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Background  Skeletal development and maintenance are complex processes known to be coordinated by multiple genetic and epigenetic signaling pathways. However, the role of long non-coding RNAs (lncRNAs), a class of crucial epigenetic regulatory molecules, has been under explored in skeletal biology.    Results  Here we report a young patient with short stature, hypothalamic dysfunction and mild macrocephaly, who carries a maternally inherited 690 kb deletion at Chr.1q24.2 encompassing a noncoding RNA gene,  DNM3OS , embedded on the opposite strand in an intron of the  DYNAMIN 3  ( DNM3)  gene. We show that lncRNA  DNM3OS  sustains the proliferation of chondrocytes independent of two co-cistronic microRNAs  miR-199a  and  miR-214 . We further show that nerve growth factor ( NGF ), a known factor of chondrocyte growth, is a key target of  DNM3OS -mediated control of chondrocyte proliferation.    Conclusions  This work demonstrates that  DNM3OS  is essential for preventing premature differentiation of chondrocytes required for bone growth through endochondral ossification.

Deletion at an 1q24 locus reveals a critical role of long noncoding RNA DNM3OS in skeletal development