The mechanoreceptor DEG-1 regulates cold tolerance in Caenorhabditis elegans
The mechanoreceptor DEG-1 regulates cold tolerance in Caenorhabditis elegans
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DOI：
10.15252/embr.201948671
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发表时间：
2020-02-03
期刊：
影响因子：
7.7
通讯作者：
Kuhara, Atsushi
中科院分区：
文献类型：
--
作者：
Takagaki, Natsune;Ohta, Akane;Kuhara, Atsushi
秀丽线虫的机械感受器位于ASG感觉神经元上，它能感知环境温度，这是动物生存的关键特征。在这里，我们发现在AIN和AVJ中间神经元中黄嘌呤脱氢酶(XDH-1)功能的实验性丧失导致耐寒性降低和对温度变化的非典型神经元反应。这些中间神经元与上游神经元连接，如机械感受器表达的ASG。钙离子成像显示，ASG神经元通过机械感受器DEG-1对温度做出反应，DEG-1是一种退行性/上皮性钠离子通道(DEG/ENaC)，进而影响下游的AIN和AVJ回路。DEG-1在ASE味觉神经元中的异位表达导致温敏的获得，而电生理分析表明DEG-1和人MDEG1参与了温觉。综上所述，这些结果表明，耐冷性是通过机械感受器介导的回路计算来调节的。
Caenorhabditis elegans mechanoreceptors located in ASG sensory neurons have been found to sense ambient temperature, which is a key trait for animal survival. Here, we show that experimental loss of xanthine dehydrogenase (XDH-1) function in AIN and AVJ interneurons results in reduced cold tolerance and atypical neuronal response to changes in temperature. These interneurons connect with upstream neurons such as the mechanoreceptor-expressing ASG. Ca2+ imaging revealed that ASG neurons respond to warm temperature via the mechanoreceptor DEG-1, a degenerin/epithelial Na+ channel (DEG/ENaC), which in turn affects downstream AIN and AVJ circuits. Ectopic expression of DEG-1 in the ASE gustatory neuron results in the acquisition of warm sensitivity, while electrophysiological analysis revealed that DEG-1 and human MDEG1 were involved in warm sensation. Taken together, these results suggest that cold tolerance is regulated by mechanoreceptor-mediated circuit calculation.