Fig. 2.

Loss of Histone H3 trimethylation restricts SKN-1gf transcriptional activity and suppresses the loss of somatic lipids. (A) ChIP-qPCR reveals SKN-1gf enrichment at the promoter of target genes relative to wild-type SKN-1. (B and C) ORO staining of lipid stores in C. elegans. (B) wdr-5lf(ok1417) mutants display normal distribution of lipids across tissues (representative image from n = 415). (C) The loss of somatic lipid stores observed in SKN-1gf mutant animals is restored in wdr-5lf(ok1417);skn-1gf(lax188) double mutants (representative image from n = 892). (D) Quantification of lipid distribution across tissues. All experiments were performed in a minimum of 3 biological replicates and lipid distribution was assessed in at least 300 animals. (See also SI Appendix, Fig. S3 for all measurements.) (E) Volcano plot of differentially expressed genes in skn-1gf compared to WT (red), genes altered by loss of wdr-5lf (green), and innate immunity genes (black); changes in immune genes analyzed by unpaired, nonparametric, t test (Mann–Whitney). (F and G) Analysis of the mRNA reads of the indicated genes related to (F) innate immunity and pathogen resistance and (G) oxidative stress and xenobiotic responses. See Datasets S2 and S4 for RNA-seq measurements. (Scale bar, 50 μm.) *P < 0.05; **P < 0.01; ****P < 0.0001. FPKM, fragments per kilobase of transcript per million mapped reads.