ZFIN Image: Flores et al., 2006, Fig. 4

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Fig. 4 Loss-of-function analyses using antisense morpholinos demonstrate which Runx proteins are essential at the onset of endochondral bone formation in the head skeleton. Embryos were injected with optimal amounts of MO at the 1-4 cell stage to inhibit gene function, and cartilage development was visualized with alcian blue staining at 3.5 (A-F) and 5 (G-L) dpf. (A,G) runx2bMM; (B,H) runx1MO; (C,I) runx2aMO; (D,J) runx2bT1MO; (E,K) runx2bT2MO; (F,L) runx3MO. Compared to runx2bMM controls, embryos treated with runx2bT1MO, runx2bT2MO, and runx3MO display significant reductions in chondrocyte differentiation at 3.5dpf (D-F). By 5dpf, runx2T1 morphants recover from an early delay in chondrogenesis (J), but those injected with runx2bt2MO and runx3MO show persistence of cartilaginous abnormalities with underdeveloped and reduced cartilage (K,L). The head skeleton of runx1 and runx2a morphants are mildly misshapen at 3.5dpf (B,C), and these become morphologically normal by 5dpf (H,I). Scale bars = 100 μm.

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Acknowledgments

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