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

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

Cell & bioscience (2021-03-04)
Ting-Ting Yu, Qiu-Fan Xu, Si-Yang Li, Hui-Jie Huang, Sarah Dugan, Lei Shao, Jennifer A Roggenbuck, Xiao-Tong Liu, Huai-Ze Liu, Betsy A Hirsch, Shen Yue, Chen Liu, Steven Y Cheng
ABSTRACT

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. 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. This work demonstrates that DNM3OS is essential for preventing premature differentiation of chondrocytes required for bone growth through endochondral ossification.

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