ArticlePloS one2013
Oct4/Sox2 binding sites contribute to maintaining hypomethylation of the maternal igf2/h19 imprinting control region.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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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.
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Who cites it
26 citing papers in PubMed, 42 citations in OpenAlex.
- Methylation profile characteristics in the H19/IGF2:IG-DMR revealed by long-read sequencing analysis in patients with Beckwith-Wiedemann syndrome having defects in the OCT4/SOX2 binding site.Clinical epigenetics · 2026Article
- TET3 protects theiScience · 2025Article
- Identification of responsible sequences which mutations cause maternal H19-ICR hypermethylation with Beckwith-Wiedemann syndrome-like overgrowth.Communications biology · 2024Article
- Differential 3D genome architecture and imprinted gene expression: cause or consequence?Biochemical Society transactions · 2024Review
- Pre-conceptional paternal diet impacts on offspring testosterone homoeostasis via epigenetic modulation of cyp19a1/aromatase activity.npj metabolic health and disease · 2024Article
- Exogenous OCT4 and SOX2 Contribution to In Vitro Reprogramming in Cattle.Biomedicines · 2023Article
- The transgenic IG-DMR sequence of the mouse Dlk1-Dio3 domain acquired imprinted DNA methylation during the post-fertilization period.Epigenetics & chromatin · 2023Article
- Review
- The long noncoding RNA H19 regulates tumor plasticity in neuroendocrine prostate cancer.Nature communications · 2021Article
- The number of the CTCF binding sites of the H19/IGF2:IG-DMR correlates with DNA methylation and expression imprinting in a humanized mouse model.Human molecular genetics · 2021Article
- High throughput screening identifies SOX2 as a super pioneer factor that inhibits DNA methylation maintenance at its binding sites.Nature communications · 2021Article
- The Role and Specific Mechanism of OCT4 in Cancer Stem Cells: A Review.International journal of stem cells · 2020Review
- PIM protein kinases regulate the level of the long noncoding RNA H19 to control stem cell gene transcription and modulate tumor growth.Molecular oncology · 2020Article
- Syndromic Disorders Caused by Disturbed Human ImprintingJournal of clinical research in pediatric endocrinology · 2020Review
- The influence of DNA methylation on monoallelic expression.Essays in biochemistry · 2019Review
- The extent of DNA methylation anticipation due to a genetic defect in ICR1 in Beckwith-Wiedemann syndrome.Journal of human genetics · 2019Article
- Novel familial distal imprinting centre 1 (11p15.5) deletion provides further insights in imprinting regulation.Clinical epigenetics · 2019Article
- Synthetic DNA fragments bearing ICR cis elements become differentially methylated and recapitulate genomic imprinting in transgenic mice.Epigenetics & chromatin · 2018Article
- Conservation of Repeats at the Mammalian KCNQ1OT1-CDKN1C Region Suggests a Role in Genomic Imprinting.Evolutionary bioinformatics online · 2017Article
- The Role of Maternal-Effect Genes in Mammalian Development: Are Mammalian Embryos Really an Exception?Stem cell reviews and reports · 2016Review
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
A central question in genomic imprinting is how parental-specific DNA methylation of imprinting control regions (ICR) is established during gametogenesis and maintained after fertilization. At the imprinted Igf2/H19 locus, CTCF binding maintains the unmethylated state of the maternal ICR after the blastocyst stage. In addition, evidence from Beckwith-Wiedemann patients and cultured mouse cells suggests that two Sox-Oct binding motifs within the Igf2/H19 ICR also participate in maintaining hypomethylation of the maternal allele. We found that the Sox and octamer elements from both Sox-Oct motifs were required to drive hypomethylation of integrated transgenes in mouse embryonic carcinoma cells. Oct4 and Sox2 showed cooperative binding to the Sox-Oct motifs, and both were present at the endogenous ICR. Using a mouse with mutations in the Oct4 binding sites, we found that maternally transmitted mutant ICRs acquired partial methylation in somatic tissues, but there was little effect on imprinted expression of H19 and Igf2. A subset of mature oocytes also showed partial methylation of the mutant ICR, which suggested that the Sox-Oct motifs provide some protection from methylation during oogenesis. The Sox-Oct motifs, however, were not required for erasure of paternal methylation in primordial germ cells, which indicated that the oocyte methylation was acquired post-natally. Maternally inherited mutant ICRs were unmethylated in blastocysts, which suggested that at least a portion of the methylation in somatic tissues occurred after implantation. These findings provide evidence that Sox-Oct motifs contribute to ICR hypomethylation in post-implantation embryos and maturing oocytes and link imprinted DNA methylation with key stem cell/germline transcription factors.
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