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Stem Cells, Neuronal and Glial Production/Differentiation

開催日 2014/9/11
時間 11:00 - 12:00
会場 Poster / Exhibition(Event Hall B)

Dynamic protein expression patterns and essential functions of Sbno1 in mouse brain development

  • P1-073
  • 中村 龍司 / Ryuji Nakamura:1 杉山 拓 / Taku Sugiyama:1 今井 英明 / Hideaki Imai:2 相沢 慎一 / Shinichi Aizawa:3 寺島 俊雄 / Toshio Terashima:3 大隅 典子 / Noriko Osumi:1 勝山 裕 / Yu Katsutama:1 
  • 1:東北大学大学院 / Division of Developmental Neuroscience, Center for Translational and Advanced Research, Tohoku University Graduate school of Medicine 2:神戸大・医学系研究科・神経発生学分野 / Div. of Devel Neurosc., Kobe Univ Grad Sch Med 3:理研・動物資源開発室 / Lab Animal Resources and Genetic Engineering, RIKEN CDB 

During brain development, proliferation of neural stem cells and production of neurons from the stem cells are strictly regulated by several molecular pathways, such as Notch, Wnt, FGF, and other signaling pathways. One possible mechanism to enable strict regulation of stem cell function is interaction of multiple molecular pathways. ,However, molecule(s) involved in such interactions are not definitely specified. We focused on Sbno1, a strawberry notch (sbno) family gene, in a screening to identify a novel gene involved in mouse brain development. Previous studies regarding sbno functions suggested that this molecule can be related to multiple molecular mechanisms, like Notch, Wnt and Ras pathways. We expected that Sbno1 was involved in multiple molecular pathways and functions as an intermediary of these pathways to allow coordication of stem cell proliferation and differentiation of cortical neurons. As a first step to know Sbno1 function in the brain development, we immunohistologically detected Sbno1 protein using an originally prepared specific antibody against Sbno1. Sbno1 protein was observed in the nucleus of differentiating cortical neurons in the cortical plate and Sbno1 expression in the cortical neurons persisted until postnatal stages. We next asked Sbno1 function by constructing Sbno1 knockout mouse strain. In this mutant mouse, neural stem cells prematurely differentiated into neuron and the neural stem cells were depleted. Although Sbno1 protein was not detected in the neural stem cells, abnormality observed in Sbno1 knockout mouse is assumed to be related to function of neural stem cells. We are now carrying out further experiments to explain the discrepancy in localization of Sbno1 protein and abnormality in the Sbno1 knockout embryos.

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