Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

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

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 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/.

PMC Copyright notice

Fig. 8 — a and b Downregulated (a) and upregulated (b) genes in whole animal RNA-seq profiles of malt-1; npr-1, ilc-17.1; npr-1 and nfki-1; npr-1 double mutants compared to npr-1 controls. Gene ontology (GO) terms and KEGG pathways significantly overrepresented among genes dysregulated in all three mutant conditions are shown (q-value <0.05, with a minimum log2(fold-change) of ±0.25). c and d Salt chemotaxis after conditioning by food-withdrawal in the absence or presence of NaCl. *P < 0.05, **P < 0.01, ***P < 0.001, one-way ANOVA with Tukey’s post hoc HSD, N = 6 assays. d The salt chemotaxis learning defect of ilcr-1 mutants is rescued by driving ilcr-1 expression in many neurons (rab-3 or flp-21 promoters), or specifically in ASE (flp-6 promoter). e–i PA14 big lawn assays. n ≥ 81 animals. ***P < 0.001, two-sided logrank test; precise n numbers and P values are provided in Supplementary Table 1. Mutants lacking malt-1 (e) or encoding protease-dead malt-1 (f), or defective in other IL-17 signaling components (g, h) are resistant to P. aeruginosa PA14 in big lawn assays, where animals cannot escape from the PA14 lawn. The enhanced survival of malt-1 mutants is rescued by pan-neuronal expression of malt-1 gDNA. n ≥ 81 animals. i The enhanced resistance of malt-1 mutants to PA14 requires TIR-1. Like tir-1 mutants, malt-1; tir-1 double mutants are hypersensitive to PA14 infection. j–m Lifespan. n ≥ 92 animals. **P < 0.01, ***P < 0.001, two-sided logrank test; precise n numbers and P values are provided in Supplementary Table 3. j and k The lifespan of malt-1 and ilc-17.1 mutants is increased compared to N2 controls. The malt-1 phenotype is rescued by expressing malt-1 gDNA pan-neuronally (j) and the ilc-17.1 phenotype can be rescued by expressing ilc-17.1 cDNA from its endogenous promoter (k). l The lifespan phenotypes of malt-1 and ilc-17.1 mutants are not additive. m The shortened lifespan of animals overexpressing ILC-17.1 is abolished in malt-1 mutants. See also Supplementary Fig. 7, Supplementary Tables 1–3 and Supplementary Data 3–6.