CEP55 promotes cilia disassembly through stabilizing Aurora A kinase

DOI PDF 被引用文献2件
  • Yu-Cheng Zhang
    State Key Laboratory of Proteomics, National Center of Biomedical Analysis, Beijing, China 1
  • Yun-Feng Bai
    State Key Laboratory of Proteomics, National Center of Biomedical Analysis, Beijing, China 1
  • Jin-Feng Yuan
    State Key Laboratory of Proteomics, National Center of Biomedical Analysis, Beijing, China 1
  • Xiao-Lin Shen
    State Key Laboratory of Proteomics, National Center of Biomedical Analysis, Beijing, China 1
  • Yu-Ling Xu
    State Key Laboratory of Proteomics, National Center of Biomedical Analysis, Beijing, China 1
  • Xiao-Xiao Jian
    State Key Laboratory of Proteomics, National Center of Biomedical Analysis, Beijing, China 1
  • Sen Li
    State Key Laboratory of Proteomics, National Center of Biomedical Analysis, Beijing, China 1
  • Zeng-Qing Song
    State Key Laboratory of Proteomics, National Center of Biomedical Analysis, Beijing, China 1
  • Huai-Bin Hu
    State Key Laboratory of Proteomics, National Center of Biomedical Analysis, Beijing, China 1
  • Pei-Yao Li
    State Key Laboratory of Proteomics, National Center of Biomedical Analysis, Beijing, China 1
  • Hai-Qing Tu
    State Key Laboratory of Proteomics, National Center of Biomedical Analysis, Beijing, China 1
  • Qiu-Ying Han
    State Key Laboratory of Proteomics, National Center of Biomedical Analysis, Beijing, China 1
  • Na Wang
    State Key Laboratory of Proteomics, National Center of Biomedical Analysis, Beijing, China 1
  • Ai-Ling Li
    State Key Laboratory of Proteomics, National Center of Biomedical Analysis, Beijing, China 1
  • Xue-Min Zhang
    State Key Laboratory of Proteomics, National Center of Biomedical Analysis, Beijing, China 1
  • Min Wu
    State Key Laboratory of Proteomics, National Center of Biomedical Analysis, Beijing, China 1
  • Tao Zhou
    State Key Laboratory of Proteomics, National Center of Biomedical Analysis, Beijing, China 1
  • Hui-Yan Li
    State Key Laboratory of Proteomics, National Center of Biomedical Analysis, Beijing, China 1

抄録

<jats:p>Primary cilia protrude from the cell surface and have diverse roles during development and disease, which depends on the precise timing and control of cilia assembly and disassembly. Inactivation of assembly often causes cilia defects and underlies ciliopathy, while diseases caused by dysfunction in disassembly remain largely unknown. Here, we demonstrate that CEP55 functions as a cilia disassembly regulator to participate in ciliopathy. Cep55−/− mice display clinical manifestations of Meckel–Gruber syndrome, including perinatal death, polycystic kidneys, and abnormalities in the CNS. Interestingly, Cep55−/− mice exhibit an abnormal elongation of cilia on these tissues. Mechanistically, CEP55 promotes cilia disassembly by interacting with and stabilizing Aurora A kinase, which is achieved through facilitating the chaperonin CCT complex to Aurora A. In addition, CEP55 mutation in Meckel–Gruber syndrome causes the failure of cilia disassembly. Thus, our study establishes a cilia disassembly role for CEP55 in vivo, coupling defects in cilia disassembly to ciliopathy and further suggesting that proper cilia dynamics are critical for mammalian development.</jats:p>

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