Genomic redistribution of GR monomers and dimers mediates transcriptional response to exogenous glucocorticoid in vivo

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Figure 6.
Figure 6.

Glucocorticoids (GCs) redistribute GR from monomeric to dimeric sites at regulated genes. (A) Density heatmap of ChIP-seq reads from GR peaks at 6 a.m. with at least 2 RPM in any condition. Prednisolone (pred) treatment of WT and GRdim mice spanned 24 h, and regulated sites in WT mice have at least a twofold difference compared with untreated controls. Top-ranked GO terms for the gained and lost sites are indicated on the left. MEME top-ranked de novo sequences are indicated on the right. See Supplemental Material for a comprehensive list of motifs. (B) GR ChIP-exo at gained sites in WT mice with or without Pred treatment. Average profiles (top) and density heatmaps (bottom) show the 5′ ends of the forward-stranded (red) and reverse-stranded (blue) sequence tags. (C) Box plot comparing CEBPB occupancy at sites with increased GR binding (gained) after Pred treatment. (D) Scatter plot comparing sequence tags from GR ChIP-seq in WT liver with and without Pred treatment, with sites containing up- or down-regulated RNAPII occupancy in response to Pred highlighted in red or blue, respectively. (E) Fraction of Pred-regulated genes with a transcription start site within 100 kb of a gained or lost GR binding site (top) or a non-Pred-regulated dimeric or monomeric GR binding site (bottom).

This Article

  1. Genome Res. 25: 836-844

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