Abstract
Vertebrates are characterized by an elongated antero-posterior (AP) body axis. This particular shape arises during embryogenesis by mophogenetic events leading to elongation. Although elongation mechanisms that lead to the formation of the anterior part of the body are well described, the ones concerning the posterior part still remain poorly studied. Here, we used tissue ablation in the chicken embryo to demonstrate that caudal presomitic mesoderm (PSM) has a key role in axis elongation. Using time-lapse microscopy, we characterized a clear posterior-to-anterior gradient of cell and tissue motility in the PSM during embryo elongation. Subtracting the tissue movement from the global motion of cells we demonstrated that this gradient correspond to a gradient of cell motility lacking any directionality, indicating that the posterior cell movements associated with axis elongation in the PSM are not intrinsic but reflect tissue deformation. Both FGF signaling gain- and loss-of-function experiments lead to disruption of the motility gradient and a slowing down of axis elongation. Finally we performed experiments indicating that FGF effect on elongation is due to its effect on cell migration and not to regulation of the cell cycle. We propose a new elongation model in which the gradient of non directional cell motility in the PSM controls posterior elongation of the embryo axis.
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