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The Drosophila F-box protein dSkp2 regulates cell proliferation by targeting Dacapo for degradation

Wen Dui1, Bin Wei, Feng He

  • 1State Key Laboratory of Brain and Cognitive Science, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China.

Molecular Biology of the Cell
|April 5, 2013
PubMed

Insights

The Drosophila Skp2 (dSkp2) protein targets Dacapo (Dap) for degradation, regulating cell cycle progression. This conserved function suggests Drosophila as a model for studying Skp2-related tumorigenesis.

Area of Science:

  • Cell Biology
  • Developmental Biology
  • Genetics

Background:

  • Cell cycle control involves complex regulatory networks with positive and negative factors.
  • Human Skp2, an F-box protein, is an oncogenic positive regulator of the cell cycle.
  • The functions of Drosophila Skp2 (dSkp2) are not well understood.

Purpose of the Study:

  • Investigate the role of dSkp2 in Drosophila.
  • Focus on the functional relationship between dSkp2 and Dacapo (Dap).
  • Explore the conservation of Skp2 functions in cell cycle regulation.

Main Methods:

  • Yeast three-hybrid assays to test protein interactions.
  • Western blotting to detect protein levels and ubiquitination.
  • RNA interference (RNAi) for gene knockdown.
  • Analysis of wing development phenotypes in Drosophila.

Main Results:

  • dSkp2 physically interacts with Dap, the Drosophila homolog of p21/p27.
  • dSkp2 targets Dap for ubiquitination and proteasomal degradation.
  • dSkp2 antagonizes Dap to regulate cell cycle progression in vivo.
  • dSkp2 knockdown reduces wing cell density by prolonging cell doubling time.
  • Phenotypes of dSkp2 knockdown resemble dap overexpression and are partially suppressed by reduced dap gene dose.

Conclusions:

  • A conserved functional relationship exists between dSkp2 and Dap in controlling cell cycle progression.
  • Drosophila serves as a valuable model system for studying Skp2-mediated tumorigenesis.
  • Understanding dSkp2-Dap interaction sheds light on fundamental cell cycle regulatory mechanisms.

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