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-beta-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.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Cells, Cultured
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Chromatin Immunoprecipitation
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Dichlororibofuranosylbenzimidazole / pharmacology
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Down-Regulation / drug effects
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Gene Expression Regulation, Viral* / drug effects
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HIV / drug effects
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HIV / genetics*
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HIV / growth & development
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HeLa Cells
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Humans
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Promoter Regions, Genetic
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Proviruses / drug effects
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Proviruses / genetics*
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Proviruses / growth & development
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RNA Polymerase II / metabolism*
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RNA, Small Interfering / pharmacology
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Transcription, Genetic
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mRNA Cleavage and Polyadenylation Factors / physiology*
Substances
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Pcf11 protein, human
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RNA, Small Interfering
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mRNA Cleavage and Polyadenylation Factors
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Dichlororibofuranosylbenzimidazole
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RNA Polymerase II