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

Jaeho Yoon, Jung Ho Kim, Sung Young Lee, SungChan Kim, Jae Bong Park, Jae Yong Lee, Jaebong Kim

Research output: Contribution to journalArticlepeer-review

5 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)673-678
Number of pages6
JournalBMB Reports
Volume47
Issue number12
DOIs
StatePublished - 2014

Keywords

  • Neurogenesis
  • PV.1
  • Xbra
  • Xenopus
  • bFGF

Fingerprint Dive into the research topics of 'PV.1 induced by FGF-Xbra functions as a repressor of neurogenesis in Xenopus embryos'. Together they form a unique fingerprint.

Cite this