Fig. 7: Pngl mutants exhibit increased lipid catabolism and supplementation on dietary lipid partially rescues their lethality. | Nature Communications

Fig. 7: Pngl mutants exhibit increased lipid catabolism and supplementation on dietary lipid partially rescues their lethality.

From: Gut barrier defects, intestinal immune hyperactivation and enhanced lipid catabolism drive lethality in NGLY1-deficient Drosophila

Fig. 7

a Images showing Nile red (red) and DAPI (blue) staining in fat body and midgut of the indicated genotypes and their quantification (n = 4 independent replicates). Scale bars are 50 µm. b Triacylglycerol (TAG) level in hemolymph and midgut of indicated genotypes (n = 3 independent replicates). c Free fatty acid (FFA) level in the hemolymph of indicated genotypes (n = 3 independent replicates). d Pie charts showing % carbohydrates, proteins and fats in different diet compositions. e Graph showing % animals that reach the pupal stage upon feeding on the indicated diets (n = 3 independent replicates). f Graph showing lethality rescue in Pngl mutants upon feeding on the indicated diets (n = 3 independent replicates). g Schematic model showing that loss of Pngl in several cell types of the Drosophila larvae results in Foxo overactivation and subsequent innate immune gene expression and lipid catabolism, leading to lethality. In all panels, each circle represents an independent replicate, and mean ± standard deviation is shown. P values are indicated on bars. Significance is ascribed as P < 0.05 using one-way ANOVA followed by Šidák correction (a, e, f) or two-way ANOVA followed by Šidák correction (b, c). Source data are provided as Source Data file.

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