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Endochondral bone formation is fundamental for skeletal development. During this process, chondrocytes undergo multiple steps of differentiation and coordinated transition from a proliferating to a hypertrophic stage, which is critical to advance skeletal development. Here, we identified the transcription factor  Dmrt2  (double-sex and mab-3 related transcription factor 2) as a Sox9-inducible gene that promotes chondrocyte hypertrophy in pre-hypertrophic chondrocytes. Epigenetic analysis further demonstrated that Sox9 regulates  Dmrt2  expression through an active enhancer located 18 kb upstream of the  Dmrt2  gene and that this enhancer’s chromatin status is progressively activated through chondrocyte differentiation.  Dmrt2 -knockout mice exhibited a dwarf phenotype with delayed initiation of chondrocyte hypertrophy. Dmrt2 augmented hypertrophic chondrocyte gene expression including  Ihh  through physical and functional interaction with Runx2. Furthermore, Dmrt2 deficiency reduced Runx2-dependent  Ihh  expression. Our findings suggest that Dmrt2 is critical for sequential chondrocyte differentiation during endochondral bone formation and coordinates the transcriptional network between Sox9 and Runx2.

Dmrt2 promotes transition of endochondral bone formation by linking Sox9 and Runx2