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Fig. 5 Dysregulated inflammatory gene expression in keap1b mutants. Relative mRNA expression of A TNF-α and B c3a in larvae after 12-h exposure to a sub-lethal concentration of 4.5 μM CuSO4 (to analyze the transcriptional inflammatory response prior to the onset of significant mortality). The lethal phenotype of keap1b−/− larvae observed at higher concentrations (Fig. 4B) is associated with a significantly blunted transcriptional induction of these key pro-inflammatory cytokines compared to wild-type, suggesting that the hypersensitivity is due to an inadequate, rather than excessive, inflammatory response. This indicates that Keap1b plays a critical role in facilitating proper inflammatory gene expression through an Nrf2-mediated response mechanism. Expression is normalized to ef1a and relative to the untreated WT group. Data are mean ± SEM (n = 3). *p < 0.05