The insulin/PI 3-kinase pathway regulates salt chemotaxis learning in Caenorhabditis elegans
The insulin/PI 3-kinase pathway regulates salt chemotaxis learning in Caenorhabditis elegans
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DOI：
10.1016/j.neuron.2006.07.024
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发表时间：
2006-09-07
期刊：
影响因子：
16.2
通讯作者：
Iino, Yuichi
中科院分区：
文献类型：
--
作者：
Tomioka, Masahiro;Adachi, Takeshi;Iino, Yuichi
已知胰岛素样信号通路调节秀丽隐杆线虫的脂肪代谢、dauer形成和寿命。在这里，我们报告说，这一途径也参与了盐的趋化性学习，其中动物先前暴露于饥饿条件下的化学吸引盐开始显示盐回避行为。ins-1，daf-2，age-1，pdk-1和akt-1的突变体，它们分别编码胰岛素，胰岛素/IGF-I受体，PI 3-激酶，磷酸肌醇依赖性激酶和Akt/PKB的同源物，在盐趋化性学习中表现出严重的缺陷。daf-2和age-1在ASER盐敏感神经元中起作用，并且在该神经元中DAF-2/AGE-1通路的活性水平决定了盐趋化性的程度和方向。另一方面，ins-1作用于AIA中间神经元，其接收来自感觉神经元的直接突触输入，并且还将突触输出发送到ASER。这些结果表明，AIA中间神经元分泌的INS-1提供反馈给ASER，以产生趋化性的可塑性。
The insulin-like signaling pathway is known to regulate fat metabolism, dauer formation, and longevity in Caenorhabditis elegans. Here, we report that this pathway is also involved in salt chemotaxis learning, in which animals previously exposed to a chemoattractive salt under starvation conditions start to show salt avoidance behavior. Mutants of ins-1, daf-2, age-1, pdk-1, and akt-1, which encode the homologs of insulin, insulin/IGF-I receptor, PI 3-kinase, phosphoinositide-dependent kinase, and Akt/PKB, respectively, show severe defects in salt chemotaxis learning. daf-2 and age-1 act in the ASER salt-sensing neuron, and the activity level of the DAF-2/AGE-1 pathway in this neuron determines the extent and orientation of salt chemotaxis. On the other hand, ins-1 acts in AIA interneurons, which receive direct synaptic inputs from sensory neurons and also send synaptic outputs to ASER. These results suggest that INS-1 secreted from AIA interneurons provides feedback to ASER to generate plasticity of chemotaxis.