A fibronectin mechanotransduction pathway translates segmentation clock oscillations into periodic somite formation

Somitogenesis starts with cyclic waves of expression of segmentation clock genes in the presomitic mesoderm (PSM) and culminates with periodic budding of somites in its anterior-most region. How cyclic clock gene expression is translated into timely morphological somite formation remains unclear. A posterior to anterior gradient of increasing fibronectin matrix complexity surrounds the PSM, suggesting that the mechanical properties of the matrix may play a role in regulating this transition. Here we interfered with the chick PSM fibronectin mechanotransduction pathway by perturbing (1) actomyosin-mediated contractility, (2) Rho-associated protein kinase function, (3) integrin-fibronectin binding and (4) fibronectin matrix assembly. Each treatment perturbed segmentation clock expression dynamics, expression and resulted in defective somitic clefts. A model is presented where the fibronectin matrix gradient participates in the PSM wavefront of maturation by activating a mechanotransduction signaling cascade ensuring the correct spatio-temporal conversion of cyclic segmentation clock gene expression into periodic somite formation.