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The axial and appendicular skeleton of vertebrates develops by endochondral ossification, in which skeletogenic tissue is initially cartilaginous and the differentiation of chondrocytes via the hypertrophic pathway precedes the differentiation of osteoblasts and the deposition of a definitive bone matrix. Results from both loss-of-function and misexpression studies have implicated the related homeobox genes  Dlx5  and  Dlx6  as partially redundant positive regulators of chondrocyte hypertrophy. However, experimental perturbations of  Dlx  expression have either not been cell type specific or have been done in the context of endogenous  Dlx5  expression. Thus, it has not been possible to conclude whether the effects on chondrocyte differentiation are cell autonomous or whether they are mediated by  Dlx  expression in adjacent tissues, notably the perichondrium. To address this question we first engineered transgenic mice in which  Dlx5  expression was specifically restricted to immature and differentiating chondrocytes and not the perichondrium.  Col2a1-Dlx5  transgenic embryos and neonates displayed accelerated chondrocyte hypertrophy and mineralization throughout the endochondral skeleton. Furthermore, this transgene specifically rescued defects of chondrocyte differentiation characteristic of the  Dlx5/6  null phenotype. Based on these results, we conclude that the role of  Dlx5  in the hypertrophic pathway is cell autonomous. We further conclude that  Dlx5  and  Dlx6  are functionally equivalent in the endochondral skeleton, in that the requirement for  Dlx5  and  Dlx6  function during chondrocyte hypertrophy can be satisfied with  Dlx5  alone.

Dlx5 Is a Cell Autonomous Regulator of Chondrocyte Hypertrophy in Mice and Functionally Substitutes for Dlx6 during Endochondral Ossification