An enhanceosome containing the Jun B/Fra-2 heterodimer and the HMG-I(Y) architectural protein controls HPV 18 transcription

• Published in: EMBO reports Vol. 1; no. 5; p. 422
• Main Authors: Bouallaga, I, Massicard, S, Yaniv, M, Thierry, F
• Format: Journal Article
• Language: English
• Published: England 01-11-2000
• Subjects: Binding Sites; Cell Nucleus - metabolism; Chloramphenicol O-Acetyltransferase - metabolism; Dimerization; DNA-Binding Proteins - chemistry; DNA-Binding Proteins - genetics; DNA-Binding Proteins - metabolism; Dose-Response Relationship, Drug; Enhancer Elements, Genetic; Fos-Related Antigen-2; Gene Deletion; Glutathione Transferase - metabolism; HeLa Cells; High Mobility Group Proteins - genetics; High Mobility Group Proteins - metabolism; HMGA1a Protein; Humans; Models, Biological; Models, Genetic; Oncogene Proteins, Viral - genetics; Oncogene Proteins, Viral - metabolism; Plasmids - metabolism; Protein Binding; Proto-Oncogene Proteins c-jun - chemistry; Proto-Oncogene Proteins c-jun - metabolism; Recombinant Fusion Proteins - metabolism; Transcription Factors - chemistry; Transcription Factors - genetics; Transcription Factors - metabolism; Transcription, Genetic
• ISSN: 1469-221X
• DOI: 10.1093/embo-reports/kvd091

Recent studies have reported new mechanisms that mediate the transcriptional synergy of strong tissue-specific enhancers, involving the cooperative assembly of higher-order nucleoprotein complexes called enhanceosomes. Here we show that the HPV18 enhancer, which controls the epithelial-specific transcription of the E6 and E7 transforming genes, exhibits characteristic features of these structures. We used deletion experiments to show that a core enhancer element cooperates, in a specific helical phasing, with distant essential factors binding to the ends of the enhancer. This core sequence, binding a Jun B/Fra-2 heterodimer, cooperatively recruits the architectural protein HMG-I(Y) in a nucleoprotein complex, where they interact with each other. Therefore, in HeLa cells, HPV18 transcription seems to depend upon the assembly of an enhanceosome containing multiple cellular factors recruited by a core sequence interacting with AP1 and HMG-I(Y).