Disruption of normal vertebral development results from abnormal formation and segmentation of the vertebral precursors, called somites. Somitogenesis, the sequential formation of a periodic pattern along the antero-posterior axis of vertebrate embryos, is one of the most obvious examples of the segmental patterning processes that take place during embryogenesis and also one of the major unresolved events in developmental biology. We review the most popular models of somite formation: Cooke and Zeeman's clock and wavefront model, Meinhardt's reaction-diffusion model and the cell cycle model of Stern and co-workers, and discuss the consistency of each in the light of recent experimental findings concerning FGF-8 signalling in the presomitic mesoderm (PSM). We present an extension of the cell cycle model to take account of this new experimental evidence, which shows the existence of a determination front whose position in the PSM is controlled by FGF-8 signalling, and which controls the ability of cells to become competent to segment. We conclude that it is, at this stage, perhaps erroneous to favour one of these models over the others.
The p38-MAPK Interacting Protein (p38IP) regulates somite and vertebral development
