Serotonergic Chemosensory Neurons Modify the C. elegans Immune Response by Regulating G-Protein Signaling in Epithelial Cells
Adult tph-1(mg280) or tph-1(n4622) animals lacking the serotonin biosynthetic enzyme TPH-1 were infected on lawns contaminated with 10% M. nematophilum. The percentage of tph-1(mg280) and tph-1(n4622) progeny with the Dar phenotype was indistinguishable from wild type (A). When animals were infected on lawns contaminated with 0.05% M. nematophilum the Dar phenotype was increased from 60.3% in wild type animals to 92.1% in tph-1(mg280) and 83.0% in tph-1(n4622) (A). This increase could be rescued by treatment with exogenous 5-HT (A) or expression of TPH-1 cDNA in ADF, but not NSM, neurons (B). tph-1(mg280) and tph-1(n4622) animals cleared SYTO13 labeled pathogen more quickly than wild type animals consistent with a role for TPH-1 in suppressing the immune response (C). This phenotype was rescued by 5-HT treatment (C) or expression of a TPH-1 cDNA in both ADF and NSM neurons or ADF neurons alone but not by expression in NSM alone (D). * indicates significance relative to wild type. § indicates significance relative to untreated mutant control (C) or tph-1(mg280) (D) (see materials and methods for details of statistical analysis).