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.
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1q24 位点的缺失揭示了长非编码 RNA DNM3OS 在骨骼发育中的关键作用

DOI:
10.1186/s13578-021-00559-8
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发表时间:
2021-03-02
期刊:
影响因子:
7.5
通讯作者:
Cheng SY
Cheng SY
中科院分区:
生物学2区
文献类型:
--
作者:
Yu TT;Xu QF;Li SY;Huang HJ;Dugan S;Shao L;Roggenbuck JA;Liu XT;Liu HZ;Hirsch BA;Yue S;Liu C;Cheng SY

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背景
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.
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发表时间: 2017-05-18
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