秀丽隐杆线虫中胰岛素样信号传导与整合行为的神经回路
Insulin-like signaling and the neural circuit for integrative behavior in C. elegans.
作者信息
Kodama Eiji, Kuhara Atsushi, Mohri-Shiomi Akiko, Kimura Koutarou D, Okumura Masatoshi, Tomioka Masahiro, Iino Yuichi, Mori Ikue
机构信息
Division of Biological Science, Graduate School of Science, Nagoya University, Nagoya, Japan.
出版信息
Genes Dev. 2006 Nov 1;20(21):2955-60. doi: 10.1101/gad.1479906.
Abstract
Caenorhabditis elegans exhibits a food-associated behavior that is modulated by the past cultivation temperature. Mutations in INS-1, the homolog of human insulin, caused the defect in this integrative behavior. Mutations in DAF-2/insulin receptor and AGE-1/phosphatidylinositol 3 (PI-3)-kinase partially suppressed the defect of ins-1 mutants, and a mutation in DAF-16, a forkhead-type transcriptional factor, caused a weak defect. In addition, mutations in the secretory protein HEN-1 showed synergistic effects with INS-1. Expression of AGE-1 in any of the three interneurons, AIY, AIZ, or RIA, rescued the defect characteristic of age-1 mutants. Calcium imaging revealed that starvation induced INS-1-mediated down-regulation of AIZ activity. Our results suggest that INS-1, in cooperation with HEN-1, antagonizes the DAF-2 insulin-like signaling pathway to modulate interneuron activity required for food-associated integrative behavior.
摘要
秀丽隐杆线虫表现出一种与食物相关的行为，这种行为会受到过去培养温度的调节。人类胰岛素同源物INS-1的突变导致了这种整合行为的缺陷。DAF-2/胰岛素受体和AGE-1/磷脂酰肌醇3（PI-3）激酶的突变部分抑制了ins-1突变体的缺陷，而叉头型转录因子DAF-16的突变则导致了轻微的缺陷。此外，分泌蛋白HEN-1的突变与INS-1表现出协同效应。在三个中间神经元AIY、AIZ或RIA中的任何一个中表达AGE-1，都能挽救age-1突变体的特征性缺陷。钙成像显示，饥饿诱导了INS-1介导的AIZ活性下调。我们的结果表明，INS-1与HEN-1协同作用，拮抗DAF-2胰岛素样信号通路，以调节与食物相关的整合行为所需的中间神经元活性。
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