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Stress, Autonomic Nervous System and Respirarion

開催日 2014/9/12
時間 9:00 - 10:00
会場 Room J(313+314)
Chairperson(s) 堀田 晴美 / Harumi Hotta (地方独立行政法人 東京都健康長寿医療センター研究所 自律神経機能 / Department of Autonomic Neuroscience, Tokyo Metropolitan Institute of Gerontology, Japan)
荒田 晶子 / Akiko Arata (兵庫医科大学 生理学・生体機能部門 / Department of Physiology, Hyogo College of Medicine, Japan)

Systematic regulation of memory-linked temperature tolerance in C. elegans

  • O2-J-1-1
  • 太田 茜 / Akane Ohta:1 宇治澤 知代 / Tomoyo Ujisawa:1,2 宇多 美里 / Misato Uda:1,2 石割 友博 / Tomohiro Ishiwari:1 五百蔵 誠 / Makoto Ioroi:1 高垣 奈式 / Natsune Takagaki:1 木村 真衣 / Mai Kimura:1 園田 悟 / Satoru Sonoda:1,2 久原 篤 / Atsushi Kuhara:1,2 
  • 1:甲南大学 / Konan University, Japan 2:甲南大学 統合ニューロバイオロジー研 / Institute for Integrative Neurobiology, Konan Univ., Japan 

Temperature is essential information for survival and proliferation. Nematode C. elegans stores temperature experiences and can induce temperature memory-linked cold tolerance, which is a phenomenon that 15°C -cultivated animals can survive at 2°C, however, 20°C - or 25°C -cultivated animals can not survive after cold shock. We are using cold tolerance as a model for studying temperature sensation and memory. Here we show that a light and pheromone-sensing neuron (ASJ) regulates cold tolerance through insulin signaling (Ohta & Ujisawa et al., under revision).

Our genetic analysis revealed that ASJ neurons, known as light and pheromone-sensing neuron, is involved in cold tolerance. Besides, Ca2+ imaging analysis revealed that ASJ respond to temperature without synaptic connection. These results suggest that ASJ senses temperature as well as light and pheromone. We examined mutants impairing light signaling in ASJ, and revealed that trimeric G-proteins and cGMP-gated channels involved in cold tolerance. These results suggest that G-protein signaling is important for temperature sensation in ASJ. We therefore hypothesized that unidentified G-protein-coupled thermoreceptor acts in ASJ sensoryneuron.
ASJ neuron express two insulin molecules DAF-28 and INS-6. Genetic epistasis analysis suggests that these insulin are involved in cold tolerance. The mutants impairing insulin receptor (DAF-2) or insulin (DAF-28 & INS-6) showed abnormal cold tolerance. Tissue-specific rescue experiments revealed that DAF-2 receives insulin at intestine and neurons in cold tolerance. DNA microarray and mutant analyses indicate that DAF-2 signaling regulates gene expression of several genes through FOXO transcriptional factor. Altogether, our study exhibited a systematic model for temperature tolerance.

Recently, we are studying temperature memory in cold tolerance. We found that only three hours after temperature shift from 25 to 15 °C cold tolerance was newly established. crh-1/CREB mutant delayed reconfiguration of cold tolerance in temperature shift assay. So far, this abnormality was rescued by expressing crh-1 cDNA in ASJ sensory neuron.

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