ArticleBMC genetics2006
Loss of imprinting at the Dlk1-Gtl2 locus caused by insertional mutagenesis in the Gtl2 5' region.
Article in BMC genetics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 55 citations in OpenAlex.
- Epigenetic changes induced by in utero dietary challenge result in phenotypic variability in successive generations of mice.Nature communications · 2022Article
- Epigenetic Contribution and Genomic Imprinting Dlk1-Dio3 miRNAs in Systemic Lupus Erythematosus.Genes · 2021Review
- Temple syndrome and Kagami-Ogata syndrome: clinical presentations, genotypes, models and mechanisms.Human molecular genetics · 2020Review
- Know Your Model: When parental origin matters.Lab animal · 2020Article
- Cadmium exposure andEnvironmental epigenetics · 2019Article
- Dysregulation of ncRNAs located at the DLK1‑DIO3 imprinted domain: involvement in urological cancers.Cancer management and research · 2019Review
- Modulating the expression of long non-coding RNAs for functional studies.EMBO reports · 2018Review
- Article
- Asymmetric DNA methylation of CpG dyads is a feature of secondary DMRs associated with theEpigenetics & chromatin · 2017Article
- The Upregulation of Genomic Imprinted DLK1-Dio3 miRNAs in Murine Lupus Is Associated with Global DNA Hypomethylation.PloS one · 2016Article
- TRIM28 Controls Genomic Imprinting through Distinct Mechanisms during and after Early Genome-wide Reprogramming.Cell reports · 2015Article
- Novel deletions affecting the MEG3-DMR provide further evidence for a hierarchical regulation of imprinting in 14q32.European journal of human genetics : EJHG · 2015Article
- Review
- Analysis of DNA methylation acquisition at the imprinted Dlk1 locus reveals asymmetry at CpG dyads.Epigenetics & chromatin · 2014Article
- Perturbations to the IGF1 growth pathway and adult energy homeostasis following disruption of mouse chromosome 12 imprinting.Acta physiologica (Oxford, England) · 2014Article
- Genomic imprinting of the type 3 thyroid hormone deiodinase gene: regulation and developmental implications.Biochimica et biophysica acta · 2013Review
- Identification of rtl1, a retrotransposon-derived imprinted gene, as a novel driver of hepatocarcinogenesis.PLoS genetics · 2013Article
- Regulation of Mammalian Gene Dosage by Long Noncoding RNAs.Biomolecules · 2013Article
- Conditional deletions refine the embryonic requirement for Dlk1.Mechanisms of development · 2013Article
- Identification of imprinting regulators at the Meg3 differentially methylated region.Genomics · 2012Article
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6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe Dlk1 and Gtl2 genes define a region of mouse chromosome 12 that is subject to genomic imprinting, the parental allele-specific expression of a gene. Although imprinted genes play important roles in growth and development, the mechanisms by which imprinting is established and maintained are poorly understood. Differentially methylated regions (DMRs), which carry methylation on only one parental allele, are involved in imprinting control at many loci. The Dlk1-Gtl2 region contains three known DMRs, the Dlk1 DMR in the 3' region of Dlk1, the intergenic DMR 15 kb upstream of Gtl2, and the Gtl2 DMR at the Gtl2 promoter. Three mouse models are analyzed here that provide new information about the regulation of Dlk1-Gtl2 imprinting.
resultsA previously existing insertional mutation (Gtl2lacZ), and a targeted deletion in which the Gtl2 upstream region was replaced by a Neo cassette (Gtl2Delta5'Neo), display partial lethality and dwarfism upon paternal inheritance. Molecular characterization shows that both mutations cause loss of imprinting and changes in expression of the Dlk1, Gtl2 and Meg8/Rian genes. Dlk1 levels are decreased upon paternal inheritance of either mutation, suggesting Dlk1 may be causative for the lethality and dwarfism. Loss of imprinting on the paternal chromosome in both Gtl2lacZ and Gtl2Delta5'Neo mice is accompanied by the loss of paternal-specific Gtl2 DMR methylation, while maternal loss of imprinting suggests a previously unknown regulatory role for the maternal Gtl2 DMR. Unexpectedly, when the Neo gene is excised, Gtl2Delta5' animals are of normal size, imprinting is unchanged and the Gtl2 DMR is properly methylated. The exogenous DNA sequences integrated upstream of Gtl2 are therefore responsible for the growth and imprinting effects.
conclusionThese data provide further evidence for the coregulation of the imprinted Dlk1 and Gtl2 genes, and support a role for Dlk1 as an important neonatal growth factor. The ability of the Gtl2lacZ and Gtl2Delta5'Neo mutations to cause long-range changes in imprinting and gene expression suggest that regional imprinting regulatory elements may lie in proximity to the integration site.
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