Cited by 556Genetic Syndromes and ImprintingGenomics and Chromatin DynamicsEpigenetics and DNA Methylation

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Interaction between differentially methylated regions partitions the imprinted genes Igf2 and H19 into parent-specific chromatin loops

Murrell, Adele, Heeson, Sarah, Reik, Wolf·2004·Nature Genetics

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Abstract

Imprinted genes are expressed from only one of the parental alleles and are marked epigenetically by DNA methylation and histone modifications. The paternally expressed gene insulin-like growth-factor 2 (Igf2) is separated by approximately 100 kb from the maternally expressed noncoding gene H19 on mouse distal chromosome 7. Differentially methylated regions in Igf2 and H19 contain chromatin boundaries, silencers and activators and regulate the reciprocal expression of the two genes in a methylation-sensitive manner by allowing them exclusive access to a shared set of enhancers. Various chromatin models have been proposed that separate Igf2 and H19 into active and silent domains. Here we used a GAL4 knock-in approach as well as the chromosome conformation capture technique to show that the differentially methylated regions in the imprinted genes Igf2 and H19 interact in mice. These interactions are epigenetically regulated and partition maternal and paternal chromatin into distinct loops. This generates a simple epigenetic switch for Igf2 through which it moves between an active and a silent chromatin domain.

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“16.1c ) (Murrell et al. 2004 ; Qiu et al. 2008 ) .”
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“…studies have demonstrated that the ICR is maternally unmethylated and paternally methylated, and that CTCF orchestrates an intrachromosomal loop by binding to both the maternal ICR and IGF2 promoter which silences the maternal allele (Murrell et al., 2004; Li et al., 2008; Zhang et al., 2011).”
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Background

Authors: Murrell, A., Heeson, S., & Reik, W.
Affiliations: Babraham Institute (GB)
Corresponding author: Murrell, Adele
Reik, Wolf
ORCID: Murrell, Adele
Reik, Wolf
Venue: Nature Genetics
Publisher: Springer Science and Business Media LLC
Published: 2004-07-25
Volume: 36
Issue: 8
Pages: 889-893
ISSN: 1061-4036 (ISSN-L)
1546-1718
DOI: 10.1038/ng1402
OpenAlex: W2085509761
Cited by: 556
References: 30
Citations by year: 2026: 7 · 2025: 4 · 2024: 13 · 2023: 5 · 2022: 8 · 2021: 8 · 2020: 10 · 2019: 13 · 2018: 16 · 2017: 15 · 2016: 18 · 2015: 26 · 2014: 27 · 2013: 30 · 2012: 50
FWCI: 22.42
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
Locations: Nature Genetics (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Syndromes and Imprinting
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
Keywords: genomic imprinting, insulin-like growth factor II, H19, differentially methylated regions, chromatin looping, DNA methylation, epigenetic regulation, chromosome conformation, epigenetic switch, mouse chromosome 7, gene silencing
MeSH terms: Animals, Chromatin, Insulin-Like Growth Factor II, Mice, Transgenic, Molecular Sequence Data, Genomic Imprinting, DNA Methylation, RNA, Untranslated, Mice, RNA, Long Noncoding

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Interaction between differentially methylated regions partitions the imprinted genes Igf2 and H19 into parent-specific chromatin loops

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