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Related Experiment Videos

The Bfa1/Bub2 GAP complex comprises a universal checkpoint required to prevent mitotic exit.

Y Wang1, F Hu, S J Elledge

  • 1Verna and Mars McLean Department of Biochemistry and Molecular Biology, Howard Hughes Medical Institute, Baylor College of Medicine, Houston, Texas 77030, USA.

Current Biology : CB
|November 21, 2000
PubMed
Summary
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The Bfa1/Bub2 complex prevents cyclin-dependent kinase (CDK) inactivation, ensuring cell cycle arrest at G2/M. This mechanism is crucial for maintaining arrest during DNA damage and spindle misorientation in budding yeast.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Genetics

Background:

  • Cyclin-dependent kinase (CDK) activity must be inactivated for mitotic exit at the end of the cell cycle.
  • Cdc14 phosphatase activates Cdh1 for cyclin B degradation and induces Sic1 to inactivate Cdk1, facilitating mitotic exit.
  • The spindle checkpoint pathway uses Bfa1/Bub2 GTPase-activating protein to keep Tem1 inactive, preventing cyclin B degradation and thus CDK inactivation during G2/M arrest.

Purpose of the Study:

  • To investigate the role of BUB2 and BFA1 in maintaining G2/M arrest in budding yeast.
  • To determine if Bfa1/Bub2 functions as a universal G2/M checkpoint pathway.

Main Methods:

  • Analysis of double mutants (cdc13-1 bub2, cdc13-1 bfa1, cdc13-1 mad2) at restrictive temperatures.
  • Observation of cell re-budding and DNA reduplication.

Related Experiment Videos

  • Assessment of mitotic exit delay in mutants with misoriented spindles.

    • Main Results:

    • BUB2 and BFA1 are required for maintaining G2/M arrest in response to DNA damage and spindle misorientation.
    • cdc13-1 bub2 and cdc13-1 bfa1 mutants, unlike cdc13-1 mad2 mutants, exhibit re-budding and DNA reduplication at the restrictive temperature.
    • The delay in mitotic exit associated with spindle misorientation depends on BUB2 and BFA1, but not MAD2.

    Conclusions:

    • The Bfa1/Bub2 pathway is essential for maintaining G2/M arrest under various stress conditions, including DNA damage and spindle misorientation.
    • Bfa1/Bub2 acts as a universal checkpoint in G2/M, preventing CDK inactivation when the cell cycle is delayed.
    • This pathway ensures proper cell cycle progression by preventing premature mitotic exit.