Journal
ONCOGENE
Volume 24, Issue 16, Pages 2589-2598Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.onc.1208428
Keywords
CHFR; cyclin B1; checkpoint; prophase; mitosis
Funding
- NCI NIH HHS [CA89630, CA09677, CA09171] Funding Source: Medline
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CHFR, a novel checkpoint gene inactivated in human cancer, delays chromosome condensation in cells treated with microtubule poisons. To understand the molecular mechanism for this delay, we characterized cells with inactivated CHFR and stably transfected derivatives expressing the wild-type gene. After exposure to microtubule poisons, the CHFR-expressing cells arrested transiently in early prophase with a characteristic ruffled morphology of the nuclear envelope and no signs of chromosome condensation. Several markers suggested that Cyclin A/Cdc2 had been activated, whereas Aur-ora-A and -B and Cyclin B1/Cdc2 were inactive. Further, Cyclin B1 was excluded from the nucleus. Ectopic expression of Cyclin B1 with a mutant nuclear export sequence induced chromosome condensation, and thus overcame the CHFR checkpoint. We conclude that the mechanism by which CHFR delays chromosome condensation involves inhibition of accumulation of Cyclin B1 in the nucleus.
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