1. Alterations in Msx 1 and Msx 2 expression correlate with inhibition of outgrowth of chick facial primordia induced by retinoic acid.
- Author
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Brown JM, Robertson KE, Wedden SE, and Tickle C
- Subjects
- Abnormalities, Drug-Induced etiology, Abnormalities, Drug-Induced pathology, Animals, Beak abnormalities, Beak ultrastructure, Chick Embryo, DNA-Binding Proteins genetics, Down-Regulation, Facial Bones abnormalities, Facial Bones ultrastructure, Homeodomain Proteins genetics, In Situ Hybridization, MSX1 Transcription Factor, Microscopy, Electron, Scanning, Abnormalities, Drug-Induced metabolism, Beak embryology, DNA-Binding Proteins metabolism, Facial Bones embryology, Homeodomain Proteins metabolism, Morphogenesis drug effects, Transcription Factors, Tretinoin toxicity
- Abstract
Spatially-restricted expression domains of Msx 1 and Msx 2 in the developing chick face suggest that they may play a role in epithelial-mesenchymal interactions governing outgrowth of facial primordia. Retinoid application to developing chick faces reproducibly inhibits upper beak outgrowth but the lower beak is unaffected. In the normal face, high levels of Msx gene transcripts in upper and lower beak primordia correlate with regions of outgrowth. Following retinoid treatment, Msx 1 and Msx 2 transcripts are rapidly down-regulated in upper beak primordia where outgrowth is inhibited, but remain largely unchanged in lower beak primordia, where outgrowth is unaffected. Decreases in gene expression precede retinoid-induced morphological changes in the upper beak, suggesting that Msx gene products are involved in mediating the effect of retinoids on facial development.
- Published
- 1997
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