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. 2013 Mar 8;6(3):768–779. doi: 10.1242/dmm.010397

Fig. 6.

Fig. 6.

Inter-premaxillary suture at P0. (A,B) H&E staining shows that mutant sutures present with aberrant trabecular overgrowth of the vertical extensions of the premaxillary bones (pm), thickening of the intervening suture mesenchyme and misalignment of the suture with the cartilage of the nasal septum (s). Widening of the mutant suture is evident in the greater separation of the cartilages (c) encapsulating the vomeronasal organs. (C,D,M) Immunofluorescent staining for Ki67 (gray channel shown) shows increased proliferation in mutant suture mesenchyme compared with unaffected littermates. (E,F) Immunofluorescent staining for Runx2 (gray channel shown) shows similar expression levels between unaffected littermates and mutant mice, although mutant suture mesenchyme is more abundant and highly Runx2-positive cells are more numerous along the bone-mesenchyme interface. (G,H,N) TUNEL staining (green) shows minimal apoptosis within the suture mesenchyme of unaffected littermates and mutant mice but a high frequency in the adjacent osteogenic domains (stained for ALP activity; red). In these regions, apoptosis is significantly higher in mutants compared with unaffected littermates. (I–L) Phospho-p38 and phospho-ERK 1/2 levels are similar in mutant and unaffected littermate sutures. (M) Proliferation is significantly increased in mutant suture mesenchyme relative to unaffected littermates; *P=0.035. (N) Apoptosis is significantly increased in bone bordering the suture mesenchyme in mutants relative to unaffected littermates; *P=0.026. Images from A–L are from near-adjacent sections from the same littermate pair. Scale bar: 100 μm.