Alterations in Msx 1 and Msx 2 expression correlate with inhibition of outgrowth of chick facial primordia induced by retinoic acid

• Published in: Anatomy and Embryology 1997-02, Vol.195 (2), p.203-207
• Main Authors: Brown, J M, Robertson, K E, Wedden, S E, Tickle, C
• Format: Article
• Language: English
• Subjects: Abnormalities, Drug-Induced - etiology; Abnormalities, Drug-Induced - metabolism; Abnormalities, Drug-Induced - pathology; Animals; Beak - abnormalities; Beak - embryology; Beak - ultrastructure; Chick Embryo; DNA-Binding Proteins - genetics; DNA-Binding Proteins - metabolism; Down-Regulation; Facial Bones - abnormalities; Facial Bones - embryology; Facial Bones - ultrastructure; Homeodomain Proteins - genetics; Homeodomain Proteins - metabolism; In Situ Hybridization; Microscopy, Electron, Scanning; Morphogenesis - drug effects; MSX1 Transcription Factor; Transcription Factors; Tretinoin - toxicity; Vitamin A
• ISSN: 0340-2061; 1863-2653; 1432-0568; 0340-2061
• DOI: 10.1007/s004290050039

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.