Exit from mitosis is regulated by Drosophila fizzy and the sequential destruction of cyclins A, B and B3

S Sigrist1, H Jacobs, R Stratmann

  • 1Friedrich-Miescher-Laboratorium der Max-Planck-Gesellschaft, Tübingen, Germany.

The EMBO Journal
|October 2, 1995
PubMed

Insights

The fizzy (fzy) gene is crucial for cell cycle progression, controlling the degradation of cyclins A, B, and B3 during mitosis. Mutations in fzy disrupt this process, leading to defects in chromosome segregation and the metaphase/anaphase transition.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Genetics

Background:

  • Mitotic exit relies on cdc2 kinase inactivation, achieved through cyclin degradation.
  • Cyclins A, B, and B3 associate with cdc2 kinase and are sequentially degraded during mitosis in higher eukaryotes.

Purpose of the Study:

  • To investigate the role of the Drosophila fizzy (fzy) gene in regulating cyclin degradation and mitotic progression.
  • To determine the specific functions of cyclins A, B, and B3 in ordered mitotic progression.

Main Methods:

  • Analysis of mutations in the Drosophila fizzy (fzy) gene.
  • Expression of mutant cyclins (delta cyclins) lacking the destruction box motif.
  • Observation of mitotic progression, sister chromosome separation, and chromosome segregation.

Main Results:

  • Mutations in fzy block the mitotic degradation of cyclins A, B, and B3.
  • Expression of delta cyclins causes distinct mitotic delays or arrests at metaphase and anaphase.
  • fzy mutations impair both sister chromosome separation and segregation, highlighting its role in the metaphase/anaphase transition.

Conclusions:

  • The sequential degradation of cyclins A, B, and B3 orders mitotic progression beyond metaphase.
  • The fizzy (fzy) gene is essential for regulating cyclin degradation and ensuring proper chromosome segregation during the metaphase/anaphase transition.

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