Reversal of Salt Preference Is Directed by the Insulin/PI3K and Gq/PKC Signaling in Caenorhabditis elegans
Reversal of Salt Preference Is Directed by the Insulin/PI3K and Gq/PKC Signaling in Caenorhabditis elegans
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DOI：
10.1534/genetics.110.119768
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发表时间：
2010-12-01
期刊：
影响因子：
3.3
通讯作者：
Iino, Yuichi
中科院分区：
文献类型：
--
作者：
Adachi, Takeshi;Kunitomo, Hirofumi;Iino, Yuichi
动物根据先前的经验寻找食物并决定自己的行为。秀丽隐杆线虫用有限数量的感觉神经元检测化学物质，使我们能够剖析每个神经元在先天和后天行为中的作用。C.在暴露于食物中的盐（NaCl）后，线虫被盐吸引。相比之下，它学会了在没有食物的情况下接触盐后避免盐。在盐吸引行为中，已知ASE味觉感觉神经元（ASEL和ASER）起主要作用。然而，很少有人知道的机制，学习盐回避。在这里，通过解剖ASE神经元的盐趋化性的贡献，我们表明，ASEL和ASER产生盐趋化可塑性。在ASER中，我们先前已经表明胰岛素/PI 3-激酶信号传导对饥饿诱导的盐趋化可塑性起作用。本研究表明PI 3-激酶信号通路促进ASER的厌恶性驱动，但不促进ASEL的厌恶性驱动.此外，由G（q）α EGL-30、二酰基甘油和nPKC（新型蛋白激酶C）TTX-4组成的G（q）信号通路促进ASER的吸引驱动，但不促进ASEL的吸引驱动。一个假定的盐受体GCY-22鸟苷酸环化酶是必需的ASER的盐吸引和回避。我们的研究结果表明，ASEL和ASER使用不同的分子机制来调节盐趋化可塑性。
Animals search for foods and decide their behaviors according to previous experience. Caenorhabditis elegans detects chemicals with a limited number of sensory neurons, allowing us to dissect roles of each neuron for innate and learned behaviors. C. elegans is attracted to salt after exposure to the salt (NaCl) with food. In contrast, it learns to avoid the salt after exposure to the salt without food. In salt-attraction behavior, it is known that the ASE taste sensory neurons (ASEL and ASER) play a major role. However, little is known about mechanisms for learned salt avoidance. Here, through dissecting contributions of ASE neurons for salt chemotaxis, we show that both ASEL and ASER generate salt chemotaxis plasticity. In ASER, we have previously shown that the insulin/PI 3-kinase signaling acts for starvation-induced salt chemotaxis plasticity. This study shows that the PI 3-kinase signaling promotes aversive drive of ASER but not of ASEL. Furthermore, the G(q) signaling pathway composed of G(q)alpha EGL-30, diacylglycerol, and nPKC (novel protein kinase C) TTX-4 promotes attractive drive of ASER but not of ASEL. A putative salt receptor GCY-22 guanylyl cyclase is required in ASER for both salt attraction and avoidance. Our results suggest that ASEL and ASER use distinct molecular mechanisms to regulate salt chemotaxis plasticity.