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Vol. 273, Issue 1, 194-199, January 2, 1998
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From the Histone genes display a peak in transcription in
early S phase and are ideal models for cell cycle-regulated gene
expression. We have previously shown that the transcription factor
interferon regulatory factor 2 (IRF-2) can activate histone H4 gene
expression. In this report we establish that a mouse histone H4 gene
and its human homolog lose stringent cell cycle control in synchronized embryonic fibroblasts in which IRF-2 has been ablated. We also show
that there are reduced mRNA levels of this endogenous mouse histone
H4 gene in the IRF-2 Department of Cell Biology and Cancer
Center, University of Massachusetts Medical Center, Worcester,
Massachusetts 01655, the § Division of Molecular Oncology,
Departments of Medicine and Pathology, Washington University School of
Medicine, St. Louis, Missouri 63110, and the ¶ Department of
Immunology, Faculty of Medicine, University of Tokyo, Hongo 7-3-1, Bunkyo-ku 113, Tokyo
/ cells. Strikingly, the
overall mRNA level and cell cycle regulation of histone H4
transcription are restored when IRF-2 is reintroduced to these cells.
IRF-2 is a negative regulator of the interferon response and has
oncogenic potential, but little is known of the mechanism of these
activities. Our results suggest that IRF-2 is an active player in
E2F-independent cell cycle-regulated gene expression at the
G1/S phase transition. IRF-2 was previously considered a
passive antagonist to the tumor suppressor IRF-1 but can now join other
oncogenic factors such as c-Myb and E2F1 that are predicted to mediate
their transforming capabilities by actively regulating genes necessary
for cell cycle progression.
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