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Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
12:02

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols

Published on: June 6, 2017

Two distinct controls of mitotic cdk1/cyclin B1 activity requisite for cell growth prior to cell division

Toru Miyazaki1, Satoko Arai

  • 1Division of Molecular Biomedicine for Pathogenesis, Center for Disease Biology and Integrative Medicine, Faculty of Medicine, The University of Tokyo, Tokyo, Japan. tm@m.u-tokyo.ac.jp

Cell Cycle (Georgetown, Tex.)
|June 27, 2007
PubMed

Insights

Death-effector domain-containing protein D (DEDD) inhibits cyclin-dependent kinase 1 (Cdk1)/cyclin B1, controlling cell growth. DEDD deficiency accelerates mitosis and reduces cell size, impacting organismal development.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Cell division is regulated by cyclin-dependent kinase 1 (Cdk1)/cyclin B1 complexes.
  • Proper cell growth prior to division is crucial for organismal development.

Purpose of the Study:

  • To investigate the role of death-effector domain-containing protein D (DEDD) in regulating cell division and cell size.
  • To elucidate the mechanism by which DEDD interacts with Cdk1/cyclin B1.

Main Methods:

  • Analysis of DEDD protein levels during the cell cycle.
  • Investigation of DEDD interaction with Cdk1/cyclin B1 in the nucleus.
  • Assessment of Cdk1/cyclin B1 kinase activity in DEDD-null and wild-type cells.
  • Evaluation of mitotic progression, cell size, and body/organ weights in DEDD-null mice.

Main Results:

  • DEDD protein levels peak during the G2/M phase, similar to cyclin B1.
  • DEDD directly binds to cyclin B1, inhibiting nuclear Cdk1/cyclin B1 kinase activity.
  • DEDD-null cells exhibit accelerated mitotic progression, reduced rRNA, and diminished cell volume.
  • DEDD-null mice display decreased body and organ weights.

Conclusions:

  • DEDD acts as a novel nuclear inhibitor of mitotic Cdk1/cyclin B1, regulating cell growth and size.
  • The DED domain is essential for DEDD's cell sizing function but not for Cdk1/cyclin B1 binding.
  • DEDD represents a new mechanism for impeditive regulation of Cdk1/cyclin B1, ensuring adequate cell growth before division.

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