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. 2009 Apr 29;106(19):7979–7984. doi: 10.1073/pnas.0900343106

Fig. 2.

Fig. 2.

Increased neonatal mortality and cranio-facial deformities in CC/FR-HrasG12V± mice. (A) Kaplan-Meier survival plot of CC/FR-HrasG12V and control mice. (B) Decreased body weight in CC/FR-HrasG12V mice at weaning. Weight of CC/FR-HrasG12V mice and control littermates at 3 and 20 weeks of age. Bars represent mean ± SE percent-change in body weight versus controls (n = 8; P = 7.7 ×10−7 at 3 weeks, P = 0.25 at 20 weeks). (C) Coronal sections (4×) across the nasal cavity of a representative WT (a) and CC/FR-HrasG12V (b) mouse. The mutant mouse exhibits marked nasal septal deviation. Low power magnification (20×) of an incisor of a WT (C) and a mutant (D) mouse. The tooth of the CC/FR-HrasG12V± mice has an abnormal ameloblast cell lining and defective enamel formation. (e) Higher magnification (40×) demonstrates detachment of the ameloblasts from the adjacent dentin, loss of polarity, and stratification of ameloblasts, as well as areas of enamel sequestration. (f) Mouse with misalignment of incisors and malocclusion. (D) (Left) Whole-body CT scan (sagittal view) illustrating the rectangular region of interest used to determine the overall cephalo-caudal and ventro-dorsal dimensions of the cranial bony structures. (Right) Abnormal cranial dimensions of CC/FR-HrasG12V mice. Mean cephalo-caudal to ventro-dorsal ratio in aged-matched control and CC/FR-HrasG12V mice. All mice studied in this article are HrasG12V heterozygous mice.