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Ectopic expression of the Drosophila Cdk1 inhibitory kinases, Wee1 and Myt1, interferes with the second mitotic wave

Donald M Price1, Zhigang Jin, Simon Rabinovitch

  • 1Department of Biological Sciences, University of Alberta, Edmonton, Alberta T6G 2E9, Canada.

Genetics
|June 20, 2002
PubMed

Insights

Drosophila Wee1 and Myt1 kinases regulate cell cycle progression. Genetic studies reveal Myt1 interacts with Notch signaling, while both kinases may inhibit apoptosis, offering new targets for developmental research.

Area of Science:

  • Cell Biology
  • Developmental Biology
  • Genetics

Background:

  • Wee1 kinases regulate the cell cycle by phosphorylating Cdk1, controlling entry into mitosis.
  • Metazoans possess two Wee1-like kinases: nuclear Wee1 and cytoplasmic Myt1.
  • Understanding their distinct roles in development is crucial.

Purpose of the Study:

  • To investigate the functions of Drosophila Wee1 (Dwee1) and Myt1 (Dmyt1) during normal development.
  • To establish transgenic models for identifying novel regulators of Wee1 and Myt1 through genetic screens.

Main Methods:

  • Gene isolation and characterization of Drosophila Wee1 and Myt1.
  • Generation of transgenic Drosophila lines overexpressing Dwee1 and Dmyt1.
  • Analysis of eye development phenotypes and genetic modifier screens using deletion collections.

Main Results:

  • Overexpression of Dwee1 or Dmyt1 in Drosophila eyes caused developmental defects.
  • Mutations in the Delta/Notch signaling pathway enhanced the Dmyt1 overexpression phenotype, suggesting Myt1 is a downstream target.
  • Interactions with p53 indicated that Wee1 and Myt1 activity can inhibit apoptosis.

Conclusions:

  • Dmyt1 plays a role in Notch-mediated eye development.
  • Wee1 and Myt1 are involved in regulating apoptosis during development.
  • These findings provide a foundation for identifying novel cell cycle regulators.

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