title: Ultrastructure of forming enamel in mouse bearing a transgene that disrupts the amelogenin self-assembly domains.
abstract: The mouse X-chromosomal amelogenin gene promoter was used to drive the expression of mutated amelogenin proteins in vivo. Two different transgenic mouse lines based on deletions to either the amino-terminal (A-domain deletions) or to the carboxyl-region (B-domain deletions) were bred. In the molars of newborn A-domain deleted transgenic mice the formation of the initial layer of aprismatic enamel was delayed. There were severe structural alterations in the enamel of incisors of newborn mice bearing the A-domain deletion which were not apparent in animals bearing the B-domain deletion. In the A-domain-deleted animals, stippled material accumulated throughout the entire thickness of the forming enamel apparently causing a disruption of the normal rod-to-inter-rod relationship. This stippled material was likened to and interpreted as being groupings of amelogenin nanospheres. In the B-domain-deleted animals the stippled material was detected only in minute defects of the forming enamel. These data suggest significant differences in nanosphere assembly properties for animals bearing either the A-domain or the B-domain-deleted transgene. The present in vivo experimental approach suggests that at early stages of enamel formation, the A-domain plays a greater role than does the B-domain in amelogenin self-assembly, and consequently in enamel architecture and structure.
authors.affiliation: Laboratoire de Biologie et Physiopathologie Crânio-faciale EA 2496 Université Paris V Groupe Matrices Extracellulaires et Biominéralisations, Faculté de Chirurgie Dentaire, 1, rue Maurice Arnoux, 92120 Montrouge, France.
authors.forename: C
authors.initials: C
authors.lastname: Dunglas
authors.forename: D
authors.initials: D
authors.lastname: Septier
authors.forename: M L
authors.initials: ML
authors.lastname: Paine
authors.forename: D H
authors.initials: DH
authors.lastname: Zhu
authors.forename: M L
authors.initials: ML
authors.lastname: Snead
authors.forename: M
authors.initials: M
authors.lastname: Goldberg
mesh_terms: D000566:Amelogenesis / Q000235:genetics*; D053523:Amelogenin; D000595:Amino Acid Sequence; D000818:Animals; D000831:Animals, Newborn; D003743:Dental Enamel / Q000254:growth & development / Q000648:ultrastructure*; D003746:Dental Enamel Proteins / Q000235:genetics*; D005818:Genetic Engineering; D007180:Incisor / Q000254:growth & development / Q000648:ultrastructure; D051379:Mice; D008810:Mice, Inbred C57BL; D008808:Mice, Inbred CBA; D008822:Mice, Transgenic; D008854:Microscopy, Electron; D008963:Molar / Q000254:growth & development / Q000648:ultrastructure; D008969:Molecular Sequence Data; D017434:Protein Structure, Tertiary / Q000235:genetics; D014083:Tooth Germ / Q000254:growth & development / Q000648:ultrastructure*
chemical_list: D053523:Amelogenin; C507200:Amelx protein, mouse; D003746:Dental Enamel Proteins