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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 2. An AKH-induced hyperglycemia model and in vivo RNAi screen.

Figure 2

(A–D) Glycemic levels (glucose + trehalose) (A, n=4, 40 larvae), immunoblots (B), and gene expression (D) in fat bodies from R4 > AKH (UAS-Akh/+; R4-Gal4/+) 3rd instar larvae. (C) Glycemic levels of R4 > AKH larvae with knockdown of AKH/glucagon signaling components (n=4, 40 larvae). Schematic (E) and results (F) of the in vivo RNAi screen of kinases and phosphatases in AKH-induced hyperglycemic flies. Glycemic levels in R4 > Akh + w-i (UAS-Akh/+; R4-Gal4/UAS-w-RNAi) and R4 > Akh + AkhR-i (UAS-Akh/+; R4-Gal4/UAS-AkhR-RNAi) were normalized to 1 (100%) and 0, respectively (n=3, 30 larvae). (G) Annotation of novel positive gene ‘hits’ identified in the in vivo RNAi screen (> 1.7 or < 0.3 as cutoffs) for signaling pathways or biological processes. (H) 30 hits modulate AKH-induced hyperglycemia via regulation of p-IRE1 or p-CREB2. Data are presented as means ± SEM. * p < 0.05.