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Overlapping YY1- and aberrant SP1-binding sites proximal to the early promoter of human papillomavirus type 16

Institute of Virology, Universität zu Köln, Fürst-Pückler Str. 56, 50935 Köln, Germany¹

Author for correspondence: Herbert Pfister.Fax +49 221 4783902. e-mail Herbert.Pfister{at}medizin.uni-koeln.de

Transcription of oncogenes E6 and E7 of human papillomavirus type 16 (HPV-16) from the P97 promoter is regulated by viral and cellular proteins. The transcription factor YY1 represses transcription through binding to cognate sequences in the long control region (LCR). In HPV-16 DNA from cervical carcinomas, mutations of YY1-binding sites have been identified that increase P97 activity 3–6-fold. A second, SP1-binding site has now been identified in the HPV-16 LCR (nt 7842–7847), which overlaps the YY1-binding site at positions 7840–7848. A point mutation within this YY1 site in viral DNA from a cervical cancer, previously shown to prevent YY1 binding, was shown to increase SP1 binding and P97 activity 4·7-fold. An engineered mutant eliminating SP1 binding showed only 1- to 1·6-fold increased P97 activity. It is concluded that competition between SP1 and YY1 for DNA binding plays a major role in YY1 repression mediated by the binding site at positions 7840–7848.

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