FGF4 and FGF8 comprise the wavefront activity that controls somitogenesis

Area of Science:

• Developmental biology
• Molecular biology
• Genetics

Background:

• Somitogenesis, the formation of embryonic segments called somites, is crucial for vertebral column development.
• Somite formation is regulated by the interplay of a 'clock' and a 'wavefront' mechanism.
• Fibroblast growth factors (FGFs) are hypothesized to be the wavefront signal, maintaining the presomitic mesoderm (PSM) in an undifferentiated state.

Purpose of the Study:

• To identify the specific FGF ligands responsible for the wavefront activity in somitogenesis.
• To elucidate the role of FGF signaling in maintaining PSM progenitor identity and preventing premature differentiation.

Main Methods:

• Gene deletion experiments in mice, specifically targeting Fgf4 and Fgf8 in the PSM.
• Analysis of gene expression patterns for PSM markers, cycling genes, WNT pathway genes, and somite progenitor markers.
• Conditional WNT signaling restoration in Fgf-deficient mutants to assess pathway interactions.

Main Results:

• Deletion of both Fgf4 and Fgf8 in the PSM resulted in the absence of most PSM gene expression and premature differentiation of the entire PSM tissue.
• This phenotype indicates a loss of wavefront activity, with somite progenitor markers expanding throughout the PSM.
• Restoring WNT signaling partially rescued PSM progenitor markers but did not prevent premature differentiation, suggesting FGF acts independently of WNT.

Conclusions:

• FGF signaling, specifically involving Fgf4 and Fgf8, constitutes the wavefront signal essential for maintaining PSM progenitor state.
• FGF signaling acts independently of WNT signaling in controlling the wavefront activity.
• Both FGF and WNT pathways function in parallel to maintain the PSM progenitor tissue during somitogenesis.