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Related Experiment Videos

Patched1 interacts with cyclin B1 to regulate cell cycle progression.

E A Barnes1, M Kong, V Ollendorff

  • 1Department of Chemistry and Biochemistry, Center for Molecular Genetics, University of California-San Diego, La Jolla, CA 92093-0367, USA.

The EMBO Journal
|May 2, 2001
PubMed
Summary

The tumor suppressor patched1 (ptc1) interacts with cyclin B1, regulating its cell localization and impacting cell division. Sonic hedgehog signaling disrupts this interaction, allowing cell cycle progression.

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • Mitosis initiation depends on M-phase promoting factor (MPF) activation.
  • MPF regulation involves cdc2 and cyclin B1 phosphorylation and localization.
  • Patched1 (ptc1) is a tumor suppressor implicated in basal cell carcinoma (BCC).

Purpose of the Study:

  • To identify novel interactions with phosphorylated cyclin B1.
  • To investigate the role of ptc1 in cell division regulation.
  • To explore the link between ptc1 tumor suppressor activity and cell cycle control.

Main Methods:

  • Yeast two-hybrid screening with a phosphorylated cyclin B1 bait.
  • Co-immunoprecipitation and subcellular localization studies in 293T cells.

Related Experiment Videos

  • Analysis of cell proliferation upon ptc1 and cyclin B1 derivative expression.
  • Main Results:

    • Identified a novel interaction between cyclin B1 and ptc1.
    • Ptc1 specifically binds phosphorylated cyclin B1, altering its localization.
    • Sonic hedgehog (shh) disrupts the ptc1-cyclin B1 interaction, promoting nuclear cyclin B1 localization.
    • Ptc1 inhibits cell proliferation, an effect reversed by a non-interacting cyclin B1 mutant.
    • Endogenous ptc1 and cyclin B1 interact in vivo.

    Conclusions:

    • Ptc1 regulates the subcellular localization of cyclin B1.
    • Ptc1's tumor suppressor function is linked to cell division regulation.
    • Ptc1 likely acts in a G(2)/M checkpoint by controlling MPF localization.