48
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Remodeling of the enhancer landscape during macrophage activation is coupled to enhancer transcription.

      Molecular Cell
      Animals, Base Sequence, CCAAT-Enhancer-Binding Proteins, metabolism, Cells, Cultured, DNA Methylation, Enhancer Elements, Genetic, Gene Expression, Gene Expression Regulation, Histone-Lysine N-Methyltransferase, Histones, genetics, Macrophage Activation, Macrophages, immunology, Male, Mice, Mice, Inbred C57BL, Myeloid-Lymphoid Leukemia Protein, NF-kappa B, Proto-Oncogene Proteins, RNA Polymerase II, antagonists & inhibitors, Sequence Analysis, DNA, Signal Transduction, Toll-Like Receptor 4, Trans-Activators, Transcription Factor RelA, Transcription, Genetic

      Read this article at

      ScienceOpenPublisherPMC
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Recent studies suggest a hierarchical model in which lineage-determining factors act in a collaborative manner to select and prime cell-specific enhancers, thereby enabling signal-dependent transcription factors to bind and function in a cell-type-specific manner. Consistent with this model, TLR4 signaling primarily regulates macrophage gene expression through a pre-existing enhancer landscape. However, TLR4 signaling also induces priming of ∼3,000 enhancer-like regions de novo, enabling visualization of intermediates in enhancer selection and activation. Unexpectedly, we find that enhancer transcription precedes local mono- and dimethylation of histone H3 lysine 4 (H3K4me1/2). H3K4 methylation at de novo enhancers is primarily dependent on the histone methyltransferases Mll1, Mll2/4, and Mll3 and is significantly reduced by inhibition of RNA polymerase II elongation. Collectively, these findings suggest an essential role of enhancer transcription in H3K4me1/2 deposition at de novo enhancers that is independent of potential functions of the resulting eRNA transcripts. Copyright © 2013 Elsevier Inc. All rights reserved.

          Related collections

          Author and article information

          Comments

          Comment on this article