Transcription termination factor Pcf11 limits the processivity of Pol II on an HIV provirus to repress gene expression
- 1 Center for Gene Regulation, Department of Biochemistry and Molecular Biology, The Pennsylvania State University, University Park, Pennsylvania 16802, USA;
- 2 Center of Molecular Immunology and Infectious Diseases, Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park, Pennsylvania 16802, USA;
- 3 Graduate Program in Pathobiology, The Pennsylvania State University, University Park, Pennsylvania 16802, USA;
- 4 Center for HIV/AIDS Care and Research, Boston University Medical Center, Boston, Massachusetts 02118, USA
Abstract
Many elongation factors in eukaryotes promote gene expression by increasing the processivity of RNA polymerase II (Pol II). However, the stability of RNA Pol II elongation complexes suggests that such complexes are not inherently prone to prematurely terminating transcription, particularly at physiological nucleotide concentrations. We show that the termination factor, Pcf11, causes premature termination on an HIV provirus. The transcription that occurs when Pcf11 is depleted from cells or an extract is no longer sensitive to 6-dichloro-1-β-D-ribofuranosylbenzimidazole (DRB), a compound that causes premature termination. Hence, Pcf11 can act as a negative elongation factor to repress RNA Pol II gene expression in eukaryotic cells.
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Footnotes
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↵5 Corresponding author.
↵5 E-MAIL dsg11{at}psu.edu; FAX (814) 863-7024.
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Article is online at http://www.genesdev.org/cgi/doi/10.1101/gad.1542707
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- Received February 15, 2007.
- Accepted May 13, 2007.
- Copyright © 2007, Cold Spring Harbor Laboratory Press