Superoxide dismutase, an enzyme that converts superoxide into less-toxic hydrogen peroxide and oxygen, has been shown to mediate behavioral response to pathogens. However, it remains largely unknown how superoxide dismutase… Click to show full abstract
Superoxide dismutase, an enzyme that converts superoxide into less-toxic hydrogen peroxide and oxygen, has been shown to mediate behavioral response to pathogens. However, it remains largely unknown how superoxide dismutase is regulated in the nervous system amid pathogen-induced gut dysbiosis. Although there are five superoxide dismutases in C. elegans, our genetic analyses suggest that SOD-1 is the primary superoxide dismutase to mediate the pathogen avoidance response. When C. elegans are fed a P. aeruginosa diet, the lack of SOD-1 contributes to enhanced lethality. We found that guanylyl cyclases GCY-5 and GCY-22 and neuropeptide receptor NPR-1 act antagonistically to regulate SOD-1 expression in the gustatory neuron ASER. After C. elegans ingests a diet that contributes to high levels of oxidative stress, the temporal regulation of SOD-1 and the SOD-1–dependent response in the gustatory system demonstrates a sophisticated mechanism to fine-tune behavioral plasticity. Our results may provide the initial glimpse of a strategy by which a multicellular organism copes with oxidative stress amid gut dysbiosis.
               
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