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Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
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Suppression of cell-cycle progression by Jun dimerization protein-2 (JDP2) involves downregulation of cyclin-A2

J Pan1, K Nakade, Y-C Huang

  • 1RIKEN BioResource Center, Ibaraki, Japan.

Oncogene
|August 31, 2010
PubMed

Insights

Jun dimerization protein-2 (JDP2) regulates cell cycle progression. Loss of JDP2 accelerates skin cell proliferation and increases cyclin-A2 gene expression, indicating JDP2 suppresses cell growth.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • Jun dimerization protein-2 (JDP2) is a transcription factor.
  • The role of JDP2 in regulating normal cell cycle progression is not well understood.

Purpose of the Study:

  • To investigate the function of JDP2 in regulating cell cycle progression.
  • To elucidate the molecular mechanisms by which JDP2 controls cell proliferation.

Main Methods:

  • Generation of Jdp2-knockout (Jdp2KO) mice.
  • Analysis of skin and fibroblast proliferation in Jdp2KO and wild-type mice.
  • Quantitative analysis of cyclin-A2 (ccna2) gene expression.
  • ChIP assays to determine JDP2 binding to the ccna2 promoter.

Main Results:

  • Jdp2KO mice exhibited accelerated epidermal thickening and increased cell proliferation after TPA treatment.
  • Fibroblasts from Jdp2KO mice showed enhanced proliferation and colony formation compared to wild-type.
  • JDP2 was recruited to the AP-1 site on the ccna2 promoter.
  • Cells lacking Jdp2 displayed elevated ccna2 mRNA levels.
  • Reintroduction of JDP2 repressed ccna2 transcription and cell-cycle progression.

Conclusions:

  • JDP2 acts as a negative regulator of normal cell cycle progression.
  • The ccna2 gene is a direct transcriptional target of JDP2.
  • JDP2 suppresses cell proliferation by repressing ccna2 transcription.

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