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Transgenic Mice that Express Normal and Mutated Amelogenins
C.W. Gibson1,*,
Z.A. Yuan1,
Y. Li1,
B. Daly2,
C. Suggs2,
M.A. Aragon1,
F. Alawi3,
A.B. Kulkarni4 and
J.T. Wright2
1 Dept. of Anatomy and Cell Biology and
3 Dept. of Pathology, School of Dental Medicine, University of Pennsylvania, 240 S. 40th Street, Philadelphia, PA 19104-6030, USA
2 Dept. of Pediatric Dentistry, School of Dentistry, University of North Carolina, Chapel Hill, NC 27599, USA; and
4 Functional Genomics Section, National Institute of Dental and Craniofacial Research, NIH, Bethesda, MD 20892, USA

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Figure 1. Map of the expression vector for M180 and the modification for the P70T vector used for the generation of transgenic mice. Vector includes 5.5-kb Amelx upstream region, exon 1, intron 1, exons 2, 3, 5, 6, 7, and 3' genomic DNA. Location of the P70T mutation is indicated. UTR: untranslated region.
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Figure 2. Western blot of extracts from Amelx null/M180, Amelx null/P70T, and Amelx null first molars. Anti-amelogenin antibody was used to detect amelogenin protein. Lanes: KOxM180-31, KOxP70T-2, or KOxP70T-16 indicates female null and male transgenic parents. M– is null male without transgene; M+ is null male with transgene. F– and F+ are heterozygous females without and with the transgene, respectively.
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Figure 3. Phenotype of wild-type, M180, and P70T molars (wild-type background). Light microscopic view of molars from wild-type (A), M180 transgenic (B), and P70T transgenic mice (C). Scanning electron micrographs of M180 (D) and P70T (E,F) molar enamel.
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Figure 4. (AQ) Histology of a normal developing tooth and an odontogenic tumor (Amelx heterozygous background). (A) Amelx +/–/P70T with tumor; (B) Amelx +/–/M180; and (C) Amelx –/0/P70T immunohistochemistry using anti-amelogenin antibody.
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Journal of Dental Research, Vol. 86, No. 4,
331-335 (2007)
DOI: 10.1177/154405910708600406

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