C. elegans pathogenic susceptibility is influenced by the worm's detection of its environment and its capacity to resist and resolve damage following infection. Here, we use a model where worms can sense, but not ingest, the pathogen Enterococcus faecalis (EF) . We identify that perception of EF without infection induces the stress-response gene fmo-2. We further identify that neural and intestinal signaling genes are necessary for fmo-2 induction without active infection. Finally, we show that fmo-2 overexpression is sufficient to extend lifespan with EF exposure, while fmo-2 KO is not detrimental, suggesting that additional fmo-2 expression benefits worms in this condition.
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