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Induction and Pattern Formation

開催日 2014/9/11
時間 16:00 - 17:00
会場 Poster / Exhibition(Event Hall B)

Prethalamus formation is regulated by Olig2, which is crucial for proper thalamocortical projection formation

  • P1-064
  • 小野 勝彦 / Katsuhiko Ono:1 Clavairoly Adrien / Adrien Clavairoly:2 野村 真 / Tadashi Nomura:1 後藤 仁志 / Hitoshi Gotoh:1 宇野 葵 / Aoi Uno:1 Armant Olivier / Olivier Armant:3 竹林 浩秀 / Hirohide Takebayashi:4 Zhang Qi / Qi Zhang:5 嶋村 健児 / Kenji Shimamura:6 糸原 重美 / Shigeyoshi Itohara:5 Parras Carlos M / Carlos M Parras:2 池中 一裕 / Kazuhiro Ikenaka:6 
  • 1:京都府立医科大学 / Dept. of Biology, Kyoto Pref. Univ. Med. 2:Institute of the Brain and Spinal Cord (ICM), Inserm-UPMC, Paris, France / Inst of Brain and Spinal Cord (ICM), Inserm-UPMC, Paris, France 3:Institute of Toxicology and Genetics, KIT Campus Nord, Eggenstein-Leopoldshafen, Germany / Inst of Toxicol and Genetics, KIT Campus Nord, Eggenstein-Leopoldshafen, Germany 4:新潟大学大学院 神経生物学・解剖分野 / Div of Neurobiol Anat, Grad Sch Medi and Dent Sci, Niigata Univ, Niigata, Japan 5:理研BSI、行動遺伝技術開発 / Lab for Behav Genetics, RIKEN BSI, Wako, Japan 6:生理学研究所、分子神経生理 / Div of Neurobiol Bioinfo, NIPS, Okazaki, Japan 

Olig2 is a transcription factor essential for oligodendrocyte and motor neuron development in the spinal cord. Although Olig2 is expressed widely in the embryonic central nervous system, the role of Olig2 in the brain development has not been elucidated. To explore new function of Olig2, we examined forebrain formation in the fetal mice. Olig2 is expressed in the ventricular zone of the prethalamus as early as E9.5, and the loss of Olig2 results in hypoplasia of the prethalamus with the expansion of the ventrally-adjacent thalamic eminence (TE). This altered diencephalon patterning is due to fate change of Olig2 lineage cells from cells of the prospective prethalamus to those of TE in the absence of Olig2. In addition, initial extension of thalamocortical axons (TCAs) is impaired by the loss of Olig2, which leads to abnormal fasciculation in later development. Microarray and in situ hybridization analyses elucidate that Epha3 and Epha5 are up-regulated in accordance with the expansion of the TE in the Olig2 deficient mouse. Dorsal thalamic neurons are inhibited their process extension in vitro on the substrate-bound form of EphA3. These results indicate that Olig2 indirectly controls initial TCA extension through the regulation of proper prethalamus formation.

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