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The CHFR mitotic checkpoint protein delays cell cycle progression by excluding Cyclin B1 from the nucleus

Matthew K Summers1, John Bothos, Thanos D Halazonetis

  • 1Molecular and Cellular Oncogenesis Program, The Wistar Institute, Philadelphia, PA 19104-4268, USA.

Oncogene
|January 28, 2005
PubMed

Insights

The CHFR gene delays chromosome condensation in cancer cells treated with microtubule poisons. This delay occurs by preventing Cyclin B1 accumulation in the nucleus, a key step in cell division.

Area of Science:

  • Cell Biology
  • Molecular Oncology
  • Genetics

Background:

  • The CHFR gene is a novel checkpoint gene.
  • CHFR is frequently inactivated in human cancers.
  • Microtubule poisons disrupt cell division by interfering with microtubule function.

Purpose of the Study:

  • To elucidate the molecular mechanism by which CHFR delays chromosome condensation.
  • To investigate the role of CHFR in cell cycle regulation following exposure to microtubule poisons.

Main Methods:

  • Characterization of cells with inactivated CHFR and stably transfected derivatives expressing wild-type CHFR.
  • Analysis of cell cycle progression and chromosome condensation markers.
  • Assessment of Cyclin A/Cdc2, Aurora-A, Aurora-B, and Cyclin B1/Cdc2 activity.
  • Investigation of Cyclin B1 localization using nuclear export sequence mutants.

Main Results:

  • CHFR-expressing cells exhibited a transient arrest in early prophase with no chromosome condensation after microtubule poison treatment.
  • Cyclin A/Cdc2 was activated, while Aurora-A, Aurora-B, and Cyclin B1/Cdc2 remained inactive.
  • Cyclin B1 was excluded from the nucleus in CHFR-expressing cells.
  • Ectopic expression of nuclear-localized Cyclin B1 overcame the CHFR-mediated checkpoint and induced chromosome condensation.

Conclusions:

  • The CHFR checkpoint delays chromosome condensation by inhibiting the nuclear accumulation of Cyclin B1.
  • Understanding CHFR's mechanism provides insights into cancer cell cycle regulation and potential therapeutic targets.

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