Transcriptional enhancer factor (TEF)-1 and its cell-specific co-activator activate human papillomavirus-16 E6 and E7 oncogene transcription in keratinocytes and cervical carcinoma cells

T Ishiji; M J Lace; S Parkkinen; Richard D Anderson; T H Haugen; T P Cripe; J H Xiao; I Davidson; P Chambon; L P Turek

doi:10.1002/j.1460-2075.1992.tb05286.x

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Transcriptional enhancer factor (TEF)-1 and its cell-specific co-activator activate human papillomavirus-16 E6 and E7 oncogene transcription in keratinocytes and cervical carcinoma cells

Journal article

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Transcriptional enhancer factor (TEF)-1 and its cell-specific co-activator activate human papillomavirus-16 E6 and E7 oncogene transcription in keratinocytes and cervical carcinoma cells

T Ishiji, M J Lace, S Parkkinen, Richard D Anderson, T H Haugen, T P Cripe, J H Xiao, I Davidson, P Chambon and L P Turek

The EMBO journal, Vol.11(6), pp.2271-2281

06/1992

DOI: 10.1002/j.1460-2075.1992.tb05286.x

PMCID: PMC556694

PMID: 1318197

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Abstract

The human papillomavirus (HPV)-16 oncogenes, E6 and E7, are transcribed preferentially in keratinocytes and cervical carcinoma cells due to a 5' enhancer. An abundant peptide binding to a 37 nt enhancer element was purified from human keratinocytes by sequence-specific DNA chromatography. This protein was identified as transcriptional enhancer factor (TEF)-1 by complex mobility, binding to wild-type and mutant SV40 and HPV-16 enhansons and antigenic reactivity with two anti-TEF-1 antibodies. TEF-1 is cell-specific, but its transactivation also depends on a limiting, cell-specific TEF-1 'co-activator'. We show that both TEF-1 and the TEF-1 co-activator are active in human keratinocytes and essential for HPV-16 transcription. TEF-1 binding in vivo was necessary for HPV-16 P97 promoter activity. Excess TEF-1 and chimeric GAL4-TEF-1 specifically inhibited the P97 promoter by 'squelching', indicating that HPV-16 transcription also requires a limiting TEF-1 co-activator. TEF-1 and the TEF-1 co-activator functions mirrored HPV-16 transcription by their presence in keratinocytes and cervical carcinoma cells and their absence from lymphoid B-cells, but also functioned in liver cells where the HPV-16 promoter is inactive. TEF-1 and its associated co-activator are thus part of a complex mechanism which determines the restricted cell range of the HPV-16 E6 and E7 oncogene promoter.

Antibodies

Oncogenes

Transfection

Humans

Repressor Proteins

Transcriptional Activation

Molecular Sequence Data

Chloramphenicol O-Acetyltransferase - metabolism

Papillomavirus E7 Proteins

Chloramphenicol O-Acetyltransferase - genetics

Recombinant Fusion Proteins - metabolism

Cell Nucleus - physiology

Papillomaviridae - genetics

DNA-Binding Proteins - metabolism

Base Sequence

Female

Oncogene Proteins, Viral - genetics

Transcription, Genetic

Cell Line

Promoter Regions, Genetic

Oligodeoxyribonucleotides

Mutagenesis, Site-Directed

Transcription Factors - genetics

DNA-Binding Proteins - genetics

DNA-Binding Proteins - isolation & purification

Uterine Cervical Neoplasms - genetics

Nuclear Proteins

Transcription Factors - metabolism

Chromatography, Affinity

Enhancer Elements, Genetic

Gene Expression Regulation, Viral

Transcription Factors - isolation & purification

Keratinocytes - physiology

Details

Title: Subtitle: Transcriptional enhancer factor (TEF)-1 and its cell-specific co-activator activate human papillomavirus-16 E6 and E7 oncogene transcription in keratinocytes and cervical carcinoma cells
Creators: T Ishiji - Department of Pathology, University of Iowa College of Medicine, Iowa City 52242
M J Lace
S Parkkinen
Richard D Anderson
T H Haugen
T P Cripe
J H Xiao
I Davidson
P Chambon
L P Turek
Resource Type: Journal article
Publication Details: The EMBO journal, Vol.11(6), pp.2271-2281
Publisher: England
DOI: 10.1002/j.1460-2075.1992.tb05286.x
PMID: 1318197
PMCID: PMC556694
ISSN: 0261-4189
eISSN: 1460-2075
Grant note: CA-49912 / NCI NIH HHS
Language: English
Date published: 06/1992
Academic Unit: Pathology
Record Identifier: 9984047760002771

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