Fig. 2 | Bone Research

Fig. 2

From: RUNX2 is essential for maintaining synchondrosis chondrocytes and cranial base growth

Fig. 2

Runx2 inactivation in Fgfr3+ cells causes craniofacial skeletal abnormalities. a Fgfr3-creER; R26R-tdTomato mice were crossed with mice carrying a runt-related transcription factor 2 (Runx2) floxed allele (flanking exon 4). Single intraperitoneal injection of tamoxifen at P3 induces cre recombination, leading to heterozygous or homozygous knockout of Runx2 in Fgfr3+ chondrocytes [Fgfr3-creER; Runx2fl/+ (Fgfr3-Runx2cHet)/Fgfr3-creER; Runx2fl/fl (Fgfr3-Runx2cKO)]. 3D renderings of Control (Fgfr3-creER), Fgfr3-Runx2cHet, and Fgfr3-Runx2cKO mice at 3 months indicate decreased anteroposterior growth of entire craniofacial complex (b), premature ossification of the synchondroses (c), and widened cranial vaults (d) in Fgfr3-Runx2cKO animals. Quantification of skull length (e), cranial base length (f), and middle cranial vault width (g) at P9 [Control (n = 6)], Fgfr3-Runx2cHet (n = 5), Fgfr3-Runx2cKO (n = 5), P42 [male-Control (n = 4), Fgfr3-Runx2cHet (n = 4), Fgfr3-Runx2cKO (n = 4); female-Control (n = 5), Fgfr3-Runx2cHet (n = 6), Fgfr3-Runx2cKO (n = 5)] and 3 months [male-Control (n = 5), Fgfr3-Runx2cHet (n = 4), Fgfr3-Runx2cKO (n = 5); female-Control (n = 4), Fgfr3-Runx2cHet (n = 5), Fgfr3-Runx2cKO (n = 6)]. *P < 0.05, **P < 0.01, Mann-Whitney’s U-test. Data are presented as mean ± s.d. Scale bar = 1 mm

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