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J. Cell Biol.,
Volume 142, Number 4, August 24, 1998 1013-1022
* Division of Molecular Medicine, Wadsworth Center, New York State Department of Health, Albany, New York 12201-0509;
and When vertebrate somatic cells are selectively
irradiated in the nucleus during late prophase (<30 min
before nuclear envelope breakdown) they progress normally through mitosis even if they contain broken chromosomes. However, if early prophase nuclei are similarly irradiated, chromosome condensation is reversed and the cells return to interphase. Thus, the G2 checkpoint that prevents entry into mitosis in response to nuclear damage ceases to function in late prophase. If one
nucleus in a cell containing two early prophase nuclei is
selectively irradiated, both return to interphase, and
prophase cells that have been induced to returned to interphase retain a normal cytoplasmic microtubule complex. Thus, damage to an early prophase nucleus is converted into a signal that not only reverses the nuclear
events of prophase, but this signal also enters the cytoplasm where it inhibits e.g., centrosome maturation and
the formation of asters. Immunofluorescent analyses reveal that the irradiation-induced reversion of prophase is correlated with the dephosphorylation of histone H1,
histone H3, and the MPM2 epitopes. Together, these
data reveal that a checkpoint control exists in early but
not late prophase in vertebrate cells that, when triggered, reverses the cell cycle by apparently downregulating existing cyclin-dependent kinase (CDK1) activity.
Department of Biomedical Sciences, State University of New York, Albany, New York 12222
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