Extended Data Fig. 3: Both JunB FKO and BKO mice display enhanced energy expenditure and cold adaptation, related to Fig. 3.
10-week-old male were individually housed in Phenotyping Systems (Sable Systems International) coupled with a temperature controllable chamber. a. Respiratory exchange ratio (RER) was decreased in adipocyte-specific JunB KO (JunB FKO) mice compared to control littermates under cold stress conditions. Food intake (b) and motor activities (c) were little affected by JunB deficiency in fat. d. mRNA levels of JunB were significantly downregulated in BAT but not in gWAT of UCP1+ cell-specific JunB KO (JunB BKO) mice compared to the controls. e. JunB BKO mice exhibited enhanced basal and cold-induced O2 consumption throughout light and dark cycles compared with controls. f. The quantified data of Extended Data Fig. 3e using CaIR. There was little difference in food intake (g) despite slightly reduced motor activities under cold stress conditions (h) between JunB BKO and control mice. i. JunB deficiency significantly increased oxygen consumption in primary brown adipocytes (4 mice/group). j. The quantified data of Extended Data Fig. 3i using CaIR. k. Ablation of JunB-expressing adipocytes upregulated the expression levels of Ucp1, Ppargc1α, and Errα (7 mice/group). Extended Data Fig. 3i was analyzed by ANOVA analysis and the unpaired two-sided T-Test was used for the rest figures. Data are presented as the mean ± SEM. *P < 0.05 or **P < 0.01.
