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(Received for publication, January 29, 1996, and in revised form, June 14, 1996)
From the Division of Hemopoiesis, Institute of Hematology, and the
Department of Hematology, Jichi Medical School, Tochigi 329-04, Japan,
§ Katsuta Research Laboratory, Hitachi Koki Co., Ltd.,
Ibaraki 312, Japan, and ¶ Tsukuba Research Institute, Banyu
Pharmaceutical Co. Ltd., Ibaraki 300-33, Japan
Apoptosis has recently been hypothesized to be
the result of aberrant cell cycle control. In this study, we have
investigated the role of cell cycle-regulatory elements in Fas-induced
apoptosis of hematopoietic cells. When HL-60 cells were treated with
anti-Fas antibody, rapid activation of growth-associated histone H1
kinase was observed without any change in cell cycle distribution. This
was accompanied by the increase in cdc2 mRNA expression
and Cdc2 kinase activity. Up-regulation of cdc2 mRNA
was similarly induced in BCL-2-overexpressing HL-60 subline by anti-Fas
treatment independently of the appearance of apoptotic phenotypes.
Fas-induced apoptosis was completely inhibited by butyrolactone I, a
specific inhibitor of Cdc2 kinase. Moreover, the same phenomenon was
observed during Fas-induced but not spontaneous apoptosis of
postmitotic granulocytes. Finally, we have found that ``Fas-responsive
element'' was located between nucleotides
Volume 271, Number 45,
Issue of November 8, 1996
pp. 28469-28477
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.
730 and 552 of the
cdc2 promoter and was responsive for transcriptional
activation of the cdc2 gene during Fas-induced apoptosis.
These results indicate that aberrant activation of Cdc2 is associated
with Fas-induced apoptosis of hematopoietic cells, and that the
mechanism of cdc2 transcription during Fas-induced
apoptosis is different from that in normal cell cycle control.
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