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Published on: July 23, 2010
NCoR1 mediates papillomavirus E8;E2C transcriptional repression.
Maria L C Powell1, Jennifer A Smith, Mathew E Sowa
1Department of Pathology, Harvard Medical School, New Research Building, Room 950, 77 Avenue Louis Pasteur, Boston, MA 02115, USA.
Journal of Virology
|February 26, 2010
Summary
The E8;E2C protein from human papillomavirus interacts with NCoR1/HDAC3 to repress viral oncogene expression. This interaction, dependent on the E8 open reading frame, reveals distinct repression mechanisms for E2 and E8;E2C proteins.
Area of Science:
- Molecular Biology
- Virology
- Cancer Research
Background:
- The papillomavirus E2 open reading frame (ORF) produces both E2 and E8;E2C proteins.
- E8;E2C regulates viral genome and represses transcription of viral oncogenes (E6 and E7).
- E8;E2C repression is mediated by its N-terminal sequence from the E8 ORF.
Purpose of the Study:
- To elucidate the mechanism of transcriptional repression by E8;E2C.
- To identify proteins interacting with E8;E2C.
Main Methods:
- Unbiased proteomic analysis to identify E8;E2C interacting proteins.
- Co-immunoprecipitation to confirm interactions with NCoR1/HDAC3 complex.
- Small interfering RNA (siRNA) knockdown studies.
Main Results:
- Identified NCoR1 and TBLR1 as high-confidence interacting proteins (HCIPs) for E8;E2C.
- Confirmed E8;E2C interaction with an NCoR1/HDAC3 complex, dependent on the wild-type E8 ORF.
- Demonstrated NCoR1/HDAC3 involvement in E8;E2C-mediated repression of the viral long control region (LCR) promoter.
Conclusions:
- E8;E2C interacts with the NCoR1/HDAC3 complex to achieve transcriptional repression.
- Papillomavirus E2 and E8;E2C proteins utilize distinct mechanisms for transcriptional repression.
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