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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. 9 — a Activation of nematode IL-17Rs ILCR-1 and ILCR-2 engages ACTL-1, the C. elegans ACT1-like adapter, probably via their SEFIR domains. ACTL-1 recruits the C. elegans IRAK and MALT1 homologs to form the ACT1-IRAK-MALT1 signalosome in the cytoplasm. This serves a scaffolding function to recruit IκBζ/NFKI-1, and modulate its actvity by an unknown mechanism. NFKI-1 probably orchestrates changes in the transcriptome of RMG and other cells. MALT1-mediated cleavage of unknown substrate(s) positively regulates NFKI-1 signaling. In parallel to this pathway, MALT-1 forms a complex of unknown function with TIR-1/SARM1, and with multiple RNA-binding proteins. b ILCR receptors and downstream signaling components including MALT-1 are expressed in many neurons. This neuronal signaling cassette alters associative learning, as well as O₂-escape behaviors, and suppresses lifespan and immunity.