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Molecular and Cellular Biology, July 2000, p. 5000-5009, Vol. 20, No. 14
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Transcriptional Regulation of the TATA-Binding Protein by Ras Cellular Signaling

Sandra A. S. Johnson, Nihar Mandavia, Horng-Dar Wang,dagger and Deborah L. Johnson*

Departments of Molecular Pharmacology and Biochemistry, Norris Comprehensive Cancer Center, University of Southern California School of Pharmacy and Keck School of Medicine, Los Angeles, California 90089-9121

Received 1 December 1999/Returned for modification 6 January 2000/Accepted 19 April 2000

Our previous studies have demonstrated that the level of the central transcription factor TATA-binding protein (TBP) is increased in cells expressing the hepatitis B virus (HBV) X protein through the activation of the Ras signaling pathway, which serves to enhance both RNA polymerase I and III promoter activities. To understand the mechanism by which TBP is regulated, we have investigated whether enhanced expression is modulated at the transcriptional level. Nuclear run-on assays revealed that the HBV X protein increases the number of active transcription complexes on the TBP gene. In transient-transfection assays with both transformed and primary hepatocytes, the human TBP promoter was shown to be induced by expression of the HBV X protein in a Ras-dependent manner, requiring both Ral guanine nucleotide dissociation stimulator (RalGDS) and Raf signaling. Transient overexpression of TBP did not affect TBP promoter activity. To further delineate the downstream Ras-mediated events contributing to TBP promoter regulation in primary rat hepatocytes, the best-characterized Ras effectors, Raf, phosphoinositide 3-kinase (PI-3 kinase), and RalGDS, were examined. Activation of either Raf or RalGDS, but not that of PI-3 kinase, was sufficient to induce TBP promoter activity. Both Raf- and RalGDS-mediated induction required the activation of mitogen-activated protein kinase kinase (MEK). In addition, another distinct Ras-activated pathway, which does not require MEK activation, appears to induce TBP promoter activity. Analysis of the DNA sequence requirement within the TBP promoter responsible for these regulatory events defined three distinct regions that modulate the abilities of Raf, RalGDS, and the Ras-dependent, MEK-independent pathways to regulate human TBP promoter activity. Together, these results provide new evidence that TBP can be regulated at the transcriptional level and identify three distinct Ras-activated pathways that modulate this central eukaryotic transcription factor.

* Corresponding author. Mailing address: Department of Molecular Pharmacology and Toxicology, University of Southern California School of Pharmacy, 1985 Zonal Ave., PSC-402, Los Angeles, CA 90089-9121. Phone: (323) 442-1446. Fax: (323) 442-1681. E-mail: johnsond{at}hsc.usc.edu.

dagger Present address: Department of Biology, California Institute of Technology, Pasadena, Calif.

Molecular and Cellular Biology, July 2000, p. 5000-5009, Vol. 20, No. 14
0270-7306/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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