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Molecular and Cellular Biology, March 2007, p. 1844-1858, Vol. 27, No. 5
0270-7306/07/$08.00+0     doi:10.1128/MCB.01363-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

The New Core Promoter Element XCPE1 (X Core Promoter Element 1) Directs Activator-, Mediator-, and TATA-Binding Protein-Dependent but TFIID-Independent RNA Polymerase II Transcription from TATA-Less Promoters{triangledown} ,{dagger}

Yumiko Tokusumi, Ying Ma, Xianzhou Song, Raymond H. Jacobson, and Shinako Takada*

Department of Biochemistry and Molecular Biology, Gene and Development Program of the Graduate School of Biomedical Science, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Blvd., Houston, Texas 77030

Received 25 July 2006/ Returned for modification 3 September 2006/ Accepted 19 December 2006

The core promoter is a critical DNA element required for accurate transcription and regulation of transcription. Several core promoter elements have been previously identified in eukaryotes, but those cannot account for transcription from most RNA polymerase II-transcribed genes. Additional, as-yet-unidentified core promoter elements must be present in eukaryotic genomes. From extensive analyses of the hepatitis B virus X gene promoter, here we identify a new core promoter element, XCPE1 (the X gene core promoter element 1), that drives RNA polymerase II transcription. XCPE1 is located between nucleotides –8 and +2 relative to the transcriptional start site (+1) and has a consensus sequence of G/A/T-G/C-G-T/C-G-G-G/A-A-G/C+1-A/C. XCPE1 shows fairly weak transcriptional activity alone but exerts significant, specific promoter activity when accompanied by activator-binding sites. XCPE1 is also found in the core promoter regions of about 1% of human genes, particularly in poorly characterized TATA-less genes. Our in vitro transcription studies suggest that the XCPE1-driven transcription can be highly active in the absence of TFIID because it can utilize either free TBP or the complete TFIID complex. Our findings suggest the possibility of the existence of a TAF1 (TFIID)-independent transcriptional initiation mechanism that may be used by a category of TATA-less promoters in higher eukaryotes.

* Corresponding author. Mailing address: Department of Biochemistry and Molecular Biology, The University of Texas M. D. Anderson Cancer Center, Unit 1000, 1515 Holcombe Blvd., Houston, TX 77030. Phone: (713) 834-6275. Fax: (713) 834-6266. E-mail: stakada{at}mdanderson.org.

{triangledown} Published ahead of print on 8 January 2007.

{dagger} Supplemental material for this article may be found at http://mcb.asm.org/.

Molecular and Cellular Biology, March 2007, p. 1844-1858, Vol. 27, No. 5
0270-7306/07/$08.00+0     doi:10.1128/MCB.01363-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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