Neuron-specific regulation of superoxide dismutase amid pathogen-induced gut dysbiosis

Alexander M. Horspool, Howard C. Chang

Research output: Contribution to journalArticlepeer-review

14 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)377-385
Number of pages9
JournalRedox Biology
Volume17
DOIs
StatePublished - Jul 2018
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Organic Chemistry
  • Clinical Biochemistry

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