The vertebrate body is segmented along the anteroposterior axis into repetitive structures, the vertebrae, which derive from embryonic precursors called somites. During development, periodic somite formation is driven by a molecular oscillator, the segmentation clock. Segmentation and elongation of the body axis depend on a population of progenitor cells located at the tail end of the embryo that contributes to axial tissues, including somitic tissue, until the entire embryonic body and the correct number of somites is produced. Although much is known about somite production, it is not known how segmentation and axial elongation come to an end. In this thesis, I show that termination of chick axial elongation is associated with decline of signals required for maintenance of progenitor cells, implying that downregulation of these signals triggers depletion of the progenitors. I also show that somite formation decreases as axial elongation comes to an end, suggesting that slow down of the segmentation clock causes somite formation to cease. I have also explored whether the dose of specific genes is limiting in determining the final somite number in mouse, and I have found that heterozygous mutations of selected genes of the Wnt signalling pathway form fewer somites, indicating that Wnt gene activity might be limiting in controlling the definitive somite number. I have also investigated the role of Greb1, a gene that our laboratory identified as being selectively expressed in the tail region where progenitors reside. I provide evidence that Greb1 controls axial morphogenesis of the zebrafish embryo by regulating movements required for normal convergence and extension of the embryonic axis during gastrulation. My results possibly provide a link between progenitor contribution to axial elongation and cell movements in the tail
