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Overexpression of Fbxo6 inactivates spindle checkpoint by interacting with Mad2 and BubR1

Han-Zhang Xu1, Zhuo-Qun Wang2, Hui-Zhuang Shan1

  • 1a Hongqiao International Institute of Medicine, Shanghai Tongren Hospital/Faculty of Basic Medicine, Chemical Biology Division of Shanghai Universities E-Institutes, Key Laboratory of Cell Differentiation and Apoptosis of the Chinese Ministry of Education , Shanghai Jiao Tong University School of Medicine , Shanghai , PR China.

Cell Cycle (Georgetown, Tex.)
|December 12, 2018
PubMed

Insights

Fbxo6 protein regulates the spindle assembly checkpoint, preventing premature sister chromatid separation during mitosis. Its overexpression disrupts cell division, leading to genomic instability in cancer cells.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Genetics

Background:

  • The spindle assembly checkpoint (SAC) is crucial for preventing chromosome mis-segregation during mitosis.
  • F-box proteins are key regulators of cell cycle progression and genome stability through ubiquitin-mediated protein degradation.

Purpose of the Study:

  • To investigate the role of Fbxo6 in regulating the spindle assembly checkpoint and chromosome segregation.
  • To elucidate the molecular mechanisms by which Fbxo6 influences mitotic progression.

Main Methods:

  • Western blotting to detect Fbxo6 phosphorylation during mitosis.
  • Cell-based assays using Fbxo6 overexpression in HeLa cells to assess mitotic exit and chromosome segregation.
  • Co-immunoprecipitation to identify interactions between Fbxo6 and SAC proteins.

Main Results:

  • Fbxo6 is phosphorylated during mitosis and critically regulates the SAC.
  • Overexpression of Fbxo6 accelerates mitotic exit and causes premature sister chromatid separation.
  • Fbxo6 interacts with SAC proteins Mad2 and BubR1, promoting an aberrant mitotic exit.
  • Fbxo6 overexpression leads to increased binuclear/multilobed nuclei and reduced cell viability.

Conclusions:

  • Fbxo6 plays a novel and critical role in regulating the spindle assembly checkpoint and chromosome segregation.
  • Fbxo6-mediated disruption of SAC contributes to genomic instability, potentially impacting cancer cell proliferation.
Keywords:
BubR1F-box proteinFbxo6Mad2Mitosisspindle checkpoint

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