Superoxide dismutase SOD-1 modulates C. elegans pathogen avoidance behavior.
Superoxide dismutase SOD-1 modulates C. elegans pathogen avoidance behavior.
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DOI：
10.1038/srep45128
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发表时间：
2017-03-21
影响因子：
4.6
通讯作者：
Chang HC
中科院分区：
文献类型：
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作者：
Horspool AM;Chang HC
线虫神经系统在感染过程中介导保护性生理和行为反应。然而，神经系统如何对感染期间病原微生物激活的活性氧（ROS）做出反应仍然很大程度上未知。在这里，我们展示了超氧化物歧化酶-1 (SOD-1)，一种将超氧化物转化为毒性较小的过氧化氢和氧气的酶，在味觉神经元 ASER 中发挥作用，介导秀丽隐杆线虫病原体回避反应。当线虫第一次遇到致病菌铜绿假单胞菌时，SOD-1 在 ASER 神经元中被诱导产生。长时间暴露于铜绿假单胞菌后，ASER 特异性 SOD-1 表达会减少。反过来，线虫开始腾出病原菌菌丛。基因敲除实验表明，病原体诱导的 ROS 可非细胞自主地激活 sod-1 依赖性行为反应。我们假设，对有害微生物的延迟厌恶反应可能会通过允许线虫暂时利用被病原体污染的食物作为额外的能量来源来提供生存益处。我们的数据提供了关于神经系统如何在氧化应激下介导食物寻求行为的机制见解，并表明氧化还原稳态的内部状态可能是对有害微生物物种的行为反应的基础。
The C. elegans nervous system mediates protective physiological and behavioral responses amid infection. However, it remains largely unknown how the nervous system responds to reactive oxygen species (ROS) activated by pathogenic microbes during infection. Here, we show superoxide dismutase-1 (SOD-1), an enzyme that converts superoxide into less toxic hydrogen peroxide and oxygen, functions in the gustatory neuron ASER to mediate C. elegans pathogen avoidance response. When C. elegans first encounters pathogenic bacteria P. aeruginosa, SOD-1 is induced in the ASER neuron. After prolonged P. aeruginosa exposure, ASER-specific SOD-1 expression is diminished. In turn, C. elegans starts to vacate the pathogenic bacteria lawn. Genetic knockdown experiments reveal that pathogen-induced ROS activate sod-1 dependent behavioral response non cell-autonomously. We postulate that the delayed aversive response to detrimental microbes may provide survival benefits by allowing C. elegans to temporarily utilize food that is tainted with pathogens as an additional energy source. Our data offer a mechanistic insight into how the nervous system mediates food-seeking behavior amid oxidative stress and suggest that the internal state of redox homeostasis could underlie the behavioral response to harmful microbial species.