Zhang Zhiqiang, Klatt Alicia, Henderson Andrew J, Gilmour David S
Center for Gene Regulation, Department of Biochemistry and Molecular Biology, The Pennsylvania State University, University Park, PA 16802, USA.
Genes Dev. 2007 Jul 1;21(13):1609-14. doi: 10.1101/gad.1542707.
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.
真核生物中的许多延伸因子通过提高RNA聚合酶II(Pol II)的持续合成能力来促进基因表达。然而,RNA Pol II延伸复合物的稳定性表明,此类复合物并非天生就易于过早终止转录,尤其是在生理核苷酸浓度下。我们发现,终止因子Pcf11会导致HIV前病毒上的转录过早终止。当从细胞或提取物中去除Pcf11时发生的转录对6-二氯-1-β-D-呋喃核糖基苯并咪唑(DRB)不再敏感,DRB是一种会导致过早终止的化合物。因此,Pcf11可作为负延伸因子,在真核细胞中抑制RNA Pol II基因表达。