Fig. 2: Enhanced innate immune response in midgut contributes to the lethality of Pngl mutants. | Nature Communications

Fig. 2: Enhanced innate immune response in midgut contributes to the lethality of Pngl mutants.

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

Fig. 2

a Graph showing immune response gene expression (relative fold change to control, y w) in the midgut of age-matched larvae of the indicated genotypes (n = 3 independent replicate). b Graph showing % lethality rescue in Pngl mutants upon removing one copy (1X) of each immune gene activator (n = 4–6 independent replicates per genotype). c Graph showing survival upon Pngl knockdown driven by the indicated GAL4 drivers (n = 4 independent replicates). d Graph showing immune gene expression (relative fold change to genetic control) in the indicated genotypes (n = 3 independent replicates). e Graph showing % lethality rescue in Pngl mutants upon tissue-specific knockdown of immune activators (foxo, Rel and Tl) using the indicated GAL4 drivers (n = 3 independent replicates). f Graph showing % lethality rescue in Pngl mutants upon overexpression of wild-type (PnglWT) and catalytically inactivate (PnglC303A) Pngl using indicated GAL4 drivers (n = 4 independent replicates). g, h Graphs showing immune gene expression in the midgut of age-matched larvae of indicated genotypes (n = 3 independent replicates). In all panels, each circle represents an independent replicate, and mean ± standard deviation is shown. Numbers on bars indicate the P values. Significance is ascribed as P < 0.05 using one-way ANOVA with multiple comparisons followed by Šidák correction in (a–c, e–h) or two-tailed unpaired t-test (d). Source data are provided as Source Data file.

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