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. 2015 Feb 1;29(3):298–307. doi: 10.1101/gad.252734.114

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© 2015 Harms et al.; Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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Figure 2. — PRDM16 deficiency reduces MED1 levels at BAT-selective genes. (A) Box plot depicting changes in gene expression of BAT-selective (BAT-sel.) genes (red), common genes (gray), and WAT-selective (WAT-sel.) genes (white) in Prdm16 knockout (KO)/wild-type (WT) BAT. (***) P < 10⁻¹⁰⁰. (B) Box plot showing changes in Pol II levels within the gene body of BAT-selective, common, and WAT-selective genes in Prdm16 knockout/wild-type BAT. (***) P < 10⁻⁷⁰. (C) Box plot showing H3K27-Ac levels within 100 kb of the TSS of BAT-selective, common, and WAT-selective genes in Prdm16 knockout/wild-type BAT. (D) Box plot depicting MED1 occupancy within 100 kb of the TSS of BAT-selective, common, and WAT-selective genes in Prdm16 knockout/wild-type BAT. (***) P < 10⁻¹⁵. (E) ChIP-seq profiles for PRDM16 (blue), Pol II in wild-type and knockout BAT (green), MED1 in wild-type and knockout BAT (red), and H3K27-Ac in wild-type and knockout BAT (magenta).