Fig 1: FBF1 controls adipose beiging through a cilia-specific PKA signaling(A and B) PKACa localization in WT and Fbf1tm/tm MEFs before and after treated with (A) CL-316,243 or (B) mirabegron. Centrosomes were stained with ?-tubulin. Scale bar, 1 µm.(C) Immunoblotting on vWAT or MEF extracts.(D) WT vWAT preadipocytes labeled with yellow fluorescent protein (YFP)-tagged CEP170C-PKI, CEP170C, and PKI. Centrosomes were stained with ?-tubulin. Scale bar, 1 µm.(E) WT vWAT preadipocytes overexpressed PKI, CEP170C, or CEP170C-PKI were treated with CL-316,243 and differentiated for 7 days in adipogenic medium (AM), then fixed, stained, and imaged. Green: lipids, blue: nuclei. Scale bar, 50 µm.(F) Relative mRNA levels of beiging genes in WT vWAT preadipocytes overexpressed PKI, CEP170C, or CEP170C-PKI.(G) Endogenous AKAP9 immunoprecipitates with FBF1 in 3T3-L1 cells.(H) AKAP9 localization in 3T3-L1 cells. FBF1 or ODF2 labeled basal bodies. Scale bar, 1 µm.(I) SIMS and 3-dimensional (3D) surface-rendering images of the basal bodies of 3T3-L1 cells stained for PKACa, AKAP9, and FBF1. Scale bar, 1 µm.(J) SIMS images of the basal bodies of 3T3-L1 cells stained for PKACa and FBF1. Scale bar, 1 µm.(K) Association between endogenous PKARI and FBF1 in 3T3-L1 cells treated with control or Akap9 siRNA.(L) 3T3-L1 cells treated with control or Akap9 siRNA were differentiated with CL-316,243 inductions for 7 days, then fixed, stained, and imaged. Green: lipids, blue: nuclei. Scale bar, 100 µm.(M) Relative mRNA levels of beiging genes in 3T3-L1 cells treated with control or Akap9 siRNA.