modulates an Rtn4a/Cxcr4a/Thbs3a axis in newly forming somites to maintain and stabilize the somite boundary formation of zebrafish embryos.

Although () is known to regulate proliferation and differentiation of muscle fibroblasts, the role of in early-stage somite development is still unknown. During somitogenesis of zebrafish embryos, () is specifically repressed by The somite boundary was defective, and actin filaments were crossing over the boundary in either -knockdown or -overexpressed embryos. In these treated embryos, C-X-C motif chemokine receptor 4a () was reduced, while thrombospondin 3a () was increased. The defective boundary was phenocopied in either -knockdown or overexpressed embryos. Repression of expression by reduced the occurrence of the boundary defect. We demonstrated that is an upstream regulator of and that defective boundary cells could not process epithelialization in the absence of intracellular accumulation of the phosphorylated focal adhesion kinase (p-FAK) in boundary cells. Therefore, in the newly forming somites, mediated downregulation of increases This activity largely decreases expression in the epithelial cells of the somite boundary, which causes epithelialization of boundary cells through mesenchymal-epithelial transition (MET) and eventually leads to somite boundary formation. Collectively, we suggest that mediates a novel pathway, the Rtn4a/Cxcr4a/Thbs3a axis, that allows boundary cells to undergo MET and form somite boundaries in the newly forming somites of zebrafish embryos.