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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.
Mechanisms of Development
|August 1, 1992
Summary
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.