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. 2013 Aug 26;210(9):1793–1806. doi: 10.1084/jem.20111790

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© 2013 Zou et al.

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Figure 7. — Dcamkl1 genetically interacts with Runx2. (A) Body weight analysis of neonatal WT, Runx2^+/−, Dcamkl1^−/−, and Dcamkl1^−/−Runx2^+/− mice. Results are presented as the mean ± SD of at least six mice per group. (B, C, and E) Alizarin red– and Alcian blue–stained skeletal preps of P3 WT, Dcamkl1^−/−, Runx2^+/−, and Dcamkl1^−/−Runx2^+/− mice demonstrates runting (B), clavicular hypoplasia (C), and delayed closure of fontanelles (E) in Runx2^+/− mice. The red arrow in C indicates the presence of a short clavicle. Results are representative of at least four mice per group. Bars: (B) 600 µm; (C) 300 µm; (E) 500 µm. (D) The clavicle length of p3 WT, Dcamkl1^−/−, Runx2^+/−, and Dcamkl1^−/−Runx2^+/− mice was quantified. Results are presented as the mean ± SD of at least eight mice per group. Statistical analysis was performed using an unpaired Student’s t test: *, P < 0.001.