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XB-ART-48510
BMB Rep 2014 Dec 01;4712:673-8. doi: 10.5483/bmbrep.2014.47.12.290.
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PV.1 induced by FGF-Xbra functions as a repressor of neurogenesis in Xenopus embryos.

Yoon J , Kim JH , Lee SY , Kim S , Park JB , Lee JY , Kim J .


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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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Species referenced: Xenopus
Genes referenced: a2m acta4 actc1 actl6a chrd egr2 fgf2 gata2 hoxb9 krt12.4 mapk1 mixer ncam1 nog odc1 otx2 smad1 tbxt ventx1 zic3
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References [+] :
Amaya, Expression of a dominant negative mutant of the FGF receptor disrupts mesoderm formation in Xenopus embryos. 1991, Pubmed, Xenbase