McGonnell, Imelda Mary; (1998) Fate maps and gene expression in normal and abnormal facial primordia of chick embryos. Doctoral thesis (Ph.D), UCL (University College London).

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Abstract

This thesis investigates the cellular and molecular basis of shaping of facial primordia during normal and abnormal primary palate formation in chick embryos. DiI fate maps of facial primordia indicate that local differences in expansion between cell populations and directed expansion of cell populations shape the face and mediate outgrowth. Examination of patterns of cell proliferation, cell death and cell intercalation showed that these cell activities make important contributions to expansion. Application of retinoic acid to chick embryos results in primary palate clefting. Fate maps showed this is due to decreased expansion and proliferation in cell populations contributing directly to primary palate formation. However, other cell populations in the upper face expanded more uniformly, apparently due to loss of tension normally created by primary palate formation. Thus changes in behaviour in a few cell populations lead to global changes in facial shape. Cellular behaviour is coordinated by signalling molecules. Connexins 43 and 32, gap junction proteins mediating cell-cell signalling, were found to be expressed in regions of greatest mesenchymal expansion in the face. Retinoic acid treatment reduces expression of connexin 43 in cell populations forming the primary palate. Application of connexin 43 antisense oligodeoxynucleotides to the chick face results in facial clefting. Signalling via epithelial-mesenchymal interactions are also necessary for shaping. Removal of ectoderm from maxillary primordia in ovo resulted in reduced outgrowth. FGF, an ectodermal signal, rescues outgrowth, but does not maintain mesenchymal Msx-1 expression. BMP, another ectodermal signal, does not increase outgrowth but maintains Msx-1 expression. Eph4A, expressed in overlapping domains with Msx-1 in the face, is also dependent on an ectodermal signal, FGF, for maintained expression. These results are consistent with the idea that cell signalling via gap junctions and between epithelium and mesenchyme control cell behaviour that lead to primary palate formation.

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