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Loss of Cdc20 causes a securin-dependent metaphase arrest in two-cell mouse embryos

Min Li1, J Philippe York, Pumin Zhang

  • 1Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, TX 77030, USA.

Molecular and Cellular Biology
|February 28, 2007
PubMed

Insights

The anaphase-promoting complex/cyclosome (APC/C) adapter Cdc20 is essential for mitosis, as Cdc20-deficient mice embryos arrest at the two-cell stage. This highlights Cdc20

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Genetics

Background:

  • The anaphase-promoting complex/cyclosome (APC/C) is a crucial E3 ubiquitin ligase regulating mitosis through targeted protein degradation.
  • APC/C activity is controlled by adapter proteins Cdc20 and Cdh1, which bind substrates via WD-40 repeat domains.
  • The specific roles and potential redundancy between APC/C-Cdc20 and APC/C-Cdh1 in mitosis remain unclear.

Purpose of the Study:

  • To investigate the essentiality of Cdc20 in mitosis and determine if its function is redundant with Cdh1.
  • To elucidate the role of Cdc20 in embryonic development and cell cycle progression.
  • To explore the contribution of securin in preventing mitotic exit.

Main Methods:

  • Gene-trapping approach in mice to generate Cdc20-deficient models.
  • Embryonic development analysis of wild-type, Cdc20-deficient, and Cdc20-securin double mutant embryos.
  • Assessment of cell cycle progression, protein levels (e.g., cyclin B1), and mitotic arrest phenotypes.

Main Results:

  • Cdc20-deficient mouse embryos exhibit failed embryogenesis, arresting at the metaphase stage in the two-cell stage.
  • High levels of cyclin B1 were observed in arrested embryos, indicating a failure in mitotic progression.
  • Cdc20 and securin double mutant embryos failed to maintain metaphase arrest, suggesting securin's role in preventing mitotic exit.

Conclusions:

  • Cdc20 plays an essential, non-redundant role in mitosis, critical for embryonic development.
  • The findings establish Cdc20 as indispensable for timely anaphase onset and mitotic exit.
  • Securin appears to play a role in maintaining metaphase arrest, potentially by inhibiting mitotic exit pathways.

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