Serotonergic Chemosensory Neurons Modify the C. elegans Immune Response by Regulating G-Protein Signaling in Epithelial Cells
Treatment of wild type animals with 3.8/ml 5-HT caused a decrease in the number of Dar animals following infection with M. nematophilum (A) and decreased the clearance of SYTO13 labeled pathogen from the rectal opening (B). Serotonin was unable to decrease the percentage of Dar animals (A) or the rate of pathogen clearance (B) when EGL-10 cDNA was overexpressed in the rectal epithelium of wild type animals suggesting that GOA-1(Gáo) signaling in the rectal epithelium is required for serotonin to suppress the immune response. Animals lacking tph-1 have wild type levels of Dar response on lawns contaminated with 10% M. nematophilum (A) but are more able to clear pathogen infections than wild type (C). Conversely activation of GOA-1(Gáo) using egl-10 loss-of-function mutants results in a decrease in the percentage of Dar animals (A) and infections clear more slowly than wild type animals (C). To determine whether GOA-1(Gáo) acts downstream of serotonin we combined egl-10(n692) with tph-1(mg280) or tph-1(n4622). The percentage of Dar animals (A) and the rate of pathogen clearance was indistinguishable between egl-10(n692) and these double mutants (C). Thus GOA-1(Gáo) signaling acts downstream of serotonin synthesis to suppress the immune response to M. nematophilum infection.