Department of Biological Sciences, Graduate School of Science, The University of Tokyo, Bunkyo-ku, Tokyo, 113-0033, Japan.
Neuroscience Institute, Graduate School of Science, Nagoya University, Nagoya, Aichi, 464-8602, Japan.
Commun Biol. 2022 Jan 11;5(1):30. doi: 10.1038/s42003-021-02956-8.
Previously, we reported that DAF-2c, an axonal insulin receptor isoform in Caenorhabditis elegans, acts in the ASER gustatory neuron to regulate taste avoidance learning, a process in which worms learn to avoid salt concentrations experienced during starvation. Here, we show that secretion of INS-1, an insulin-like peptide, after starvation conditioning is sufficient to drive taste avoidance via DAF-2c signaling. Starvation conditioning enhances the salt-triggered activity of AIA neurons, the main sites of INS-1 release, which potentially promotes feedback signaling to ASER to maintain DAF-2c activity during taste avoidance. Genetic studies suggest that DAF-2c-Akt signaling promotes high-salt avoidance via a decrease in PLCβ activity. On the other hand, the DAF-2c pathway promotes low-salt avoidance via PLCε and putative Akt phosphorylation sites on PLCε are essential for taste avoidance. Our findings imply that animals disperse from the location at which they experience starvation by controlling distinct PLC isozymes via DAF-2c.
先前，我们报道过 DAF-2c，秀丽隐杆线虫轴突胰岛素受体同工型，在 ASER 味觉神经元中发挥作用，以调节味觉回避学习，这是一种蠕虫学会避免饥饿期间经历的盐浓度的过程。在这里，我们表明，饥饿条件作用后 INS-1（一种胰岛素样肽）的分泌足以通过 DAF-2c 信号驱动味觉回避。饥饿条件作用增强了 AIA 神经元（INS-1 释放的主要部位）对盐的触发活性，这可能促进了反馈信号传递到 ASER，以在味觉回避期间维持 DAF-2c 的活性。遗传研究表明，DAF-2c-Akt 信号通过降低 PLCβ 活性促进高盐回避。另一方面，DAF-2c 途径通过 PLCε 促进低盐回避，并且 PLCε 上的假定 Akt 磷酸化位点对于味觉回避是必需的。我们的发现表明，动物通过 DAF-2c 控制不同的 PLC 同工型，从它们经历饥饿的位置分散。
