Architectural epigenetics: mitotic retention of mammalian transcriptional regulatory information
Department of Cell Biology
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
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.
DOI of Published Version
Mol Cell Biol. 2010 Oct;30(20):4758-66. Epub 2010 Aug 9. Link to article on publisher's site
Molecular and cellular biology
Zaidi SK, Young DW, Montecino MA, Lian JB, Stein JL, Van Wijnen AJ, Stein GS. (2010). Architectural epigenetics: mitotic retention of mammalian transcriptional regulatory information. Stein, Stein, Lian, vanWijnen Lab Publications. https://doi.org/10.1128/MCB.00646-10. Retrieved from https://escholarship.umassmed.edu/stein/7