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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 5. Baboa responds to Actβ regarding modulation of AKH action and glycemia.

Figure 5

(A) Schematic and relative FPKM value of different Babo isoforms indicated by RNA-seq of 3rd instar larval fat body (n=3, 30 larval fat bodies). (B, C) Fat body immunoblots (B) and glycemic levels (C) (n=4, 40 larvae) of CG > Actβ larvae with knockdown of Babo isoforms. Genotype is CG-Gal4, tub-Gal80ts /+; UAS-Actβ/UAS-RNAi. (D, E) Fat body immunoblots (D) and glycemic levels (E) (n=4, 40 larvae) of R4 > Akh larvae with knockdown of Babo isoforms. Genotype is UAS-Akh/+; R4-Gal4/UAS-RNAi. (F) Glycemic levels in Actin > Daw-i larvae (left, n=4, 40 larvae) and in larvae with fat body overexpression of Actβ or Daw (right, n=4, 40 larvae). (G) Immunoblots of fat body in larvae with fat body overexpression of Actβ or Daw. (H) Glycemic levels in 3rd instar larvae with fat body overexpression of Daw plus knockdown of AkhR or Babo (n=4, 40 larvae). The genotype is CG-Gal4, tub-Gal80ts/+; UAS-Daw/UAS-RNAi. Data are presented as means ± SEM. * p < 0.05.