MALT-1 mediates IL-17 neural signaling to regulate C. elegans behavior, immunity and longevity.


Journal

Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555

Informations de publication

Date de publication:
29 04 2020
Historique:
received: 22 05 2019
accepted: 26 03 2020
entrez: 1 5 2020
pubmed: 1 5 2020
medline: 30 7 2020
Statut: epublish

Résumé

Besides pro-inflammatory roles, the ancient cytokine interleukin-17 (IL-17) modulates neural circuit function. We investigate IL-17 signaling in neurons, and the extent it can alter organismal phenotypes. We combine immunoprecipitation and mass spectrometry to biochemically characterize endogenous signaling complexes that function downstream of IL-17 receptors in C. elegans neurons. We identify the paracaspase MALT-1 as a critical output of the pathway. MALT1 mediates signaling from many immune receptors in mammals, but was not previously implicated in IL-17 signaling or nervous system function. C. elegans MALT-1 forms a complex with homologs of Act1 and IRAK and appears to function both as a scaffold and a protease. MALT-1 is expressed broadly in the C. elegans nervous system, and neuronal IL-17-MALT-1 signaling regulates multiple phenotypes, including escape behavior, associative learning, immunity and longevity. Our data suggest MALT1 has an ancient role modulating neural circuit function downstream of IL-17 to remodel physiology and behavior.

Identifiants

pubmed: 32350248
doi: 10.1038/s41467-020-15872-y
pii: 10.1038/s41467-020-15872-y
pmc: PMC7190641
doi:

Substances chimiques

Caenorhabditis elegans Proteins 0
Interleukin-17 0
Green Fluorescent Proteins 147336-22-9
Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 Protein EC 3.4.22.-
Oxygen S88TT14065

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

2099

Subventions

Organisme : Medical Research Council
ID : MC_U105178786
Pays : United Kingdom
Organisme : Wellcome Trust
ID : 209504/Z/17/Z
Pays : United Kingdom
Organisme : NIH HHS
ID : P40 OD010440
Pays : United States

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Auteurs

Sean M Flynn (SM)

Cell Biology Division, Medical Research Council Laboratory of Molecular Biology, Cambridge, CB2 0QH, United Kingdom.

Changchun Chen (C)

Cell Biology Division, Medical Research Council Laboratory of Molecular Biology, Cambridge, CB2 0QH, United Kingdom.
Umeå Center for Molecular Medicine, Wallenberg Center for Molecular Medicine, Umeå University, SE-901 87, Umeå, Sweden.

Murat Artan (M)

Cell Biology Division, Medical Research Council Laboratory of Molecular Biology, Cambridge, CB2 0QH, United Kingdom.

Stephen Barratt (S)

Cell Biology Division, Medical Research Council Laboratory of Molecular Biology, Cambridge, CB2 0QH, United Kingdom.

Alastair Crisp (A)

Cell Biology Division, Medical Research Council Laboratory of Molecular Biology, Cambridge, CB2 0QH, United Kingdom.

Geoffrey M Nelson (GM)

Cell Biology Division, Medical Research Council Laboratory of Molecular Biology, Cambridge, CB2 0QH, United Kingdom.
Department of Biomedical Informatics, Harvard Medical School, Boston, MA, 02115, USA.

Sew-Yeu Peak-Chew (SY)

Biological Mass Spectrometry and Proteomics, Cell Biology Division, Medical Research Council Laboratory of Molecular Biology, Cambridge, CB2 0QH, United Kingdom.

Farida Begum (F)

Biological Mass Spectrometry and Proteomics, Cell Biology Division, Medical Research Council Laboratory of Molecular Biology, Cambridge, CB2 0QH, United Kingdom.

Mark Skehel (M)

Biological Mass Spectrometry and Proteomics, Cell Biology Division, Medical Research Council Laboratory of Molecular Biology, Cambridge, CB2 0QH, United Kingdom.

Mario de Bono (M)

Cell Biology Division, Medical Research Council Laboratory of Molecular Biology, Cambridge, CB2 0QH, United Kingdom. mdebono@ist.ac.at.
Institute of Science and Technology Austria (IST Austria), Am Campus 1, 3400, Klosterneuburg, Austria. mdebono@ist.ac.at.

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