TY - JOUR
T1 - Identification and Characterization of Enhancers Controlling the Inflammatory Gene Expression Program in Macrophages
AU - Ghisletti, Serena
AU - Barozzi, Iros
AU - Mietton, Flore
AU - Polletti, Sara
AU - De Santa, Francesca
AU - Venturini, Elisa
AU - Gregory, Lorna
AU - Lonie, Lorne
AU - Chew, Adeline
AU - Wei, Chia Lin
AU - Ragoussis, Jiannis
AU - Natoli, Gioacchino
PY - 2010/3
Y1 - 2010/3
N2 - Enhancers determine tissue-specific gene expression programs. Enhancers are marked by high histone H3 lysine 4 mono-methylation (H3K4me1) and by the acetyl-transferase p300, which has allowed genome-wide enhancer identification. However, the regulatory principles by which subsets of enhancers become active in specific developmental and/or environmental contexts are unknown. We exploited inducible p300 binding to chromatin to identify, and then mechanistically dissect, enhancers controlling endotoxin-stimulated gene expression in macrophages. In these enhancers, binding sites for the lineage-restricted and constitutive Ets protein PU.1 coexisted with those for ubiquitous stress-inducible transcription factors such as NF-κB, IRF, and AP-1. PU.1 was required for maintaining H3K4me1 at macrophage-specific enhancers. Reciprocally, ectopic expression of PU.1 reactivated these enhancers in fibroblasts. Thus, the combinatorial assembly of tissue- and signal-specific transcription factors determines the activity of a distinct group of enhancers. We suggest that this may represent a general paradigm in tissue-restricted and stimulus-responsive gene regulation.
AB - Enhancers determine tissue-specific gene expression programs. Enhancers are marked by high histone H3 lysine 4 mono-methylation (H3K4me1) and by the acetyl-transferase p300, which has allowed genome-wide enhancer identification. However, the regulatory principles by which subsets of enhancers become active in specific developmental and/or environmental contexts are unknown. We exploited inducible p300 binding to chromatin to identify, and then mechanistically dissect, enhancers controlling endotoxin-stimulated gene expression in macrophages. In these enhancers, binding sites for the lineage-restricted and constitutive Ets protein PU.1 coexisted with those for ubiquitous stress-inducible transcription factors such as NF-κB, IRF, and AP-1. PU.1 was required for maintaining H3K4me1 at macrophage-specific enhancers. Reciprocally, ectopic expression of PU.1 reactivated these enhancers in fibroblasts. Thus, the combinatorial assembly of tissue- and signal-specific transcription factors determines the activity of a distinct group of enhancers. We suggest that this may represent a general paradigm in tissue-restricted and stimulus-responsive gene regulation.
KW - MOLIMMUNO
KW - SYSBIO
UR - http://www.scopus.com/inward/record.url?scp=77949977555&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=77949977555&partnerID=8YFLogxK
U2 - 10.1016/j.immuni.2010.02.008
DO - 10.1016/j.immuni.2010.02.008
M3 - Article
C2 - 20206554
AN - SCOPUS:77949977555
SN - 1074-7613
VL - 32
SP - 317
EP - 328
JO - Immunity
JF - Immunity
IS - 3
ER -