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Rough deal and Zw10 are required for the metaphase checkpoint in Drosophila

R Basto1, R Gomes, R E Karess

  • 1CNRS, Centre de Génétique Moléculaire, Avenue de la Terrasse, 91198 Gif-sur-Yvette, France.

Nature Cell Biology
|January 9, 2001
PubMed

Insights

The metaphase checkpoint ensures accurate chromosome segregation during cell division. Drosophila Rough deal (Rod) and Zeste-White 10 (Zw10) proteins are vital for this checkpoint, preventing errors like aneuploidy.

Area of Science:

  • Cell Biology
  • Genetics
  • Molecular Biology

Background:

  • Mitotic progression requires precise regulation of the metaphase-anaphase transition.
  • The spindle-assembly checkpoint (SAC) prevents premature anaphase by monitoring kinetochore-microtubule attachments.
  • SAC dysfunction leads to aneuploidy, a hallmark of many diseases.

Purpose of the Study:

  • To identify novel components of the SAC in Drosophila.
  • To investigate the roles of Rough deal (Rod) and Zeste-White 10 (Zw10) in SAC function.

Main Methods:

  • Utilized Drosophila melanogaster as a model organism.
  • Investigated the phenotypes of Drosophila cells lacking ROD or Zw10.
  • Observed cellular responses to spindle damage, including metaphase arrest and cyclin B degradation.

Main Results:

  • Drosophila Rough deal (Rod) and Zeste-White 10 (Zw10) are essential for SAC function.
  • Loss of ROD or Zw10 results in failure to arrest in metaphase upon spindle damage.
  • Cells lacking ROD or Zw10 prematurely degrade cyclin B and exit mitosis, similar to bub1 mutants.

Conclusions:

  • Rod and Zw10 are critical kinetochore components required for SAC-mediated metaphase arrest.
  • These findings identify novel SAC proteins in Drosophila with no apparent budding yeast homologs.
  • Defects in Rod and Zw10 function contribute to aneuploidy due to SAC failure.

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