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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Viral DNA synthesis-dependent titration of a cellular repressor activates transcription of the human adenovirus type 2 IVa2 gene.
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Viral DNA synthesis-dependent titration of a cellular repressor activates transcription of the human adenovirus type 2 IVa2 gene.

机译：细胞阻遏物的病毒DNA合成依赖性滴定激活了人类2型腺病毒IVa2基因的转录。

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摘要

Synthesis of progeny DNA genomes in cells infected by human subgroup C adenoviruses leads to several changes in viral gene expression. These changes include transcription from previously silent, late promoters, such as the IV(a2) promoter, and a large increase in the efficiency of major-late (ML) transcription. Some of these changes appear to take place sequentially, because the product of the IV(a2) gene has been implicated in stimulation of ML transcription. Our previous biochemical studies suggested that IV(a2) transcription is regulated by viral DNA synthesis-dependent relief of transcriptional repression by a cellular protein that we termed IV(a2)-RF. To test the relevance of such a repressor-titration mechanism during the viral infectious cycle, we introduced into the endogenous IV(a2) promoter two mutations that impair in vitro-binding of IV(a2)-RF, but introduce no change (Rep7) or one conservative amino acid substitution (Rep6) into the overlapping coding sequence for the viral DNA polymerase.The results of run-on transcription assays indicated that both mutations induced earlier-than-normal and more efficient IV(a2) transcription. Both mutations were also observed to result in modest increases in the efficiency of viral DNA synthesis. However, measurement of the concentration of IV(a2) transcripts as a function of IV(a2) template concentration demonstrated that the Rep mutations increased by up to 60-fold the efficiency with which IV(a2) templates were used during the initial period of the late phase of infection, as predicted by the repressor titration hypothesis. These mutations also increased the efficiency of ML transcription in infected cells.
机译：在人类亚组C腺病毒感染的细胞中，子代DNA基因组的合成导致病毒基因表达发生若干变化。这些变化包括从以前沉默的晚期启动子（例如IV（a2）启动子）转录，以及主要后期（ML）转录效率的大幅提高。这些变化中的某些变化似乎是顺序发生的，因为IV（a2）基因的产物与ML转录的刺激有关。我们以前的生化研究表明，IV（a2）转录受病毒DNA合成依赖性转录抑制的调控，而这种抑制作用是由我们称为IV（a2）-RF的细胞蛋白进行的。为了测试这种阻抑剂滴定机制在病毒感染周期中的相关性，我们向内源性IV（a2）启动子引入了两个突变，这些突变会削弱IV（a2）-RF的体外结合，但不会引起变化（Rep7）病毒DNA聚合酶的重叠编码序列中包含一个或一个保守的氨基酸取代（Rep6）。连续转录分析的结果表明，这两个突变均诱导了比正常情况更早且更有效的IV（a2）转录。还观察到两种突变均导致病毒DNA合成效率的适度提高。但是，对IV（a2）转录本浓度作为IV（a2）模板浓度的函数进行测量，结果表明，Rep突变在初始阶段使用IV（a2）模板的效率提高了60倍。如阻遏滴定假设所预测的，是感染的晚期。这些突变还提高了感染细胞中ML转录的效率。

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