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      Architectural protein subclasses shape 3D organization of genomes during lineage commitment.

      Cell

      Sequence Analysis, DNA, metabolism, Repressor Proteins, Promoter Regions, Genetic, analysis, Nuclear Proteins, chemistry, Neural Stem Cells, Mice, genetics, Mediator Complex, Genome-Wide Association Study, Genome, Gene Knockdown Techniques, Gene Expression Regulation, Developmental, Enhancer Elements, Genetic, Embryonic Stem Cells, Chromosomal Proteins, Non-Histone, Chromatin, Cell Lineage, Cell Cycle Proteins, Animals

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          Abstract

          Understanding the topological configurations of chromatin may reveal valuable insights into how the genome and epigenome act in concert to control cell fate during development. Here, we generate high-resolution architecture maps across seven genomic loci in embryonic stem cells and neural progenitor cells. We observe a hierarchy of 3D interactions that undergo marked reorganization at the submegabase scale during differentiation. Distinct combinations of CCCTC-binding factor (CTCF), Mediator, and cohesin show widespread enrichment in chromatin interactions at different length scales. CTCF/cohesin anchor long-range constitutive interactions that might form the topological basis for invariant subdomains. Conversely, Mediator/cohesin bridge short-range enhancer-promoter interactions within and between larger subdomains. Knockdown of Smc1 or Med12 in embryonic stem cells results in disruption of spatial architecture and downregulation of genes found in cohesin-mediated interactions. We conclude that cell-type-specific chromatin organization occurs at the submegabase scale and that architectural proteins shape the genome in hierarchical length scales. Copyright © 2013 Elsevier Inc. All rights reserved.

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          Author and article information

          Journal
          10.1016/j.cell.2013.04.053
          3712340
          23706625

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