Fig. 6 |. JunB suppresses the formation of high-thermogenic adipocytes by binding to PGC-1α effector ERRα.

a, Schematic showing the JunB binding site TRE (TGA(C/G)TCA) on the Erra promoter at the −1,305/−1,315 region. TSS, transcription start site. b, Overexpression of JunB suppressed basal and PGC-1α-induced activation of the Erra promoter in HEK293T cells (n = 3, independent experiments). c, Knockdown of JunB increased basal and PGC1α-induced activation of the Erra promoter in primary preadipocytes (n = 3, independent experiments). d, ChIP assay showed that JunB bound to the Erra promoter in BAT (n = 3 mice per group). e, The EMSA showed the direct interaction between JunB recombinant protein and DNA probe of the Erra promoter at the −1,305/−1,315 region (n = 3, independent experiments). WT, wild type. f,g, The ability of JunB to induce basal and PGC-1α-induced Erra gene activation was blocked when the TRE site was mutated (n = 3, independent experiments) (f) or TRE site was depleted (n = 3, independent experiments) (g) on the luciferase reporter of the Erra promoter. h, Suppressing JunB increased the mRNA of ERRα in primary preadipocytes. i–l, Suppressing ERRα abolished increased oxygen consumption (n = 3, independent experiments) (i), maximum respiration capacity (n = 3, independent experiments) (j) and mitochondria^hi adipocytes (k and l) (n = 3, independent experiments) in JunB KO differentiated brown adipocytes. Data were analysed using an unpaired two-sided t-test. OCR, oxygen consumption rate.