ArticleNucleic acids research2022
Epigenome editing reveals core DNA methylation for imprinting control in the Dlk1-Dio3 imprinted domain.
Article in Nucleic acids research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 28 citations in OpenAlex.
- From epigenetic mark detection to rational design of epigenetic editing strategies.Molecular therapy. Advances · 2026Review
- Regulatory mechanisms of maternal imprinting at the murine Dlk1-Dio3 domain.Nature communications · 2026Article
- Reciprocal, methylation-dependent binding of Zfp57 and Gzf1 safeguards Dlk1-Dio3 imprinting during developmental reprogramming.Nature communications · 2026Article
- Paternal Caffeine Exposure Programs Offspring Stress Vulnerability via Sperm Dlk1-Dio3 Imprinting-Directed Remodeling of a Novel Neural Circuit.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Allele-specific CRISPR perturbation of the imprinted Dlk1-Dio3 domain reveals regulation of BMP-NOTCH-VEGF signaling in embryonic organogenesis.Cell death and differentiation · 2026Article
- Article
- Dual Role of DLK1 in GnRH Neuron Ontogeny.Stem cell reviews and reports · 2025Article
- A molecular circuit regulates fate plasticity in emerging and adult AT2 cells.Nature communications · 2025Article
- NamiRNA-Enhancer Network: The Changing Era Challenge and Chance of miRNA.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Dissecting the epigenetic regulation of the fetal hemoglobin genes to unravel a novel therapeutic approach for β-hemoglobinopathies.Nucleic acids research · 2025Article
- Identification of the Notch ligand DLK1 as an immunotherapeutic target and regulator of tumor cell plasticity and chemoresistance in adrenocortical carcinoma.Nature communications · 2025Article
- DLK1 Distinguishes Subsets of NF1-Associated Malignant Peripheral Nerve Sheath Tumors with Divergent Molecular Signatures.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Article
- Activation of the imprinted Prader-Willi syndrome locus by CRISPR-based epigenome editing.Cell genomics · 2025Article
- DNA methylation shapes the Polycomb landscape during the exit from naive pluripotency.Nature structural & molecular biology · 2025Article
- Identification of maternal allele sequences of IG-DMR that are essential for neonatal viability.PloS one · 2025Article
- Epigenome editing technologies for discovery and medicine.Nature biotechnology · 2024Review
- Epigenome editing revealed the role of DNA methylation of T-DMR/CpG island shore on Runx2 transcription.Biochemistry and biophysics reports · 2024Article
- Article
- Novel 14q32.2 paternal deletion encompassing the whole DLK1 gene associated with Temple syndrome.Clinical epigenetics · 2024Article
- Maternal RNA transcription in Dlk1-Dio3 domain is critical for proper development of the mouse placental vasculature.Communications biology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Dlk1-Dio3 imprinted domain is controlled by an imprinting control region (ICR) called IG-DMR that is hypomethylated on the maternal allele and hypermethylated on the paternal allele. Although several genetic mutation experiments have shown that IG-DMR is essential for imprinting control of the domain, how DNA methylation itself functions has not been elucidated. Here, we performed both gain and loss of DNA methylation experiments targeting IG-DMR by transiently introducing CRISPR/Cas9 based-targeted DNA methylation editing tools along with one guide RNA into mouse ES cells. Altered DNA methylation, particularly at IG-DMR-Rep, which is a tandem repeat containing ZFP57 methylated DNA-binding protein binding motifs, affected the imprinting state of the whole domain, including DNA methylation, imprinted gene expression, and histone modifications. Moreover, the altered imprinting states were persistent through neuronal differentiation. Our results suggest that the DNA methylation state at IG-DMR-Rep, but not other sites in IG-DMR, is a master element to determine whether the allele behaves as the intrinsic maternal or paternal allele. Meanwhile, this study provides a robust strategy and methodology to study core DNA methylation in cis-regulatory elements, such as ICRs and enhancers.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.