Krauskopf A, Ben-Asher E, Aloni Y
Department of Molecular Genetics and Virology, Weizmann Institute of Science, Rehovot, Israel.
J Virol. 1994 Apr;68(4):2741-5. doi: 10.1128/JVI.68.4.2741-2745.1994.
Our previous observations indicated that upon infection with minute virus of mice (MVM), Ehrlich ascites cells lose a transcription elongation activity which is essential for the readthrough of the MVM attenuator. This was monitored by the ability of extracts from uninfected but not from infected cells to support readthrough of the P4 attenuator when added to partially purified transcription elongation complexes. We have investigated the nature of this change in transcription elongation following MVM infection. In this communication, we show that infection of Ehrlich ascites cells with MVM leads to a general shift in the length of nascent mRNA synthesized in isolated nuclei and separated by sucrose gradients. Furthermore, infection leads to attenuation of transcription of the cellular gene c-fos but not c-myc. We show biochemical evidence to support a model by which, following MVM infection, there is a functional reduction in the activity of a TFIIS-like general transcriptional elongation activity.
我们之前的观察结果表明，感染小鼠微小病毒（MVM）后，艾氏腹水细胞会失去一种转录延伸活性，这种活性对于MVM弱化子的通读至关重要。当将未感染细胞而非感染细胞的提取物添加到部分纯化的转录延伸复合物中时，通过其支持P4弱化子通读的能力来监测这一情况。我们研究了MVM感染后这种转录延伸变化的本质。在本通讯中，我们表明用MVM感染艾氏腹水细胞会导致在分离的细胞核中合成并通过蔗糖梯度分离的新生mRNA长度发生总体变化。此外，感染会导致细胞基因c-fos的转录减弱，但不会导致c-myc的转录减弱。我们提供了生化证据来支持一个模型，即MVM感染后，一种类似TFIIS的一般转录延伸活性的功能会降低。
