ArticleNature communications2015
A cohesin-OCT4 complex mediates Sox enhancers to prime an early embryonic lineage.
Article in Nature communications, 2015. 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 32 citations in OpenAlex.
- SOX17 in pulmonary arterial hypertension: from development to clinical phenotype.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- Genomic locus of lncRNA-Gm26793 forms an inter-chromosomal interaction with Cubn to ensure proper stem cell differentiation in vitro and in vivo.Cell discovery · 2025Article
- Liquid condensates: a new barrier to loop extrusion?Cellular and molecular life sciences : CMLS · 2025Review
- Review
- Sall4 and Gata4 induce cardiac fibroblast transition towards a partially multipotent state with cardiogenic potential.Scientific reports · 2024Article
- Upregulation of the Oct3/4 Network in Basal Breast Cancer Is Associated with Its Metastatic Potential and Shows Tissue Dependent Variability.International journal of molecular sciences · 2023Article
- Cohesin: an emerging master regulator at the heart of cardiac development.Molecular biology of the cell · 2023Article
- Identification of SALL4 Expressing Islet-1+ Cardiovascular Progenitor Cell Clones.International journal of molecular sciences · 2023Article
- Multidimensional scaling methods can reconstruct genomic DNA loops using Hi-C data properties.PloS one · 2023Article
- OCT4-mediated inflammation induces cell reprogramming at the origin of cardiac valve development and calcification.Science advances · 2021Article
- RNA Biogenesis Instructs Functional Inter-Chromosomal Genome Architecture.Frontiers in genetics · 2021Article
- IRX3/5 regulate mitotic chromatid segregation and limb bud shape.Development (Cambridge, England) · 2020Article
- The expanding phenotypes of cohesinopathies: one ring to rule them all!Cell cycle (Georgetown, Tex.) · 2019Review
- SALL4 promotes the tumorigenicity of cervical cancer cells through activation of the Wnt/β-catenin pathway via CTNNB1.Cancer science · 2019Article
- Review
- DNA N6-methyladenine is dynamically regulated in the mouse brain following environmental stress.Nature communications · 2017Article
- Dynamic Protein Interactions of the Polycomb Repressive Complex 2 during Differentiation of Pluripotent Cells.Molecular & cellular proteomics : MCP · 2016Article
- Article
- Review
- Epigenetic Regulation of Cardiac Differentiation of Embryonic Stem Cells and Tissues.Journal of visualized experiments : JoVE · 2016Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Short- and long-scales intra- and inter-chromosomal interactions are linked to gene transcription, but the molecular events underlying these structures and how they affect cell fate decision during embryonic development are poorly understood. One of the first embryonic cell fate decisions (that is, mesendoderm determination) is driven by the POU factor OCT4, acting in concert with the high-mobility group genes Sox-2 and Sox-17. Here we report a chromatin-remodelling mechanism and enhancer function that mediate cell fate switching. OCT4 alters the higher-order chromatin structure at both Sox-2 and Sox-17 loci. OCT4 titrates out cohesin and switches the Sox-17 enhancer from a locked (within an inter-chromosomal Sox-2 enhancer/CCCTC-binding factor CTCF/cohesin loop) to an active (within an intra-chromosomal Sox-17 promoter/enhancer/cohesin loop) state. SALL4 concomitantly mobilizes the polycomb complexes at the Soxs loci. Thus, OCT4/SALL4-driven cohesin- and polycombs-mediated changes in higher-order chromatin structure mediate instruction of early cell fate in embryonic cells.
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Registered trials
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.