ArticleNucleic acids research2016
Imprinting control regions (ICRs) are marked by mono-allelic bivalent chromatin when transcriptionally inactive.
Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed.
- The elongation of Mest transcript into MestXL sustains, but does not initiate, the maternal allele bias of its convergent gene Copg2 during neurogenesis.Nature communications · 2026Article
- Reciprocal, methylation-dependent binding of Zfp57 and Gzf1 safeguards Dlk1-Dio3 imprinting during developmental reprogramming.Nature communications · 2026Article
- The Complex Path from Mammary Ductal Hyperplasia to Breast Cancer: Elevated Malignancy Risk in Atypical Forms.Biomedicines · 2026Review
- The superpowers of imprinting control regions.Genome research · 2026Review
- Non-canonical imprinting, manifesting as post-fertilization placenta-specific parent-of-origin dependent methylation, is not conserved in humans.Human molecular genetics · 2025Article
- Rescuing DNMT1 fails to fully reverse the molecular and functional repercussions of its loss in mouse embryonic stem cells.Nucleic acids research · 2025Article
- Allelic reprogramming of chromatin states in human early embryos.National science review · 2024Article
- Detection of DNA methylation signatures through the lens of genomic imprinting.Scientific reports · 2024Article
- Imprinting disorders.Nature reviews. Disease primers · 2023Review
- Genome-wide detection of imprinted differentially methylated regions using nanopore sequencing.eLife · 2022Article
- Intragenic CpG Islands and Their Impact on Gene Regulation.Frontiers in cell and developmental biology · 2022Review
- Genomic Imprinting in the New Omics Era: A Model for Systems-Level Approaches.Frontiers in genetics · 2022Review
- The Transcriptome and Epigenome Reveal Novel Changes in Transcription Regulation During Pancreatic Rat Islet Maturation.Endocrinology · 2021Article
- Widespread overexpression from the four DNA hypermethylated HOX clusters in aggressive (IDHwt) glioma is associated with H3K27me3 depletion and alternative promoter usage.Molecular oncology · 2021Article
- TET3 controls the expression of the H3K27me3 demethylase Kdm6b during neural commitment.Cellular and molecular life sciences : CMLS · 2021Article
- Article
- HOX gene cluster (de)regulation in brain: from neurodevelopment to malignant glial tumours.Cellular and molecular life sciences : CMLS · 2020Review
- The fusiform gyrus exhibits an epigenetic signature for Alzheimer's disease.Clinical epigenetics · 2020Article
- Altered Transcription Factor Binding and Gene Bivalency in Islets of Intrauterine Growth Retarded Rats.Cells · 2020Article
- Role of genomic imprinting in mammalian development.Journal of biosciences · 2020Review
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parental allele-specific expression of imprinted genes is mediated by imprinting control regions (ICRs) that are constitutively marked by DNA methylation imprints on the maternal or paternal allele. Mono-allelic DNA methylation is strictly required for the process of imprinting and has to be faithfully maintained during the entire life-span. While the regulation of DNA methylation itself is well understood, the mechanisms whereby the opposite allele remains unmethylated are unclear. Here, we show that in the mouse, at maternally methylated ICRs, the paternal allele, which is constitutively associated with H3K4me2/3, is marked by default by H3K27me3 when these ICRs are transcriptionally inactive, leading to the formation of a bivalent chromatin signature. Our data suggest that at ICRs, chromatin bivalency has a protective role by ensuring that DNA on the paternal allele remains unmethylated and protected against spurious and unscheduled gene expression. Moreover, they provide the proof of concept that, beside pluripotent cells, chromatin bivalency is the default state of transcriptionally inactive CpG island promoters, regardless of the developmental stage, thereby contributing to protect cell identity.
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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.