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Comment
. 2011 Apr 20;30(8):1418-9.
doi: 10.1038/emboj.2011.80.

Adipogenic hotspots: where the action is

David J Steger  1 , Mitchell A Lazar
Affiliations
Comment

Adipogenic hotspots: where the action is

David J Steger et al. EMBO J. .

Abstract

EMBO J 30 8, 1459–1472 (2011); published online March 22 2011

Transcription factors (TFs) orchestrate cell-fate decisions by programming the expression of many genes, including those of other TFs that further drive lineage specification. C/EBP proteins and glucocorticoid receptor (GR) activate transcription of the master regulator of adipocyte differentiation, PPARγ. A study in this issue of The EMBO Journal sheds light on how C/EBPs, GR, STAT5, and RXR cooperate during early adipogenesis to globally remodel the epigenome.

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Conflict of interest statement

The authors declare that they have no conflict of interest.

Figures

Figure 1
Figure 1
Chromatin opening during adipogenesis. Temporary exposure of preadipocytes to adipogenic stimuli induces DNase I hypersensitive ‘hotspots’ with characteristics of enhancers including binding of multiple TFs, coactivator recruitment (e.g. p300), histone acetylation (stars), and increased chromatin accessibility. (A) Transient DNase I hypersensitive sites (DHSs). These represent a transition state not observed in either the preadipocyte or the adipocyte. They are present within the first day and disappear later in adipogenesis. One such hotspot functions as an enhancer of the master adipogenic TF, PPARγ. (B) Stable DHSs. Chromatin hotspots that open early and remain open through differentiation, with early TFs replaced by PPARγ and C/EBPα about 2 days after the start of adipogenesis. (C) De novo DHSs. Many DHSs are adipocyte specific and bound by PPARγ, which may be sufficient to open chromatin at these regions.
See this image and copyright information in PMC

Comment on

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