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. 2019 Apr 4;12(4):dmm037259. doi: 10.1242/dmm.037259

Fig. 3.

Fig. 3.

Increased FOXO activity drives pathophysiology in fat body fs(1)h knockdowns. (A) Survival of male fs(1)h knockdowns and controls, wild-type or heterozygous for foxo, at 25°C. Number of flies in this experiment: 30-40 per genotype. (B,C) Expression of antimicrobial peptide (AMP) genes in control (c564>0) and fs(1)h knockdown (c564>fs(1)h-IR) flies, either wild-type or heterozygous for foxo. Values represent mean+s.e.m.; genotypes were compared using ANOVA (*P<0.05, ****P<0.0001). (B) Isolated fat body, uninjected flies. (C) Francisella novicida-injected whole flies. (D) Triglyceride (TG) levels in control and fs(1)h fat-body-knockdown flies, either wild-type or heterozygous for foxo, under normal conditions and following 24 h starvation (F, fed; S, starved; n.d., no TG detected). Values shown as mean. (E) Free sugar (trehalose and glucose) and stored carbohydrate (glycogen) levels in control and fs(1)h fat-body-knockdown flies, either wild-type or heterozygous for foxo. Values as mean+s.e.m.; genotypes were compared using unpaired two-tailed t-test (*P<0.05). Number of samples: six replicates per genotype.