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研究発表を行った学会；
・第１回グローバルCOEサマーリトリートセミナー、2007年 9月28~29日(熊本)

タイトル；A Role for Glycogen Synthase Kinase 3β and β-Catenin in Coordinating Proliferation and Differentiation of Telencephalic Neural Precursor Cells.
発表者；　清水　健史　氏
　　　（熊本大学　発生医学研究センター　転写制御分野）
Abstract；
Proliferation of neural precursor cells and their neuronal differentiation are mutually exclusive, suggesting (an) unidentified molecular link(s) between proliferation and differentiation. In our previous report, through misexpression studies with dominant-active GSK3β and β-catenin we proposed a model in which nuclear β-catenin concurrently coactivated LEF/TCF transcription factors for inducing cell proliferation and Notch/RBPJκ transcription factors for inhibiting neuronal differentiation. In this study, we perform loss-of-function analyses of them. Pharmacological inhibition of GSK3β activity increased BrdU-positive proliferating cells and decreased Tuj1-positive neurons. Knockdown of β-catenin expression by siRNA reduced the FGF2-induced promoter activation of hes1, a major Notch signaling target. Taken together, inactivation of endogenous GSK3β and subsequent accumulation of β-catenin manage two distinct transcriptional machineries involved in proliferation and differentiation of neural precursor cells.