil relevant epigenetic factors could play a significant role in the treatment of periodontal disease in a personalized mode, evidencing that public health approach should coexist with precision individualized treatment.]]> Wed, 31 Dec 1969 19:00:00 EST Understanding osteoarthritis pathogenesis: a multiomics system-based approach. Ratneswaran A, Rockel JS, Kapoor M
Curr Opin Rheumatol (Jan 2020)

Osteoarthritis is a heterogeneous, multifactorial condition regulated by complex biological interactions at multiple levels. Comprehensive understanding of these regulatory interactions is required to develop feasible advances to improve patient outcomes. Improvements in technology have made extensive genomic, transcriptomic, epigenomic, proteomic, and metabolomic profiling possible. This review summarizes findings over the past 20 months related to omics technologies in osteoarthritis and examines how using a multiomics approach is necessary for advancing our understanding of osteoarthritis as a disease to improve precision osteoarthritis treatments.]]> Wed, 31 Dec 1969 19:00:00 EST Museum Epigenomics: Charting the Future by Unlocking the Past. Hahn EE, Grealy A, Alexander M, Holleley CE
Trends Ecol Evol (Jan 2020)

Epigenomic state preserved in museum specimens could be leveraged to provide unique insights into gene regulation trends associated with accelerating environmental change during the Anthropocene. We address the challenges facing museum epigenomics and propose a collaborative framework for researchers and curators to explore this new field.]]> Wed, 31 Dec 1969 19:00:00 EST Epigenetic Modifications in T Cells: The Role of DNA Methylation in Salt-Sensitive Hypertension. Dasinger JH, Alsheikh AJ, Abais-Battad JM, Pan X, Fehrenbach DJ, Lund H, Roberts ML, Cowley AW, Kidambi S, Kotchen TA, Liu P, Liang M, Mattson DL
Hypertension (Feb 2020)

The SS (Dahl salt sensitive) rat is an established model of hypertension and renal damage that is accompanied with immune system activation in response to a high-salt diet. Investigations into the effects of sodium-independent and dependent components of the diet were shown to affect the disease phenotype with SS/MCW (JrHsdMcwi) rats maintained on a purified diet (AIN-76A) presenting with a more severe phenotype relative to grain-fed SS/CRL (JrHsdMcwiCrl) rats. Since contributions of the immune system, environment, and diet are documented to alter this phenotype, this present study examined the epigenetic profile of T cells isolated from the periphery and the kidney from these colonies. T cells isolated from kidneys of the 2 colonies revealed that transcriptomic and functional differences may contribute to the susceptibility of hypertension and renal damage. In response to high-salt challenge, the methylome of T cells isolated from the kidney of SS/MCW exhibit a significant increase in differentially methylated regions with a preference for hypermethylation compared with the SS/CRL kidney T cells. Circulating T cells exhibited similar methylation profiles between colonies. Utilizing transcriptomic data from T cells isolated from the same animals upon which the DNA methylation analysis was performed, a predominant negative correlation was observed between gene expression and DNA methylation in all groups. Lastly, inhibition of DNA methyltransferases blunted salt-induced hypertension and renal damage in the SS/MCW rats providing a functional role for methylation. This study demonstrated the influence of epigenetic modifications to immune cell function, highlighting the need for further investigations.]]> Wed, 31 Dec 1969 19:00:00 EST CHROMATIX: computing the functional landscape of many-body chromatin interactions in transcriptionally active loci from deconvolved single cells. Perez-Rathke A, Sun Q, Wang B, Boeva V, Shao Z, Liang J
Genome Biol (Jan 2020)

Chromatin interactions are important for gene regulation and cellular specialization. Emerging evidence suggests many-body spatial interactions play important roles in condensing super-enhancer regions into a cohesive transcriptional apparatus. Chromosome conformation studies using Hi-C are limited to pairwise, population-averaged interactions; therefore unsuitable for direct assessment of many-body interactions. We describe a computational model, CHROMATIX, which reconstructs ensembles of single-cell chromatin structures by deconvolving Hi-C data and identifies significant many-body interactions. For a diverse set of highly active transcriptional loci with at least 2 super-enhancers, we detail the many-body functional landscape and show DNase accessibility, POLR2A binding, and decreased H3K27me3 are predictive of interaction-enriched regions.]]> Wed, 31 Dec 1969 19:00:00 EST Using What We Already Have: Uncovering New Drug Repurposing Strategies in Existing Omics Data. Pulley JM, Rhoads JP, Jerome RN, Challa AP, Erreger KB, Joly MM, Lavieri RR, Perry KE, Zaleski NM, Shirey-Rice JK, Aronoff DM
Annu Rev Pharmacol Toxicol (Jan 2020)

The promise of drug repurposing is to accelerate the translation of knowledge to treatment of human disease, bypassing common challenges associated with drug development to be more time- and cost-efficient. Repurposing has an increased chance of success due to the previous validation of drug safety and allows for the incorporation of omics. Hypothesis-generating omics processes inform drug repurposing decision-making methods on drug efficacy and toxicity. This review summarizes drug repurposing strategies and methodologies in the context of the following omics fields: genomics, epigenomics, transcriptomics, proteomics, metabolomics, microbiomics, phenomics, pregomics, and personomics. While each omics field has specific strengths and limitations, incorporating omics into the drug repurposing landscape is integral to its success.]]> Wed, 31 Dec 1969 19:00:00 EST Brain Development in School-Age and Adolescent Girls: Effects of Turner Syndrome, Estrogen Therapy, and Genomic Imprinting. O'Donoghue S, Green T, Ross JL, Hallmayer J, Lin X, Jo B, Huffman LC, Hong DS, Reiss AL
Biol Psychiatry (Jan 2020)

The study of Turner syndrome (TS) offers a unique window of opportunity for advancing scientific knowledge of how X chromosome gene imprinting, epigenetic factors, hormonal milieu, and chronologic age affect brain development in females.]]> Wed, 31 Dec 1969 19:00:00 EST Understanding epigenomics based on the rice model. Lu Y, Zhou DX, Zhao Y
Theor Appl Genet (Jan 2020)

The purpose of this paper provides a comprehensive overview of the recent researches on rice epigenomics, including DNA methylation, histone modifications, noncoding RNAs, and three-dimensional genomics. The challenges and perspectives for future research in rice are discussed. Rice as a model plant for epigenomic studies has much progressed current understanding of epigenetics in plants. Recent results on rice epigenome profiling and three-dimensional chromatin structure studies reveal specific features and implication in gene regulation during rice plant development and adaptation to environmental changes. Results on rice chromatin regulator functions shed light on mechanisms of establishment, recognition, and resetting of epigenomic information in plants. Cloning of several rice epialleles associated with important agronomic traits highlights importance of epigenomic variation in rice plant growth, fitness, and yield. In this review, we summarize and analyze recent advances in rice epigenomics and discuss challenges and directions for future research in the field.]]> Wed, 31 Dec 1969 19:00:00 EST Placental effects on the maternal brain revealed by disrupted placental gene expression in mouse hybrids. Arévalo L, Campbell P
Proc Biol Sci (Jan 2020)

The mammalian placenta is both the physical interface between mother and fetus, and the source of endocrine signals that target the maternal hypothalamus, priming females for parturition, lactation and motherhood. Despite the importance of this connection, the effects of altered placental signalling on the maternal brain are insufficiently studied. Here, we show that placental dysfunction alters gene expression in the maternal brain, with the potential to affect maternal behaviour. Using a cross between the house mouse and the Algerian mouse, in which hybrid placental development is abnormal, we sequenced late-gestation placental and maternal medial preoptic area transcriptomes and quantified differential expression and placenta-maternal brain co-expression between normal and hybrid pregnancies. The expression of and was significantly altered in the brains of females exposed to hybrid placentas. Most strikingly, expression patterns of placenta-specific gene families and in the brains of house mouse females carrying hybrid litters matched those of female Algerian mice, the paternal species in the cross. Our results indicate that the paternally derived placental genome can influence the expression of maternal-fetal communication genes, including placental hormones, suggesting an effect of the offspring's father on the mother's brain.]]> Wed, 31 Dec 1969 19:00:00 EST Single Cell Omics: From Assay Design to Biomedical Application. Chen W, Li S, Kulkarni AS, Huang L, Cao J, Qian K, Wan J
Biotechnol J (Jan 2020)

Given the existence of cell heterogeneity, single cell analysis is undergoing a rapid expansion for life science and precision medicine. Recent numerous innovations in analytical platforms and instruments have re-energized the field and led to the emergence of single cell omics with high sensitivity, throughput and multiplexity. The omics knowledge builds the bridge between underlying molecular changes and cell behavior, and facilitates a deeper understanding of disease development processes. Here, the authors highlight important achievements of single cell omics mainly including genomics, epigenomics, transcriptomics, proteomics, and metabolomics, and discuss the biomedical applications of single cell omics in stem cells differentiation, immune cells function, nerve cells development and activity, and circulating tumor cells based cancer research.]]> Wed, 31 Dec 1969 19:00:00 EST Identification of a Novel Imprinted Transcript in the Porcine Complex Locus Using Methylome and Transcriptome of Parthenogenetic Fetuses. Ahn J, Wu H, Lee J, Hwang IS, Yu D, Ahn JS, Lee JW, Hwang S, Lee K
Genes (Basel) (Jan 2020)

Genomic imprinting in domestic animals contributes to the variance of performance traits. However, research remains to be done on large-scale detection of epigenetic landscape of porcine imprinted loci including the GNAS complex locus. The purpose of this study was to generate porcine parthenogenetic fetuses and comprehensively identify imprinting patterns of the GNAS locus in transcript levels. To this end, both normally fertilized and bimaternal (uniparental) parthenogenetic porcine fetuses were generated, and whole genome bisulfite sequencing (WGBS) and RNA sequencing (RNA-seq) were performed to construct methylome and transcriptome, respectively. Differentially methylated regions (DMRs) between the fetuses were identified through methylome analysis, and parental-origin-specific expression patterns of transcripts were examined with transcriptome. As a result, three major DMRs were identified: paternally methylated DMR, maternally methylated - DMR, and maternally methylated DMR. Parental-origin-specific expressions of those five DMR-affected transcripts were found, including a novel imprinted transcript, Exon1B, in pigs. In conclusion, using parthenotes, parental-origin-specific imprinting patterns in the porcine GNAS locus was comprehensively identified, and our approach paves the way for the discovery of novel imprinted genes and loci in a genomic context across species.]]> Wed, 31 Dec 1969 19:00:00 EST The Promises and Challenges of Toxico-Epigenomics: Environmental Chemicals and Their Impacts on the Epigenome. Chung FF, Herceg Z
Environ Health Perspect (Jan 2020)

It has been estimated that a substantial portion of chronic and noncommunicable diseases can be caused or exacerbated by exposure to environmental chemicals. Multiple lines of evidence indicate that early life exposure to environmental chemicals at relatively low concentrations could have lasting effects on individual and population health. Although the potential adverse effects of environmental chemicals are known to the scientific community, regulatory agencies, and the public, little is known about the mechanistic basis by which these chemicals can induce long-term or transgenerational effects. To address this question, epigenetic mechanisms have emerged as the potential link between genetic and environmental factors of health and disease.]]> Wed, 31 Dec 1969 19:00:00 EST Imprinted Cdkn1c genomic locus cell-autonomously promotes cell survival in cerebral cortex development. Laukoter S, Beattie R, Pauler FM, Amberg N, Nakayama KI, Hippenmeyer S
Nat Commun (Jan 2020)

The cyclin-dependent kinase inhibitor p57 is encoded by the imprinted Cdkn1c locus, exhibits maternal expression, and is essential for cerebral cortex development. How Cdkn1c regulates corticogenesis is however not clear. To this end we employ Mosaic Analysis with Double Markers (MADM) technology to genetically dissect Cdkn1c gene function in corticogenesis at single cell resolution. We find that the previously described growth-inhibitory Cdkn1c function is a non-cell-autonomous one, acting on the whole organism. In contrast we reveal a growth-promoting cell-autonomous Cdkn1c function which at the mechanistic level mediates radial glial progenitor cell and nascent projection neuron survival. Strikingly, the growth-promoting function of Cdkn1c is highly dosage sensitive but not subject to genomic imprinting. Collectively, our results suggest that the Cdkn1c locus regulates cortical development through distinct cell-autonomous and non-cell-autonomous mechanisms. More generally, our study highlights the importance to probe the relative contributions of cell intrinsic gene function and tissue-wide mechanisms to the overall phenotype.]]> Wed, 31 Dec 1969 19:00:00 EST DNA methylation analysis of multiple imprinted DMRs in Sotos syndrome reveals IGF2-DMR0 as a DNA methylation-dependent, P0 promoter-specific enhancer. Watanabe H, Higashimoto K, Miyake N, Morita S, Horii T, Kimura M, Suzuki T, Maeda T, Hidaka H, Aoki S, Yatsuki H, Okamoto N, Uemura T, Hatada I, Matsumoto N, Soejima H
FASEB J (Jan 2020)

Haploinsufficiency of NSD1, which dimethylates histone H3 lysine 36 (H3K36), causes Sotos syndrome (SoS), an overgrowth syndrome. DNMT3A and DNMT3B recognizes H3K36 trimethylation (H3K36me3) through PWWP domain to exert de novo DNA methyltransferase activity and establish imprinted differentially methylated regions (DMRs). Since decrease of H3K36me3 and genome-wide DNA hypomethylation in SoS were observed, hypomethylation of imprinted DMRs in SoS was suggested. We explored DNA methylation status of 28 imprinted DMRs in 31 SoS patients with NSD1 defect and found that hypomethylation of IGF2-DMR0 and IG-DMR in a substantial proportion of SoS patients. Luciferase assay revealed that IGF2-DMR0 enhanced transcription from the IGF2 P0 promoter but not the P3 and P4 promoters. Chromatin immunoprecipitation-quantitative PCR (ChIP-qPCR) revealed active enhancer histone modifications at IGF2-DMR0, with high enrichment of H3K4me1 and H3 lysine 27 acetylation (H3K27ac). CRISPR-Cas9 epigenome editing revealed that specifically induced hypomethylation at IGF2-DMR0 increased transcription from the P0 promoter but not the P3 and P4 promoters. NSD1 knockdown suggested that NSD1 targeted IGF2-DMR0; however, IGF2-DMR0 DNA methylation and IGF2 expression were unaltered. This study could elucidate the function of IGF2-DMR0 as a DNA methylation dependent, P0 promoter-specific enhancer. NSD1 may play a role in the establishment or maintenance of IGF2-DMR0 methylation during the postimplantation period.]]> Wed, 31 Dec 1969 19:00:00 EST