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Fig. 2. Targeted disruption of Axin2 in mice induces craniosynostosis. Histological sections show that cranial sutures are prematurely fused in the Axin2^–/– mice. The sutures of control (A,C,F) and Axin2-null (B,D,E,G) mice at postnatal day 0 (A,B), 8 (C-E) and 17 (F,G) were analyzed by histology. In the controls (A,C,F), the metopic suture remains patent (indicated by arrowheads) in the first 4 weeks of postnatal development. The Axin2^–/– suture did not show fusion at birth (B). However, unilateral (D) or bilateral (E) fusion of the Axin2^–/– suture (arrows) occurred at day 8. The overlaying of cranial bones and endocranial bridging (arrows) is evident by day 17 (G). Compared with controls, the Axin2^–/– sutures are morphologically more advanced with increased ossification (orange). The skeletogenesis stimulated in the Axin2 mutant was characterized by expression of FGFR1, a marker for osteoblast precursor (H-K). Immunohistochemical staining reveals an increase in FGFR1-expressing osteoblast precursors (asterisks) in the Axin2^–/– suture at P17 (I,K). Sections were immunostained with -FGFR1 antibody (brown) and counterstained with Hematoxylin (blue). Enlargements of the insets (H,I) are shown in J and K. Scale bars: 100 µm in A,B; 200 µm in C-G; 50 µm in H,I.

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