Toll-like receptors (TLRs) play critical roles in innate immunity in many animal species. The sole TLR of C. elegans--TOL-1--is required for a pathogen-avoidance behavior, yet how it promotes this behavior is unknown. We show that for pathogen avoidance TOL-1 signaling is required in the chemosensory BAG neurons, where it regulates gene expression and is necessary for their chemosensory function. Genetic studies revealed that TOL-1 acts together with many conserved components of TLR signaling. BAG neurons are activated by carbon dioxide (CO₂), and we found that this modality is required for pathogen avoidance. TLR signaling can therefore mediate host responses to microbes through an unexpected mechanism: by promoting the development and function of chemosensory neurons that surveil the metabolic activity of environmental microbes.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4642686 | PMC |
http://dx.doi.org/10.1016/j.cub.2015.07.037 | DOI Listing |
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