Cited by 289Genomics and Chromatin DynamicsCancer-related Molecular PathwaysNuclear Structure and Function

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Repression of RNA Polymerase I Transcription by the Tumor Suppressor p53

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Zhai, Weiguo, Comai, Lucio·2000·Molecular and Cellular Biology

DOI 10.1128/mcb.20.16.5930-5938.2000PMC PMC86070

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Abstract

The tumor suppressor protein p53 is frequently inactivated in tumors. It functions as a transcriptional activator as well as a repressor for a number of viral and cellular promoters transcribed by RNA polymerase II (Pol II) and by RNA Pol III. Moreover, it appears that p53 also suppresses RNA Pol I transcription. In this study, we examined the molecular mechanism of Pol I transcriptional inhibition by p53. We show that wild-type, but not mutant, p53 can repress Pol I transcription from a human rRNA gene promoter in cotransfection assays. Furthermore, we show that recombinant p53 inhibits rRNA transcription in a cell-free transcription system. In agreement with these results, p53-null epithelial cells display an increased Pol I transcriptional activity compared to that of epithelial cells that express p53. However, both cell lines display comparable Pol I factor protein levels. Our biochemical analysis shows that p53 prevents the interaction between SL1 and UBF. Protein-protein interaction assays indicate that p53 binds to SL1, and this interaction is mostly mediated by direct contacts with TATA-binding protein and TAF(I)110. Moreover, template commitment assays show that while the formation of a UBF-SL1 complex can partially relieve the inhibition of transcription, only the assembly of a UBF-SL1-Pol I initiation complex on the rDNA promoter confers substantial protection against p53 inhibition. In summary, our results suggest that p53 represses RNA Pol I transcription by directly interfering with the assembly of a productive transcriptional machinery on the rRNA promoter.

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Authors: Zhai, W., & Comai, L.
Affiliations: University of Southern California (US)
Corresponding author: Comai, Lucio
ORCID: Comai, Lucio
Venue: Molecular and Cellular Biology
Publisher: Informa UK Limited
Published: 2000-08
Volume: 20
Issue: 16
Pages: 5930-5938
ISSN: 0270-7306 (ISSN-L)
1098-5549
DOI: 10.1128/mcb.20.16.5930-5938.2000
PMC: PMC86070
OpenAlex: W2146842824
Cited by: 289
References: 53
Citations by year: 2026: 4 · 2025: 6 · 2024: 8 · 2023: 9 · 2022: 10 · 2021: 14 · 2020: 7 · 2019: 14 · 2018: 13 · 2017: 13 · 2016: 6 · 2015: 14 · 2014: 24 · 2013: 21 · 2012: 7
FWCI: 2.53
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: journals.asm.org/non-commercial-tdm-license (tdm)
Locations: Molecular and Cellular Biology (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health
National Institute of General Medical Sciences (R01GM053949, R01 GM53949)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Structure and Function
Keywords: p53, RNA polymerase I transcription, transcriptional repression, UBF, TATA-binding protein, protein-protein interaction, transcription initiation complex, tumor suppressor
MeSH terms: HeLa Cells, Humans, Plasmids, RNA Polymerase I, Transcription, Genetic, Transfection, Genes, Tumor Suppressor, Genes, p53, Tumor Suppressor Protein p53

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Repression of RNA Polymerase I Transcription by the Tumor Suppressor p53

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