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
U2 - 10.1128/MCB.00646-10
DO - 10.1128/MCB.00646-10
M3 - Short survey
C2 - 20696837
AN - SCOPUS:78049404909
SN - 0270-7306
VL - 30
SP - 4758
EP - 4766
JO - Molecular and Cellular Biology
JF - Molecular and Cellular Biology
IS - 20
ER -