Social feeding in Caenorhabditis elegans is induced by neurons that detect aversive stimuli

Social feeding in Caenorhabditis elegans is induced by neurons that detect aversive stimuli
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DOI:
10.1038/nature01169
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发表时间:
2002-10-31
期刊:
影响因子:
64.8
通讯作者:
Bargmann, CI
Bargmann, CI
中科院分区:
综合性期刊1区
文献类型:
--
作者:
de Bono, M;Tobin, DM;Bargmann, CI

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天然秀丽隐杆线虫分离株表现出社会或孤独的细菌喂养。我们在这里表明,社会喂养是由伤害性神经元,检测不利或压力条件。伤害感受神经元ASH和ADL的消融将社会动物转变为孤独的饲养者。社会喂养可能是由于ASH和ADL神经元对有害化学物质的感觉;它需要编码TRP相关转导通道的基因ocr-2和osm-9,以及将感觉化学感受器定位于纤毛所需的odr-4和odr-8。其他感觉神经元可能抑制社会进食,ocr-2和odr-4突变体中的社会进食通过osm-3突变恢复,osm-3是26个纤毛感觉神经元发育所需的基因。我们的数据提出了一个通过相反的感觉输入来调节社会喂养的模型:对伤害性神经元的厌恶性输入促进社会喂养,而来自表达osm-3的神经元的拮抗性输入抑制聚集。
Natural Caenorhabditis elegans isolates exhibit either social or solitary feeding on bacteria. We show here that social feeding is induced by nociceptive neurons that detect adverse or stressful conditions. Ablation of the nociceptive neurons ASH and ADL transforms social animals into solitary feeders. Social feeding is probably due to the sensation of noxious chemicals by ASH and ADL neurons; it requires the genes ocr-2 and osm-9, which encode TRP-related transduction channels, and odr-4 and odr-8, which are required to localize sensory chemoreceptors to cilia. Other sensory neurons may suppress social feeding, as social feeding in ocr-2 and odr-4 mutants is restored by mutations in osm-3, a gene required for the development of 26 ciliated sensory neurons. Our data suggest a model for regulation of social feeding by opposing sensory inputs: aversive inputs to nociceptive neurons promote social feeding, whereas antagonistic inputs from neurons that express osm-3 inhibit aggregation.