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Molecular and Cellular Biology, May 1999, p. 3485-3495, Vol. 19, No. 5
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Transcriptional Cross Talk between NF-kappa B and p53

Gill A. Webster and Neil D. Perkins*

Department of Biochemistry, Division of Gene Regulation and Expression, University of Dundee, Dundee DD1 5EH, Scotland, United Kingdom

Received 29 July 1998/Returned for modification 28 October 1998/Accepted 12 February 1999

Many cellular stimuli result in the induction of both the tumor suppressor p53 and NF-kappa B. In contrast to activation of p53, which is associated with the induction of apoptosis, stimulation of NF-kappa B has been shown to promote resistance to programmed cell death. These observations suggest that a regulatory mechanism must exist to integrate these opposing outcomes and coordinate this critical cellular decision-making event. Here we show that both p53 and NF-kappa B inhibit each other's ability to stimulate gene expression and that this process is controlled by the relative levels of each transcription factor. Expression of either wild-type p53 or the RelA(p65) NF-kappa B subunit suppresses stimulation of transcription by the other factor from a reporter plasmid in vivo. Moreover, endogenous, tumor necrosis factor alpha-activated NF-kappa B will inhibit endogenous wild-type p53 transactivation. Following exposure to UV light, however, the converse is observed, with p53 downregulating NF-kappa B-mediated transcriptional activation. Both p53 and RelA(p65) interact with the transcriptional coactivator proteins p300 and CREB-binding protein (CBP), and we demonstrate that these results are consistent with competition for a limiting pool of p300/CBP complexes in vivo. These observations have many implications for regulation of the transcriptional decision-making mechanisms that govern cellular processes such as apoptosis. Furthermore, they suggest a previously unrealized mechanism through which dysregulated NF-kappa B can contribute to tumorigenesis and disease.

* Corresponding author. Mailing address: Department of Biochemistry, Division of Gene Regulation and Expression, MSI/WTB Complex, Dow St., University of Dundee, Dundee DD1 5EH, Scotland, United Kingdom. Phone: 44 1382 345 606. Fax: 44 1382 348 072. E-mail: nperkins{at}bad.dundee.ac.uk.

Molecular and Cellular Biology, May 1999, p. 3485-3495, Vol. 19, No. 5
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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