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. 2020 Apr 29;11:2099. doi: 10.1038/s41467-020-15872-y

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 7 — a Immunoblot analysis of IL-17 signaling components from nuclear and cytoplasmic fractions of C. elegans lysate. I, input, C, cytosolic, N, nuclear. NFKI-1 is predominately nuclear; ACTL-1 and MALT-1 are distributed between the nucleus and cytoplasm. Similar results were obtained in 5 experiments. b and c Overexpressing malt-1 in neurons, using the rab-3 promoter, restores the arousal response to 21% O₂ to ilc-17.1 and ilcr-1 mutants (b), and actl-1 and pik-1 mutants (c). b n = 52 animals (npr-1), n = 104 animals (npr-1; ilcr-1), n = 71 animals (npr-1; ilcr-1; rab-3p::malt-1), n = 86 animals (npr-1; ilc-17.1), n = 61 animals (npr-1; ilc-17.1; rab-3p::malt-1). c n = 19 animals (npr-1), n = 46 animals (npr-1; actl-1), n = 26 animals (npr-1; actl-1; rab-3p::malt-1), n = 33 animals (npr-1; pik-1), n = 28 animals (npr-1; pik-1; rab-3p::malt-1). Plots show average speed (line) and SEM (shaded regions). ***P < 0.001, two-sided Mann-Whitney U test. d and e Overexpressing malt-1 gDNA also rescues the aggregation phenotype (d), but not the arousal defect (e) of nfki-1 mutants. d N = 7 assays (npr-1), N = 6 assays (npr-1; nfki-1 and npr-1; nfki-1; malt-1::gfp). ***P = 3.5e−05, one-way ANOVA with Tukey’s post hoc HSD. e n = 47 animals (npr-1), n = 79 animals (npr-1; nfki-1), n = 39 animals (npr-1; nfki-1; malt-1::gfp). **P = 0.0067, two-sided Mann-Whitney U test. f and g The aggregation phenotype of malt-1 is rescued by overexpressing nfki-1 cDNA (f), while speed defects are partially rescued (g). f N = 5 assays (npr-1), N = 4 assays (npr-1; malt-1 and npr-1; malt-1; nfki-1::gfp). ***P = 7e−07, one-way ANOVA with Tukey’s post hoc HSD. g n = 36 animals (npr-1), n = 50 animals (npr-1; malt-1), n = 44 animals (npr-1; malt-1; nfki-1::gfp). ***P = 7e−07, one-way ANOVA with Tukey’s post hoc HSD. ***P = 4.7e−4, two-sided Mann-Whitney U test.