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. Author manuscript; available in PMC: 2018 Feb 7.
Published in final edited form as: Cell Metab. 2017 Feb 7;25(2):386–399. doi: 10.1016/j.cmet.2017.01.002

Figure 3. Babo signaling regulates AKH action and glycemic control.

Figure 3

(A) Effects of knockdown of individual TGF-β-like receptors (left) or downstream transcription factors (right) in the fat body on glycemic levels (glucose + trehalose) in R4 > Akh 3rd instar larvae (UAS-Akh/+; R4-Gal4/UAS-RNAi) (n=4, 40 larvae). (B) Glycemic levels in CG > Babo-i larvae (CG-Gal4/+; UAS-babo-RNAi/+) fed with normal or high-sugar food (n=4, 40 larvae). (C–D) Immunoblots of protein from freshly isolated larval fat bodies that were treated with or without 1 µM synthetic AKH peptide for 30 min (C, left) or freshly isolated fat bodies of 3rd instar larvae fed a high-sugar diet (C, right) or a normal diet (D). (E) Glycemic levels in Babo or dSmad2 overexpressing 3rd instar larvae (n=4, 40 larvae). (F) Glycemic levels in 3rd instar larvae bearing Babo knockdown (left, CG-Gal4/+; UAS-AkhR-RNAi/UAS-Babo-RNAi) or dSmad2 overexpression (right, CG-Gal4/+; UAS-AkhR-RNAi/UAS-dSmad2) in the context of AkhR deficiency in fat body (n=4, 40 larvae). Data are presented as means ± SEM. * p < 0.05.