By David Hukins
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Additional info for Connective Tissue Matrix: Part 2
1981). More recently, Tucker and Erickson (1986) have shown that those newt NC cells that encounter glycosaminoglycans (GAGs) while differentiating will become xanthophores, while those that do not are more likely to become melanophores. Cells other than those of the NC can also have their fates controlled by ECM macromolecules; an unknown component of bone matrix causes muscle cells to become chondrocytes (reviewed by Nathanson, 1986) and collagen substrata in vitro promote muscle cells to form clones of differentiated, striated muscle (Hauschka and Konigsberg, 1966).
1987) demonstrates the functions of another CAM, N-cadherin, in somitogenesis, the process by which the mesenchyme lateral to the early neural tube segments into blocks of tissue which later break up to form bone, muscle and dermis. N-Cadherin appears when the presomitic mesenchyme aggregates to form somites and disappears when the somite breaks up into sclerotome, myotome and dermotome. It is noteworthy that N-CAM appears when the somite forms but is not lost when it breaks up; this maintenance of some CAM on the cell surface may help to ensure that the somitic cells retain a degree of coherence and, unlike the migrating NC cells which express no CAMs, do not colonize the entire embryo.
1975) and into the primary stroma of the cornea after hyaluronic acid-induced swelling (Toole and Trelstad, 1971). A further role is in controlling the expansion of mesenchymal tissue (Brinkley and Morris-Wiman, 1987). Fibronectin and Other Substratum-adhesion Molecules (SAMs) These molecules mediate the adhesive process between cells and their substrata and there are in turn membrane-bound receptors that allow cells to adhere to the SAMs. Fibronectin and chondronectin are the best-known members of the family for mesenchymal cells and laminin for epithelial cells.
Connective Tissue Matrix: Part 2 by David Hukins