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

Sean M. Flynn, Changchun Chen, Murat Artan, Stephen Barratt, Alastair Crisp, Geoffrey M. Nelson, Sew-Yeu Peak-Chew, Farida Begum, Mark Skehel and Mario de Bono ()
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Sean M. Flynn: Medical Research Council Laboratory of Molecular Biology
Changchun Chen: Medical Research Council Laboratory of Molecular Biology
Murat Artan: Medical Research Council Laboratory of Molecular Biology
Stephen Barratt: Medical Research Council Laboratory of Molecular Biology
Alastair Crisp: Medical Research Council Laboratory of Molecular Biology
Geoffrey M. Nelson: Medical Research Council Laboratory of Molecular Biology
Sew-Yeu Peak-Chew: Medical Research Council Laboratory of Molecular Biology
Farida Begum: Medical Research Council Laboratory of Molecular Biology
Mark Skehel: Medical Research Council Laboratory of Molecular Biology
Mario de Bono: Medical Research Council Laboratory of Molecular Biology

Nature Communications, 2020, vol. 11, issue 1, 1-15

Abstract: Abstract 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.

Date: 2020
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DOI: 10.1038/s41467-020-15872-y

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