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Intracellular signalling pathways involved in mesoderm induction by FGF

L L Gillespie1, G D Paterno, L C Mahadevan

  • 1Terry Fox Cancer Research Laboratories, Faculty of Medicine, Memorial University, St. John's, NF, Canada.

Insights

Fibroblast growth factor (FGF) induces mesoderm in Xenopus, involving tyrosine phosphorylation. Protein kinase C (PKC) activation alone is insufficient and may act as a negative feedback mechanism during FGF signaling.

Area of Science:

  • Developmental Biology
  • Cell Signaling

Background:

  • Fibroblast growth factor (FGF) is crucial for mesoderm induction in Xenopus embryos.
  • Signal transduction pathways, including tyrosine phosphorylation and protein kinase C (PKC) activation, are implicated in developmental processes.

Purpose of the Study:

  • To investigate the roles of tyrosine phosphorylation and PKC activation in FGF-induced mesoderm induction in Xenopus.
  • To determine if these pathways are sufficient or inhibitory for mesoderm formation.

Main Methods:

  • Utilized a monoclonal anti-phosphotyrosine antibody to detect tyrosine phosphorylation.
  • Administered sodium orthovanadate to elevate phosphotyrosine levels.
  • Measured PKC activity and used phorbol ester (TPA) to activate PKC in ectodermal explants.

Main Results:

  • Sodium orthovanadate induced mesoderm and synergized with FGF, enhancing dorsal induction.
  • PKC activation was detected in FGF-treated explants, but TPA alone did not induce mesoderm.
  • Simultaneous TPA and FGF treatment inhibited mesoderm induction, suggesting a negative feedback role for PKC.

Conclusions:

  • Tyrosine phosphorylation is a key component of FGF-induced mesoderm induction.
  • PKC activation is not sufficient for mesoderm induction and may negatively regulate the FGF signaling pathway.
  • PKC activation does not affect mesoderm induction by activin A.

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