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DDB1 promotes the proliferation and hypertrophy of chondrocytes during mouse skeleton development.
Zhao, Lianzheng; Wang, Xiaodan; Pomlok, Kumpanat; Liao, Hongwei; Yang, Guan; Yang, Xiao; Chen, Ye-Guang.
Affiliation
  • Zhao L; The State Key Laboratory of Membrane Biology, Tsinghua-Peking Center for Life Sciences, School of Life Sciences, Tsinghua University, Beijing, 100084, China.
  • Wang X; The State Key Laboratory of Membrane Biology, Tsinghua-Peking Center for Life Sciences, School of Life Sciences, Tsinghua University, Beijing, 100084, China.
  • Pomlok K; The State Key Laboratory of Membrane Biology, Tsinghua-Peking Center for Life Sciences, School of Life Sciences, Tsinghua University, Beijing, 100084, China.
  • Liao H; The State Key Laboratory of Membrane Biology, Tsinghua-Peking Center for Life Sciences, School of Life Sciences, Tsinghua University, Beijing, 100084, China.
  • Yang G; State Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences, Beijing Institute of Lifeomics, Beijing, 102206, China.
  • Yang X; State Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences, Beijing Institute of Lifeomics, Beijing, 102206, China.
  • Chen YG; The State Key Laboratory of Membrane Biology, Tsinghua-Peking Center for Life Sciences, School of Life Sciences, Tsinghua University, Beijing, 100084, China. Electronic address: ygchen@tsinghua.edu.cn.
Dev Biol ; 465(2): 100-107, 2020 09 15.
Article in En | MEDLINE | ID: mdl-32479761
The proliferation and hypertrophy of chondrocytes play important roles in endochondral ossification, which is tightly regulated during skeleton development. However, the regulation mechanism remains largely unknown. Here we show that DDB1 (Damaged DNA Binding Protein 1) has a critical function in the development of growth plates. Using chondrocyte-specific DDB1 knockout mice, we found that DDB1 deletion in chondrocytes results in dwarfism due to the aberrant skeleton development. The structure of growth plate in tibia becomes disordered at P21, not in femur. But at P70, the changes are severer in femur than tibia. Chondrocyte proliferation and differentiation are attenuated and asynchronous in both tibia and femur at P7 and P21. Furthermore, DDB1 deficiency induces p27 upregulation and subsequent cell cycle arrest in primary chondrocytes. Therefore, our data reveal that DDB1 is essential for the skeleton development by controlling chondrocyte proliferation and differentiation.
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Tibia / Chondrocytes / Musculoskeletal Development / DNA-Binding Proteins / Femur / Cell Cycle Checkpoints / Growth Plate Limits: Animals Language: En Journal: Dev Biol Year: 2020 Document type: Article Affiliation country: China Country of publication: United States

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Tibia / Chondrocytes / Musculoskeletal Development / DNA-Binding Proteins / Femur / Cell Cycle Checkpoints / Growth Plate Limits: Animals Language: En Journal: Dev Biol Year: 2020 Document type: Article Affiliation country: China Country of publication: United States