Figure 7. PGC1a-mediated induction of Bmal1 by ADIPOQ.
(A) Circadian profile of Pgc1a mRNA levels in the MBH of WT (black) and Adipoq deficient (MT) mice (red; n = 3 per time point). (B) Induction of Pgc1a mRNA levels in N44 cells after Adn treatment and in the mediobasal hypothalamus (MBH) after i.v. Adn injection in wild-type mice (n = 5). (C) Expression of Pgc1a in N44 cells and in the MBH after shRNA-mediated knockdown of Adipor1 or Adipor2 (n = 3 for N44 cells and 7 (Con)/10 (KD) in MBH). (D) mRNA levels of Pgc1a (left) and Bmal1 (right) in non-synchronized N44 cells after shRNA-mediated knockdown of Pgc1a (n = 4). (E) Bmal1 mRNA levels in unsynchronized N44 cells in response to Adn with (right) or without (left) prior knockdown of Pgc1a (n = 4). (F) Bmal1 mRNA levels in unsynchronized N44 cells in response to Adn with (right) or without (left) prior treatment with 5 µM VPR66 (n = 4). (G) ChIP-qPCR for PGC1a binding to Bmal1 RORE (and Bmal1 3’-UTR as negative control) in unsynchronized N44 cells in response to Adn treatment (n = 3). (H, I) Response of Bmal1-luc luminescence rhythms in synchronized N44 cells to Adn treatment at 23 hr after synchronization (arrow) with or without prior knockdown of Pgc1a. (H) Normalized luminescence data (n = 3 per condition). (I) Phasing of the first and second peak after Adn treatment relative to solvent (n = 8). All data are means ± SEM. Box plots show medians, quartiles and min/max. p-values: (B) 0.0116 (N44, +Adn vs. -Adn), ANOVA dF = F(1, 16)=0.299 (interaction)/0.294 (tissue)/15.60 (treatment); (C) 0.0001 (N44, Adipor1 KD vs. Con), 0.0020 (MBH, Adipor1 KD vs. Con), ANOVA dF = F(1, 19)=0.028 (interaction)/0.044 (tissue)/40.90 (treatment); (D) < 0.0001 (Pgc1a, Pgc1a KD vs. Con),<0.0001 (Bmal1, Pgc1a KD vs. Con), ANOVA dF = F(1, 12)=9.693 (interaction)/8.566 (gene)/151.5 (treatment). (E) 0.0019 (Con, +Adn vs. -Adn), ANOVA dF = F(1, 12)=4.894 (interaction)/37.05 (genotype)/15.39 (treatment); (F) 0.0087 (PBS, +Adn vs. -Adn), ANOVA dF = F(1, 12)=2.044 (interaction)/9.281 (inhibition)/12.45 (treatment); (G) 0.0013 (RORE, +Adn vs. -Adn), ANOVA dF = F(1, 8)=13.17 (interaction)/87.25 (site)/16.20 (treatment); (I) < 0.0001 (peak 1, Con vs. KD), 0.0258 (peak 2, Con vs. KD), ANOVA dF = F(1, 24)=2.809 (interaction)/3.192 (peak)/29.93 (genotype).

