Neuron-specific regulation of superoxide dismutase amid pathogen-induced gut dysbiosis.
Neuron-specific regulation of superoxide dismutase amid pathogen-induced gut dysbiosis.
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DOI:
10.1016/j.redox.2018.05.007
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发表时间:
2018-07
期刊:
影响因子:
11.4
通讯作者:
Chang HC
中科院分区:
文献类型:
--
作者:
Horspool AM;Chang HC
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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