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Vol. 10, Issue 11, 3607-3622, November 1999
and
*Department of Molecular Biology, Lerner Research Institute, The
Cleveland Clinic Foundation, Cleveland, Ohio 44195;
Overexpression of p53 causes G2 arrest, attributable in part
to the loss of CDC2 activity. Transcription of cdc2 and
cyclin B1, determined using reporter constructs driven
by the two promoters, was suppressed in response to the induction of
p53. Suppression requires the regions Department of Molecular Microbiology and Immunology and
Kenneth Norris, Jr., Comprehensive Cancer Center, Los Angeles,
California 90033-1034; and Department of Biology,
University of North Carolina at Greensboro, Greensboro, North Carolina
27402-6174
287 to 123 of the
cyclin B1 promoter and 104 to 74 of the
cdc2 promoter. p53 did not affect the inhibitory phosphorylations of CDC2 at threonine 14 or tyrosine 15 or the activity
of the cyclin-dependent kinase that activates CDC2 by phosphorylating it at threonine 161. Overexpression of p53 may also
interfere with the accumulation of CDC2/cyclin B1 in the nucleus,
required for cells to enter mitosis. Constitutive expression of cyclin
B1, alone or in combination with the constitutively active CDC2 protein
T14A Y15F, did not reverse p53-dependent G2 arrest. However, targeting
cyclin B1 to the nucleus in cells also expressing CDC2 T14A Y15F did
overcome this arrest. It is likely that several distinct pathways
contribute to p53-dependent G2 arrest.
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