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Dental phenotype of a mouse model expressing a truncated form of ameloblastin
Author(s) -
Wazen Rima Marie,
Moffatt Pierre,
Zalzal Sylvia Francis,
Yamada Yoshihiko,
Nanci Antonio
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.651.3
Subject(s) - ameloblast , enamel paint , phenotype , amelogenin , enamel organ , immunohistochemistry , chemistry , microbiology and biotechnology , biology , gene , dentistry , biochemistry , medicine , immunology
Ameloblastin (AMBN) is the second most abundant protein produced by ameloblasts and is found mainly in forming enamel. Our aim was to characterize the tooth phenotype in a mouse model lacking expression of full‐length AMBN (AMBN −FL ). Since after building enamel ameloblasts and associated cells participate in the formation of the gingival attachment to the tooth (junctional epithelium, JE), we have also examined its integrity. Materials and Methods Mandibles from normal and AMBN −FL mice were processed for morphological analyses and immunohistochemical detection of AMBN. Freeze‐dried enamel organs and enamel were prepared for molecular and biochemical analyses. Results Our data show that absence of full‐length AMBN causes structural changes at the level of the enamel organ, shows displatic enamel layer, and loss of integrity of the JE. Immunohistochemical staining indicated that the enamel organ in these mice continued to produce an AMBN‐related peptide that is translated from a truncated RNA missing exons 5 and 6. The protein was deduced to have 295 amino acids and an apparent molecular weight of 32‐35 kDa. Conclusion Our study shows that AMBN influences both cells and matrix events. Identification of the portion of AMBN protein still produced in this AMBN −FL mouse model provides new insights on the functional domains that may be implicated in these activities. Supported by the CIHR.