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Ritva Rice, Bradley Spencer-Dene, Elaine C. Connor, Amel Gritli-Linde, Andrew P. McMahon, Clive Dickson, Irma Thesleff, David P.C. Rice
Published in Volume 113, Issue 12
J Clin Invest. 2004; 113(12):1692–1700 doi:10.1172/JCI20384
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Figure 1

Palatal abnormalities in Fgfr2b_/_ and Fgf10_/_ mice. (A_C) View of the palate with mandible removed from NB mice. (A) WT palate was completely closed with clear symmetrical rugae. (B and C) Fgfr2b_/_ and Fgf10_/_ mutants exhibited a similar wide cleft of the secondary palate, with a view into the nasal cavity (asterisks). (D_L) E13 and E15 hematoxylin stained coronal sections through the oral cavity. (G_I) Higher-magnification views of D_F. By E13 the epithelium of WT mice had begun to thicken and stratify into a squamous pattern. That of both mutants was thin and lacked organization. Occasional patches of thicker epithelium did form, notably in Fgf10_/_ mice either at the MEE (I) or as outgrowths from the dorsum of the tongue (F, arrow). However, cells in these patches underwent apoptosis (see Figure 4). (K and L) Palatal shelves were positioned above the tongue but neither met nor fused. (L) Epithelial fusion between the palatal shelf and mandible (arrow). C, cranial base; f, floor of the mouth; m, Meckel’s cartilage; nc, nasal cavity; p, palatal shelf; t, tongue; tb, molar tooth bud. Scale bars: A, 2 mm (A_C, same magnification); D, 200 ∝m (D_F, same magnification); and J, 200 ∝m (J_L, same magnification).