Effects of heat shock on the pattern of fibronectin and laminin during somitogenesis in Xenopus laevis.

Abstract

Heat shock causes partial disruption of the segmentation pattern during somitogenesis in Xenopus as well as in other vertebrates. However, Xenopus undergoes a different type of somite formation than that of most vertebrates: Somites are formed by rotation of cell blocks out of the paraxial mesoderm. We attempted to determine whether or not the segmentation disorder following heat shock is caused by an altered pattern of fibronectin and/or laminin, that could then effect the rotation of cell blocks. Therefore, we carried out heat shock experiments and analyzed the distribution of both ECM proteins in correlation to the position of somitic cells. Our results reveal that heat shock causes an incorrect deposition of fibronectin as well as laminin during somite formation. This leads to an intermingling of cells from different segments and to an anchorage of cells at the lateral matrix. Immunoblots show that the defects in the pattern of these ECM proteins do not correlate with a decrease of both proteins. However, immunohistological staining patterns demonstrate that oversized blocks of 20-cell width, instead of the normal ones of about 9-cell width, are separated out of the paraxial mesoderm following heat shock treatment. This indicates that the altered pattern of fibronectin and laminin might be a secondary effect caused by incorrect segregation and detachment of cell blocks during somitogenesis. Since anchorage of somitic cells is mostly affected by the altered distribution of fibronectin and laminin, it is more likely that both ECM proteins function in anchorage of migrating presomitic cells and in maintaining of segment borders rather than in stimulating cell rotation movements.