Poster Sessions

DEV-10

Naiche Adler

L.A. Naiche, N. Holder, M. Lewandoski

Collapsing the Wavefront: Fibroblast Growth Factor (FGF) Signaling Maintains the Presomitic Mesoderm in an Undifferentiated State

During somitogenesis, a posterior Wavefront signal maintains the undifferentiated state of the presomitic mesoderm (PSM). Previous work suggests that FGF activity may be the Wavefront signal. However, it is unclear which (if any) of the six FGFs expressed in the PSM encode this activity, as removal of any one ligand is insufficient to disrupt early somitogenesis. We show that when both Fgf4 and Fgf8 are ablated in the PSM, only a few abnormal somites form and axis elongation arrests prematurely. Expression of undifferentiated PSM markers, cycling genes, and WNT genes are lost in mutant PSM. Somite markers are expanded into the PSM, suggesting that the PSM prematurely differentiates into somitic tissue. Loss of WNT signaling also causes axis truncation, so we investigated whether the phenotype of the mutants was a secondary effect. We restored WNT signaling with a gain-of-function B-catenin allele, and we found that undifferentiated PSM markers are partially restored, but axis elongation and somite formation are not rescued. This study provides the first genetic evidence identifying FGF ligands that encode Wavefront activity. Furthermore, these data suggest that FGF action is required to maintain WNT signaling, and that both signaling pathways are required in parallel to maintain undifferentiated PSM tissue.