NHR-86 binds to the promoters of innate immune genes to drive their transcription.

(A) Venn diagram showing the number of nhr-86-dependent, R24-induced genes in the mRNA-seq experiment, the genes whose promoters were bound by NHR-86 following R24 treatment in the ChIP-seq experiment, and the overlap between these datasets. The overlap between these datasets is significantly more than is expected by chance alone (1.1 gene overlap expected by chance, hypergeometric p-value = 2x10-39). ChIP-seq profiles, mRNA-seq profiles and confirmatory ChIP-PCR are presented for the representative immune effectors irg-4 (B), irg-5 (C), mul-1 (F49F1.6) (D) and drd-50 (F49F1.1) (E) in animals of the indicated genotype exposed to R24 or the control. The y-axis is the number of reads (log2). A gene model shows the location of the exons (blue) of the indicated genes. ChIP was performed with an anti-GFP antibody in C. elegans wild-type and transgenic NHR-86::GFP animals. Final set of peaks were called if the difference in intensity values of samples had a significance level of p-value S3 Table) for the indicated comparison. In the ChIP-PCR data, the percent input for each condition was normalized to the abundance of a random intergenic region of chromosome four. ** pirg-5 (C) and a random intergenic region on chromosome six (F) were not enriched by control or R24 treatment. Each data point in the ChIP-qPCR data is from an independent biological replicate.