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Drosophila melanogaster is an excellent model to dissect the molecular components and pathways of the innate anti-pathogen immune response. The nematode parasite Steinernema carpocapsae and its mutualistic bacterium Xenorhabdus nematophila form a complex that is highly pathogenic to insects, including D. melanogaster . We have used symbiotic (carrying X. nematophila ) and axenic (lacking X. nematophila ) nematodes to probe the regulation of genes belonging to different immune signaling pathways in D. melanogaster larvae and assess the survival response of certain mutants to these pathogens. We found that both types of S. carpocapsae upregulate MyD88 (Toll), but not PGRP-LE (Imd); whereas axenic S. carpocapsae strongly upregulate Wengen (Jnk), Domeless (Jak/Stat), Dawdle (TGFβ, Activin), and Decapentaplegic (TGFβ, BMP). We further found that inactivation of Wengen and Decapentaplegic confers a survival advantage to larvae infected with axenic S. carpocapsae , whereas mutating PGRP-LE promotes the survival of larvae infected with symbiotic nematodes.

Differential Regulation of Immune Signaling and Survival Response in Drosophila melanogaster Larvae upon Steinernema carpocapsae Nematode Infection