Architectural epigenetics: mitotic retention of mammalian transcriptional regulatory information

Mol Cell Biol. 2010 Oct;30(20):4758-66. doi: 10.1128/MCB.00646-10. Epub 2010 Aug 9.

Abstract

Epigenetic regulatory information must be retained during mammalian cell division to sustain phenotype-specific and physiologically responsive gene expression in the progeny cells. Histone modifications, DNA methylation, and RNA-mediated silencing are well-defined epigenetic mechanisms that control the cellular phenotype by regulating gene expression. Recent results suggest that the mitotic retention of nuclease hypersensitivity, selective histone marks, as well as the lineage-specific transcription factor occupancy of promoter elements contribute to the epigenetic control of sustained cellular identity in progeny cells. We propose that these mitotic epigenetic signatures collectively constitute architectural epigenetics, a novel and essential mechanism that conveys regulatory information to sustain the control of phenotype and proliferation in progeny cells by bookmarking genes for activation or suppression.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Adenosine Triphosphatases / metabolism
  • Animals
  • Cell Differentiation
  • Cell Proliferation
  • DNA Methylation
  • DNA-Binding Proteins / metabolism
  • Epigenesis, Genetic*
  • Gene Expression Regulation
  • Histones / metabolism
  • Humans
  • Mammals / genetics*
  • Mammals / metabolism
  • Mitosis / genetics
  • Models, Genetic
  • Multiprotein Complexes / metabolism
  • Phenotype
  • Protein Processing, Post-Translational
  • RNA, Untranslated / genetics
  • Transcription Factors / metabolism

Substances

  • DNA-Binding Proteins
  • Histones
  • Multiprotein Complexes
  • RNA, Untranslated
  • Transcription Factors
  • condensin complexes
  • Adenosine Triphosphatases