Figure 7: Deficiency of NFIA causes an impaired brown fat gene signature and reciprocal elevation of skeletal muscle gene expression in vivo.
From: NFIA co-localizes with PPARγ and transcriptionally controls the brown fat gene program
(a) Macroscopic pictures (scale bar, 2.5 mm) and haematoxylin and eosin (HE) staining (scale bar, 100 μm) of BAT sections from neonates. (b) RT-qPCR analysis of the Ucp1 gene (mean ± s.e.m.; n = 11 mice for WT, 24 mice for Nfia+/−, and 15 mice for Nfia−/−, respectively; ∗P < 0.05). (c) Western blot analysis of UCP1 protein. β-actin was used as a loading control. Representative images of two independent experiments are shown. (d) ChIP-qPCR analysis of in vivo BAT. Ucp1 9.5 kb is a background site (mean ± s.e.m.; n = 3 independent samples; ∗P < 0.05; NS, not significant). Representative results of two independent experiments are shown. (e) Volcano plot of RNA-seq analysis. BAT- and SKM-selective genes are depicted in red and blue, respectively. The definitions of BAT- and SKM-selective genes (n = 254 and n = 312, respectively) are shown in the Methods. (f) Top GO terms of genes down- or upregulated by NFIA-KO. (g) Scatter plot showing fold changes of gene expression by NFIA introduction into C2C12 myoblasts and NFIA-KO in BAT. BAT- and SKM-selective genes are depicted in red and blue, respectively. The genome-wide analyses were performed once on the basis of the RNA-seq data set. Unprocessed original scans of blots are shown in Supplementary Fig. 8.
