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Cdc20 hypomorphic mice fail to counteract de novo synthesis of cyclin B1 in mitosis

Liviu Malureanu1, Karthik B Jeganathan, Fang Jin

  • 1Department of Pediatric and Adolescent Medicine, Mayo Clinic College of Medicine, Rochester, MN 55905, USA.

The Journal of Cell Biology
|October 20, 2010
PubMed

Insights

Cdc20 (anaphase-promoting complex activator) is essential for cell division, but its absence in mice doesn't cause cancer. New cyclin B1 synthesis delays cell cycle progression in Cdc20-deficient cells.

Area of Science:

  • Cell Biology
  • Genetics
  • Molecular Biology

Background:

  • Cdc20 is a key regulator of the anaphase-promoting complex/cyclosome (APC/C).
  • APC/C activation by Cdc20 triggers anaphase onset through cyclin B1 and securin degradation.
  • Understanding Cdc20's role is crucial for comprehending cell cycle control and potential disease implications.

Purpose of the Study:

  • To investigate the physiological importance of Cdc20 in higher eukaryotes.
  • To determine the consequences of reduced Cdc20 levels on organismal health and cancer predisposition.
  • To elucidate the mechanisms underlying cell cycle delays in Cdc20-deficient cells.

Main Methods:

  • Generation of hypomorphic mice with reduced Cdc20 expression.
  • Analysis of aneuploidy, chromatin bridging, and chromosome-microtubule attachment in these mice.
  • Investigation of cyclin B1 synthesis and degradation dynamics during mitosis using techniques like translation inhibition.

Main Results:

  • Hypomorphic mice exhibited significant aneuploidy but remained healthy and cancer-free.
  • Cdc20 deficiency led to chromatin bridging and chromosome misalignment, indicating a role in sister chromatid separation and attachment.
  • De novo synthesis of cyclin B1 during mitosis in Cdc20-hypomorphic cells caused its accumulation and significantly delayed anaphase onset.

Conclusions:

  • Cdc20 is essential for accurate chromosome segregation and timely anaphase onset.
  • Regulated de novo synthesis of cyclin B1 during mitosis is a critical factor that makes Cdc20 rate-limiting for its degradation.
  • Despite causing aneuploidy, Cdc20 deficiency does not inherently lead to cancer in mice, suggesting complex regulatory networks.

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