Fig. 3.

Oxidative stress redirects SKN-1gf transcriptional activity while restoring somatic lipid distribution. (A–C) The absence of somatic lipids in SKN-1gf mutants treated with vehicle (control) (A) is restored in animals exposed to 75 µM PQ (B) (representative image from n = 237); arrows indicate somatic lipids. (C) Quantification of lipid distribution across tissues. All experiments were performed in a minimum of biological triplicates and lipid distribution was assessed in at least 300 animals. (See also SI Appendix, Fig. S5 and Dataset S3 for all measurements.) (D) Volcano plot of differentially expressed genes in skn-1gf compared to WT (red), genes altered by PQ exposure (blue), and innate immunity genes (black); changes in immune genes analyzed by unpaired, nonparametric, t test (Mann–Whitney). (E and F) Analysis of the mRNA reads of the indicated genes related to (E) oxidative stress and xenobiotic responses and (F) innate immunity and pathogen resistance. See also Datasets S3 and S4 for RNA-seq measurements. (G) ChIP-qPCR reveals PQ treatment redirection of SKN-1gf activity is associated with a loss of recruitment at innate immunity gene promoters. (Scale bar, 50 μm.) *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001. FPKM, fragments per kilobase of transcript per million mapped reads.