Richman, Joy Marion; (1990) Factors controlling differential growth of facial primordia of the chick embryo. Doctoral thesis (Ph.D), UCL (University College London).

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Abstract

The embryonic chick face is composed of a series of facial primordia, epithelium-covered buds of mesenchyme, which surround the presumptive mouth. The frontonasal mass forms most of the upper beak, the paired maxillary primordia only grow out a small amount to form the corners of the beak, while the lower beak is entirely derived from the paired mandibular primordia. The aims of this thesis are to discover the factors that control this differential outgrowth and to uncover which of these factors goes awry in abnormal facial development. I initially tested whether the quantity of outgrowth was controlled by the mesenchyme or epithelium by exchanging epithelia between primordia. The mesenchyme determined the amount of outgrowth and all facial epithelia were interchangeable. In exchanges of limb and face tissues, the morphology of frontonasal mass/limb combinations most resembled the homotypic controls. A functional assay was then developed to study growth of facial mesenchyme in vitro. I first defined conditions where no increase in cell number occurred. I then added serum and growth factors in order to see which substances stimulated proliferation. A general stimulation of proliferation was achieved by the addition of serum. Basic fibroblast growth factor stimulated a subpopulation of chondrocytes represented only in the frontonasal mass. Retinoic acid affects facial development in vivo and in vitro. I cultured cells from retinoid treated embryos to see whether they differed in their response to bFGF. I found that the same population that normally would be stimulated by bFGF is inhibited by retinoic acid pretreatment. The basis of the retinoic acid-induced facial cleft was explored further by mapping the distribution of a nuclear receptor for retinoic acid (RAR-β) in normal and retinoid-treated embryos. The distribution of type II collagen transcripts was also investigated. In normal embryos RAR-β transcripts are concentrated in the mesenchyme of upper beak primordia and are unevenly distributed within the maxilla and frontonasal mass. Type II collagen RNA's were mainly found in the surface epithelium and chondrogenic regions. Retinoid treatment changed the expression of the receptor in all the primordia but did not change the distribution of type II collagen transcripts.

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