Extended Data Figure 8 : Disrupting pik-1/IRAK causes ilc-17.1-like phenotypes.

From: IL-17 is a neuromodulator of Caenorhabditis elegans sensory responses

Extended Data Figure 8

a, Schematic of the exon/intron structure of pik-1, highlighting the db842 and tm2167 mutations used in this study. The allele db842 was found in strain AX3604; tm2167 was obtained from the Japanese knockout consortium. b, The pik-1 mutants exhibit an ilc-17.1-like defect and fail to sustain rapid movement at 21% O2. The pik-1 and ilc-17.1 phenotypes are non-additive, suggesting the proteins encoded by these genes act in the same pathway; n = 4 assays, 120 animals. **P < 0.01, Mann–Whitney U-test. c, The bordering and aggregation defects of pik-1 mutants can be rescued by expressing pik-1 cDNA from the pik-1 or flp-5 promoters (RMG); n = 4 assays. ***P < 0.001, ****P < 0.0001, Mann–Whitney U-test. d, A functional ppik-1::pik-1::SL2::mCherry polycistronic transgene is expressed broadly in the nervous system. RMG expression was confirmed using a pflp-5::gfp fiduciary marker. e, f, Sustained rapid movement of ilc-17.1 overexpressing animals at 21% O2 is blocked by mutations in the pik-1 gene. Speed assays were performed 10 min (e) and 2 h (f) after picking animals to the assay plates; n = 4 assays, 120 animals. ***P < 0.001, Mann–Whitney U-test.