Revisiting the involvement of signaling gradients in somitogenesis

Abstract

During embryonic development, formation of individual vertebrae requires that the paraxial mesoderm becomes divided into regular segmental units known as somites. Somites are sequentially formed at the anterior end of the presomitic mesoderm (PSM) resulting from functional interactions between the oscillatory activity of signals promoting segmentation and a moving wavefront of tissue competence to those signals, eventually generating a constant flow of new somites at regular intervals. According to the current model for somitogenesis, the wavefront results from the combined activity of two opposing functional gradients in the PSM involving the Fgf, Wnt and retinoic acid (RA) signaling pathways. Here, I use published data to evaluate the wavefront model. A critical analysis of those studies seems to support a role for Wnt signaling, but raise doubts regarding the extent to which Fgf and RA signaling contribute to this process. Somite formation is thought to result from the combined activity of a molecular clock and a moving wavefront of tissue competence generated by gradients of Fgf, Wnt and RA signaling activity. Available genetic evidence supports the role that has been suggested for Wnt signaling, but raises doubts about the contribution of the Fgf and RA signaling gradients to this process.