ArticleNucleic acids research2013
Promoter cross-talk via a shared enhancer explains paternally biased expression of Nctc1 at the Igf2/H19/Nctc1 imprinted locus.
Article in Nucleic acids research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 29 citations in OpenAlex.
- Igf2 adult-specific skeletal muscle enhancer activity revealed in mice with intergenic CTCF boundary deletion.PLoS genetics · 2025Article
- Differential 3D genome architecture and imprinted gene expression: cause or consequence?Biochemical Society transactions · 2024Review
- Human IGF2 Gene Epigenetic and Transcriptional Regulation: At the Core of Developmental Growth and Tumorigenic Behavior.Biomedicines · 2023Review
- Hi-TrAC reveals division of labor of transcription factors in organizing chromatin loops.Nature communications · 2022Article
- Exploring chromatin structural roles of non-coding RNAs at imprinted domains.Biochemical Society transactions · 2021Review
- Artificial Intelligence to Decode Cancer Mechanism: Beyond Patient Stratification for Precision Oncology.Frontiers in pharmacology · 2020Review
- CTCF modulates allele-specific sub-TAD organization and imprinted gene activity at the mouse Dlk1-Dio3 and Igf2-H19 domains.Genome biology · 2019Article
- The insulin-like growth factor 2 gene in mammals: Organizational complexity within a conserved locus.PloS one · 2019Article
- Paternal bias expression of Igf2as is enhancer-dependent on the imprinting cluster of Igf2, H19 and Nctc1 in muscle cells.Animal cells and systems · 2019Article
- Article
- The complex genetics of human insulin-like growth factor 2 are not reflected in public databases.The Journal of biological chemistry · 2018Article
- Onco-Multi-OMICS Approach: A New Frontier in Cancer Research.BioMed research international · 2018Review
- Loss of imprinting mutations define both distinct and overlapping roles for misexpression of IGF2 and of H19 lncRNA.Nucleic acids research · 2017Article
- H19ICR mediated transcriptional silencing does not require target promoter methylation.Biochemical and biophysical research communications · 2016Article
- Characterizing a distal muscle enhancer in the mouse Igf2 locus.Physiological genomics · 2016Article
- H19 lncRNA alters DNA methylation genome wide by regulating S-adenosylhomocysteine hydrolase.Nature communications · 2015Article
- Methylome-wide Sequencing Detects DNA Hypermethylation Distinguishing Indolent from Aggressive Prostate Cancer.Cell reports · 2015Article
- Human endogenous retroviruses sustain complex and cooperative regulation of gene-containing loci and unannotated megabase-sized regions.Retrovirology · 2015Article
- Novel principles of gamma-retroviral insertional transcription activation in murine leukemia virus-induced end-stage tumors.Retrovirology · 2014Article
- Long noncoding RNAs, emerging players in muscle differentiation and disease.Skeletal muscle · 2014Article
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5 authors at 2 institutions in 1 country.
Funding
Abstract
Developmentally regulated transcription often depends on physical interactions between distal enhancers and their cognate promoters. Recent genomic analyses suggest that promoter-promoter interactions might play a similarly critical role in organizing the genome and establishing cell-type-specific gene expression. The Igf2/H19 locus has been a valuable model for clarifying the role of long-range interactions between cis-regulatory elements. Imprinted expression of the linked, reciprocally imprinted genes is explained by parent-of-origin-specific chromosomal loop structures between the paternal Igf2 or maternal H19 promoters and their shared tissue-specific enhancer elements. Here, we further analyze these loop structures for their composition and their impact on expression of the linked long non-coding RNA, Nctc1. We show that Nctc1 is co-regulated with Igf2 and H19 and physically interacts with the shared muscle enhancer. In fact, all three co-regulated genes have the potential to interact not only with the shared enhancer but also with each other via their enhancer interactions. Furthermore, developmental and genetic analyses indicate functional significance for these promoter-promoter interactions. Altogether, we present a novel mechanism to explain developmental specific imprinting of Nctc1 and provide new information about enhancer mechanisms and about the role of chromatin domains in establishing gene expression patterns.
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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.