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Blood, Vol. 95 No. 8 (April 15), 2000:
pp. 2645-2650
Abundance of cyclin B1 regulates  -radiation-induced apoptosis
Lisa A. Porter,
Gurmit Singh, and
Jonathan M. Lee
From the Hamilton Regional Cancer Center, Hamilton, Ontario, Canada;
and Medical Sciences Graduate Programme, Faculty of Health Sciences,
and Department of Pathology and Molecular Medicine, McMaster
University, Hamilton, Ontario, Canada.
 -Radiation is a potent inducer of apoptosis. There are multiple
pathways regulating DNA damage-induced apoptosis, and we set out to
identify novel mechanisms regulating -radiation-induced apoptosis in hematopoietic cells. In this report, we present
data implicating the cyclin B1 protein as a regulator of apoptotic fate
following DNA damage. Cyclin B1 is the regulatory subunit of the cdc2
serine/threonine kinase, and accumulation of cyclin B1 in late G2 phase
of the cell cycle is a prerequisite for mitotic initiation in mammalian
cells. We find that abundance of the cyclin B1 protein rapidly
increases in several mouse and human hematopoietic cells (Ramos, DP16,
HL60, thymocytes) undergoing -radiation-induced apoptosis. Cyclin
B1 accumulation occurs in all phases of the cell cycle. Antisense
inhibition of cyclin B1 accumulation decreases apoptosis, and ectopic
cyclin B1 expression is sufficient to induce apoptosis. These
observations are consistent with the idea that cyclin B1 is both
necessary and sufficient for -radiation-induced apoptosis.
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