| First Author | Diekwisch T | Year | 1993 |
| Journal | Development | Volume | 117 |
| Issue | 2 | Pages | 471-82 |
| PubMed ID | 8392462 | Mgi Jnum | J:4657 |
| Mgi Id | MGI:53140 | Doi | 10.1242/dev.117.2.471 |
| Citation | Diekwisch T, et al. (1993) Antisense inhibition of AMEL translation demonstrates supramolecular controls for enamel HAP crystal growth during embryonic mouse molar development. Development 117(2):471-82 |
| abstractText | During tooth development, enamel organ epithelial cells express a tissue-specific gene product (amelogenin) which presumably functions to control calcium hydroxyapatite crystal growth patterns during enamel biomineralization. The present studies were designed to test the hypothesis that amelogenin as a supramolecular aggregate regulates crystal growth during enamel biomineralization. Antisense oligodeoxynucleotide strategy was used in a simple organ culture system to inhibit amelogenin translation. Under these experimental conditions, antisense treatment prior to and during amelogenin expression resulted in inhibition of amelogenin translation products within immunoprecipitated [35S]methionine metabolically labeled proteins. To determine the efficiency of antisense treatment in this model system, digoxigenin-labeled oligodeoxynucleotides were observed to diffuse throughout the tooth explants including the target ameloblast cells within 24 hours. Ultrastructural analyses of amelogenin supramolecular assembly as electron-dense stippled materials in antisense treated cultures demonstrated dysmorphology of the extracellular enamel matrix with a significant reduction in crystal length and width. We conclude that secreted extracellular proteins form a supramolecular aggregate, which controls both the orientation and dimensions of enamel crystal formation during tooth development. |
