The role of epithelial coliagen and proteoglycan in the initiation of osteogenesis by avian neural crest cells

Abstract

Osteogenesis was inhibited when mandibular processes from 3 1/2-day-old embryos were cultured in BUdR, LACA, alpha, alpha'-Dipyridyl, 4-Methylumbelliferone, and 4-Methylumbelliferyl-beta-D-glucoside or beta-D-xyloside. Mandibular processes were then cultured in the test substances for 3 days, enzymatically separated into their epithelial and ectomesenchymal components, combined with mandibular components from untreated embros, and either organ-cultured or grafted to chorioallantoic membranes of host embryos. Osteogenesis was inhibited when treated epithelium, but not when treated ectomesenchyme, was present in the tissue recombinations. Analysis of the known action of these inhibitors indicates that proliferation, hydroxylation of collagen, and synthesis of proteoglycans by epithelial cells are all necessary components of this osteogenic epithelial-ectomesenchymal interaction.

Extracellular matrix synthesis is required for the movement of sclerotome and neural crest cells on collagen

“…As proline analogs, cis-HP and LACA are well established as agents that inhibit the secretion and deposition of triple helical procollagen from cells [4, 16, 271. However, although the primary biochemical targets of these drugs is in the collagen biosynthetic pathway, it must be emphasized that effects due to perturbation of interlinked processes cannot be entirely eliminated. Both cis-HP [18,20,21,29,42,501 and LACA [l, 8,9,18,20,29,38,421 have been used repeatedly for such inhibition, frequently with chick embryo tissue [5,17,40,49,511. The capacity of NPXP to inhibit proteoglycan synthesis is also well known [6,26,36,371.…”

Mesenchyme-dependent BMP signaling directs the timing of mandibular osteogenesis

“…The epithelial signal appears to be a proteinaceous component located in the basal lamina (Bradamante and Hall, 1980;Hall and Van Exan, 1982;Hall et al, 1983), which is transmitted via cell-cell contact to mesenchyme (Van Exan and Hall, 1984). Because our quail-duck transplants accelerate the timing of epithelial-mesenchymal interactions, as well as the subsequent formation of bone, we expect that, at earlier stages, donor mesenchyme induces premature signaling from the overlying host epithelium, and/or that epithelial signals stay continuously expressed before their period of necessity, and that mesenchyme regulates its own competence to respond to these signals (Fig.…”

“…That these interactions are osteo-inductive and stage dependent has been demonstrated primarily through tissue recombination and epithelial removal experiments involving chick and mouse embryos (Tyler and Hall, 1977;Hall, 1978;Bradamante and Hall, 1980;Tyler and McCobb, 1980;Hall, 1982;Van Exan and Hall, 1984;Wedden, 1987;Hall and Coffin-Collins, 1990;Dunlop and Hall, 1995;Francis-West et al, 1998;Vaglia and Hall, 1999). What remain to be clarified are the molecular and cellular mechanisms that control the timing of these interactions and the ensuing formation of bone.…”

Quail-duck chimeras reveal spatiotemporal plasticity in molecular and histogenic programs of cranial feather development

“…The most common approach employed to define the role of either the epithelium or the mesenchyme at each step of the process has involved recombination of dissected tissues in vitro. In this context, cranial osteogenesis has been shown to be regulated by stage-specific interactions between neural crest mesenchyme and adjacent epithelia (Hall, 1978;Hall and Tremaine, 1979;Bee and Thorogood, 1980;Bradamante and Hall, 1980;Tyler and McCobb, 1980;Hall, 1982;Hall and Coffin-Collins, 1990;Mina et al, 1994;Dunlop and Hall, 1995;Vaglia and Hall, 1999;Couly et al, 2002). Although the epithelium is required in this process, its role appears to be permissive rather than instructive.…”