Architectural epigenetics: mitotic retention of mammalian transcriptional regulatory information

UMMS Affiliation

Department of Cell Biology



Document Type


Medical Subject Headings

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


Cell Biology


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.

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Citation: Mol Cell Biol. 2010 Oct;30(20):4758-66. Epub 2010 Aug 9. Link to article on publisher's site

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