Architectural epigenetics: Mitotic retention of mammalian transcriptional regulatory information

Sayyed K. Zaidi, Daniel W. Young, Martin Montecino, Jane B. Lian, Janet L. Stein, Andre J van Wijnen, Gary S. Stein

Research output: Contribution to journalArticle

33 Citations (Scopus)

Abstract

Epigenetic regulatory information must be retained during mammalian cell division to sustain phenotypespecific 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.

Original languageEnglish (US)
Pages (from-to)4758-4766
Number of pages9
JournalMolecular and Cellular Biology
Volume30
Issue number20
DOIs
StatePublished - Oct 2010
Externally publishedYes

Fingerprint

Epigenomics
Histone Code
Phenotype
Gene Expression
DNA Methylation
RNA Interference
Cell Division
Transcriptional Activation
Hypersensitivity
Transcription Factors

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

Cite this

Zaidi, S. K., Young, D. W., Montecino, M., Lian, J. B., Stein, J. L., van Wijnen, A. J., & Stein, G. S. (2010). Architectural epigenetics: Mitotic retention of mammalian transcriptional regulatory information. Molecular and Cellular Biology, 30(20), 4758-4766. https://doi.org/10.1128/MCB.00646-10

Architectural epigenetics : Mitotic retention of mammalian transcriptional regulatory information. / Zaidi, Sayyed K.; Young, Daniel W.; Montecino, Martin; Lian, Jane B.; Stein, Janet L.; van Wijnen, Andre J; Stein, Gary S.

In: Molecular and Cellular Biology, Vol. 30, No. 20, 10.2010, p. 4758-4766.

Research output: Contribution to journalArticle

Zaidi, SK, Young, DW, Montecino, M, Lian, JB, Stein, JL, van Wijnen, AJ & Stein, GS 2010, 'Architectural epigenetics: Mitotic retention of mammalian transcriptional regulatory information', Molecular and Cellular Biology, vol. 30, no. 20, pp. 4758-4766. https://doi.org/10.1128/MCB.00646-10
Zaidi, Sayyed K. ; Young, Daniel W. ; Montecino, Martin ; Lian, Jane B. ; Stein, Janet L. ; van Wijnen, Andre J ; Stein, Gary S. / Architectural epigenetics : Mitotic retention of mammalian transcriptional regulatory information. In: Molecular and Cellular Biology. 2010 ; Vol. 30, No. 20. pp. 4758-4766.
@article{6a21b1fa3d8c41b999bafc0137e4b08a,
title = "Architectural epigenetics: Mitotic retention of mammalian transcriptional regulatory information",
abstract = "Epigenetic regulatory information must be retained during mammalian cell division to sustain phenotypespecific 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.",
author = "Zaidi, {Sayyed K.} and Young, {Daniel W.} and Martin Montecino and Lian, {Jane B.} and Stein, {Janet L.} and {van Wijnen}, {Andre J} and Stein, {Gary S.}",
year = "2010",
month = "10",
doi = "10.1128/MCB.00646-10",
language = "English (US)",
volume = "30",
pages = "4758--4766",
journal = "Molecular and Cellular Biology",
issn = "0270-7306",
publisher = "American Society for Microbiology",
number = "20",

}

TY - JOUR

T1 - Architectural epigenetics

T2 - Mitotic retention of mammalian transcriptional regulatory information

AU - Zaidi, Sayyed K.

AU - Young, Daniel W.

AU - Montecino, Martin

AU - Lian, Jane B.

AU - Stein, Janet L.

AU - van Wijnen, Andre J

AU - Stein, Gary S.

PY - 2010/10

Y1 - 2010/10

N2 - Epigenetic regulatory information must be retained during mammalian cell division to sustain phenotypespecific 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.

AB - Epigenetic regulatory information must be retained during mammalian cell division to sustain phenotypespecific 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.

UR - http://www.scopus.com/inward/record.url?scp=78049404909&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=78049404909&partnerID=8YFLogxK

U2 - 10.1128/MCB.00646-10

DO - 10.1128/MCB.00646-10

M3 - Article

C2 - 20696837

AN - SCOPUS:78049404909

VL - 30

SP - 4758

EP - 4766

JO - Molecular and Cellular Biology

JF - Molecular and Cellular Biology

SN - 0270-7306

IS - 20

ER -