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KMID : 0624620140470120673
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BMB Reports
2014 Volume.47 No. 12 p.673 ~ p.678
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PV.1 induced by FGF-Xbra functions as a repressor of neurogenesis in Xenopus embryos
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Yoon Jae-Ho
Kim Jung-Ho
Lee Sung-Young
Kim Sung-Chan
Park Jae-Bong
Lee Jae-Yong
Kim Jae-Bong
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Abstract
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During Xenopus early development, FGF signaling is involved in mesoderm formation and neurogenesis by modulating various signaling cascades. FGF-MAPK signaling induces Xbra expression, which maintains mesodermal fate through an autocatalytic-loop. Interestingly, previous reports have demonstrated that basic FGF (bFGF) treatment alone does not induce neurogenesis in ectodermal explants, even though FGF signaling inhibits BMP signaling via phosphorylation in Smad1 linker region. In addition, the overexpression of dominantnegative Xbra induces neurogenesis in ectodermal explants. However, the detailed mechanism underlying these phenomena has not yet been clarified. In this work, we showed that bFGF-Xbra signaling increased the PV.1 expression. DN-Xbra was found to decrease PV.1 expression, and the co-injection of PV.1 with DN-Xbra reduced neurogenesis in ectodermal explants. Furthermore, the knockdown of PV.1 induced neurogenesis in bFGF-treated ectodermal explants. Taken together, our results demonstrate that FGF-Xbra signaling induces PV.1 expression and that PV.1 functions as a neural repressor in the FGF-treated ectoderm.
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KEYWORD
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bFGF, Neurogenesis, PV.1, Xbra, Xenopus
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