The role of extracellular matrix in the formation of the sclerotome

Abstract

The development of the sclerotome is considered as a model for the formation of mesenchyme from an epithelium. In early epithelial somites, transmission and scanning electron microscopy indicate considerable ultrastructural similarity between the future sclerotome and dermamyotomal regions. Subsequently, these two regions diverge in their development. In the forming dermamyotome, junctional complexes become more extensive and the cells become elongated, closely applied to each other, and have angular surface contours. In the forming sclerotome, there is an early reduction in apical junctions. The cells elongate, keeping their original polarity, and acquire numerous filopodia which contain punctate junctions at sites of cell-to-cell contact. Associated with cellular extension is an expansion of the intercellular spaces which do not contain any ultrastructurally recognizable material. Evidence for a role of hyaluronic acid in the expansion of the intercellular spaces is presented. As identified by the susceptibility of cetylpyridinium chloride precipitates to Streptomyces hyaluronidase and chromatographic separation of chondroitinase ABC digestion products, as much as 64--68% of the [3H]glucosamine-labeled glycosaminoglycans synthesized by explanted somites is hyaluronic acid. In addition, hyaluronidase-sensitive label is localized in the intercellular spaces of the sclerotome, as demonstrated by autoradiography. When Streptomyces hyaluronidase is injected in ovo into living embryos, the sclerotomal mesenchyme differentiates morphologically, but intercellular spaces are drastically reduced. It is hypothesized that the sclerotomal cells produce a hyaluronate-enriched extracellular matrix which is inflated by hydration to mediate the expansion of the sclerotomal mass towards the notochord.