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J. Biol. Chem., Vol. 276, Issue 19, 15720-15727, May 11, 2001
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From the Department of Biochemistry and Molecular Biology, Colorado
State University, Fort Collins, Colorado 80523-1870
The Tax protein, encoded by the human T-cell
leukemia virus type I (HTLV-I), is required for high level viral
transcription and HTLV-I-associated malignant transformation. Although
the precise mechanism of malignant transformation by Tax is unclear, it
is well established that Tax represses the transcription function of
the tumor suppressor p53, possibly accelerating the accumulation of
genetic mutations that are critical in HTLV-I-mediated malignant transformation. Tax repression of p53 transcription function appears to
occur, at least in part, through competition for the cellular coactivator CBP/p300. In this study, we characterize the effect of Tax
on the p53 family member, p73. We demonstrate that Tax also represses
the transcription function of p73
Human T-cell Leukemia Virus Type I Tax Repression of p73
Is
Mediated through Competition for the C/H1 Domain of CBP*
and
and that the repression is
reciprocal in vivo, consistent with the idea that both
transcription factors may compete for CBP/p300 in vivo. We provide evidence showing that both Tax and p73 interact strongly with
the C/H1 domain of CBP and that their binding to this region is
mutually exclusive in vitro. This finding provides evidence supporting the idea that reciprocal transcriptional repression between
Tax and p73 is mediated through coactivator competition.
*
The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed. Tel.: 970-491-5017;
E-mail: il@lamar.colostate.edu.
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