Involvement of TFIID and USA Components in Transcriptional Activation of the Human Immunodeficiency Virus Promoter by NF-κB and Sp1
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The purified Rel/NF-kappaB (p50/p65) complex and Sp1 markedly activate transcription from the human immunodeficiency virus type 1 (HIV-1) promoter in a highly purified HeLa reconstituted transcription system. Transcriptional activation by NF-kappaB and Sp1 requires both TFIID and the USA fraction. The USA-derived coactivators PC2 and PC4 fully reconstitute the USA coactivator activity, both by repressing the basal level of transcription and by potentiating activator function to yield large increases in the levels of transcription induction. Under limiting concentrations, PC2 and PC4 also show synergistic effects. The C-terminal portion (amino acids 416 to 550) of the p65 subunit of NF-kappaB is a potent activator when assayed as a Gal fusion in the reconstituted transcription system and interacts both with TATA-binding protein (TBP) and with several human TBP-associated factors (TAFs) that include TAFII250. The p65 activation domain mediates transcription activation in the presence of partially reconstituted TFIID species that include a minimal complex containing only TBP and TAFII250. These studies also show that, like USA components, TAFs can serve both to repress TBP-mediated transcription and, following activator interactions, to reverse the repression and effect a net increase in activity. Taken together, these data underscore the importance of both TAFs and specific USA-derived coactivators for optimal activation of the HIV-1 promoter, as well as certain parallels in their overall mechanisms of action.
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Mediator subunits might limit how strongly pro-inflammatory NF-κB signaling induces gene expression, beyond their known role in recruiting active RNA polymerase-II to DNA-bound transcription factors including p65.
“These results suggest that, apart from the well-studied function of the Mediator complex in recruiting active RNA polymerase-II to DNA-bound transcription factors (Malik and Roeder, 2005) including to p65 (Guermah et al., 1998), Mediator components may be involved in restricting the transcriptional response of induced genes during pro-inflammatory NF-κB signaling.”
From Optical Pooled Screens in Human Cells (2019) · cites this paper as Guermah et al., 1998
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The Mediator complex and transcription regulation
Poss, Z. C., Ebmeier, C. C., & Taatjes, D. J. (2013) · Critical Reviews in Biochemistry and Molecular Biology · doi:10.3109/10409238.2013.840259 · Cited by 364 · see citing works
Optical Pooled Screens in Human Cells
Feldman, D., Singh, A., Schmid-Burgk, J. L., Carlson, R. J., Mezger, A., Garrity, A. J., Zhang, F., & Blainey, P. C. (2019) · Cell · doi:10.1016/j.cell.2019.09.016 · Cited by 321 · see citing works
- Authors
- Guermah, M., Malik, S., & Roeder, R. G.
- Affiliations
- Rockefeller University (US)
- ORCID
- Roeder, Robert G.
- Venue
- Molecular and Cellular Biology
- Publisher
- Informa UK Limited
- Published
- 1998-06-01
- Volume
- 18
- Issue
- 6
- Pages
- 3234-3244
- ISSN
- 0270-7306 (ISSN-L)
- 1098-5549
- PMC
- PMC108905
- OpenAlex
- W2108930620
- Cited by
- 91
- References
- 80
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 3 · 2023: 2 · 2022: 1 · 2020: 1 · 2019: 2 · 2018: 1 · 2017: 1 · 2016: 1 · 2013: 5 · 2012: 2
- FWCI
- 3.84
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Molecular and Cellular Biology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r35ca042567-12)
- National Cancer Institute (CA 42567)
- National Institute of Allergy and Infectious Diseases (AI32737)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Life Sciences › Immunology and Microbiology › Virology › HIV Research and Treatment
- Keywords
- HIV-1 promoter, transcriptional activation, NF-κB, Sp1, TFIID, PC2, PC4, TATA-binding protein, TAF, HeLa cells, transcriptional repression
- MeSH terms
- DNA-Binding Proteins, HeLa Cells, Humans, Membrane Proteins, Nuclear Proteins, Promoter Regions, Genetic, Repressor Proteins, Transcription Factors, HIV-1, Transcriptional Activation, Trans-Activators, NF-kappa B, Sp1 Transcription Factor, TATA Box, Immediate-Early Proteins, Transcription Factors, TFII, TATA-Box Binding Protein, Transcription Factor TFIID, TATA-Binding Protein Associated Factors, Macromolecular Substances, Histone Acetyltransferases, Transcription Factor RelA
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