We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
MALT-1 mediates IL-17 neural signaling to regulate C. elegans behavior, immunity and longevity.
- Authors
Flynn, Sean M.; Chen, Changchun; Artan, Murat; Barratt, Stephen; Crisp, Alastair; Nelson, Geoffrey M.; Peak-Chew, Sew-Yeu; Begum, Farida; Skehel, Mark; de Bono, Mario
- 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. IL-17 is a pro-inflammatory molecule that can also regulate neural circuit function. Here the authors use C. elegans to show that the paracaspase MALT-1 lies downstream of IL-17 signaling and regulates many aspects of C. elegans biology, including escape behavior, associative learning, immunity and longevity.
- Subjects
IRAQ; CAENORHABDITIS elegans; NEURAL circuitry; ASSOCIATIVE learning; NERVOUS system; IMMUNITY; LONGEVITY
- Publication
Nature Communications, 2020, Vol 11, Issue 1, p1
- ISSN
2041-1723
- Publication type
Article
- DOI
10.1038/s41467-020-15872-y