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PV.1 induced by FGF-Xbra functions as a repressor of neurogenesis in Xenopus embryos

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During Xenopus early development, FGF signaling is involvedin mesoderm formation and neurogenesis by modulatingvarious signaling cascades. FGF-MAPK signaling induces Xbraexpression, which maintains mesodermal fate through anautocatalytic-loop. Interestingly, previous reports havedemonstrated that basic FGF (bFGF) treatment alone does notinduce neurogenesis in ectodermal explants, even though FGFsignaling inhibits BMP signaling via phosphorylation in Smad1linker region. In addition, the overexpression of dominantnegativeXbra induces neurogenesis in ectodermal explants. However, the detailed mechanism underlying these phenomenahas not yet been clarified. In this work, we showed thatbFGF-Xbra signaling increased the PV.1 expression. DN-Xbrawas found to decrease PV.1 expression, and the co-injection ofPV.1 with DN-Xbra reduced neurogenesis in ectodermalexplants. Furthermore, the knockdown of PV.1 inducedneurogenesis in bFGF-treated ectodermal explants. Takentogether, our results demonstrate that FGF-Xbra signalinginduces PV.1 expression and that PV.1 functions as a neuralrepressor in the FGF-treated ectoderm.

Abstract

During Xenopus early development, FGF signaling is involvedin mesoderm formation and neurogenesis by modulatingvarious signaling cascades. FGF-MAPK signaling induces Xbraexpression, which maintains mesodermal fate through anautocatalytic-loop. Interestingly, previous reports havedemonstrated that basic FGF (bFGF) treatment alone does notinduce neurogenesis in ectodermal explants, even though FGFsignaling inhibits BMP signaling via phosphorylation in Smad1linker region. In addition, the overexpression of dominantnegativeXbra induces neurogenesis in ectodermal explants. However, the detailed mechanism underlying these phenomenahas not yet been clarified. In this work, we showed thatbFGF-Xbra signaling increased the PV.1 expression. DN-Xbrawas found to decrease PV.1 expression, and the co-injection ofPV.1 with DN-Xbra reduced neurogenesis in ectodermalexplants. Furthermore, the knockdown of PV.1 inducedneurogenesis in bFGF-treated ectodermal explants. Takentogether, our results demonstrate that FGF-Xbra signalinginduces PV.1 expression and that PV.1 functions as a neuralrepressor in the FGF-treated ectoderm.

참고문헌 (32)

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