Transcriptional activation with concurrent or nonconcurrent template replication has differential effects on transient expression from herpes simplex virus promoters.

Transcriptional activation with concurrent or nonconcurrent template replication has differential effects on transient expression from herpes simplex virus promoters.
复制标题

并发或非并发模板复制的转录激活对单纯疱疹病毒启动子的瞬时表达具有不同的影响。

DOI:
10.1007/bf00315257
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发表时间:
1989
期刊:
影响因子:
1.6
通讯作者:
Wagner,EK
Wagner,EK
中科院分区:
医学4区
文献类型:
--
作者:
Snowden,BW;Blair,ED;Wagner,EK

文献摘要

相似文献

我们使用了两种方法来诱导模板复制,以评估对 1 型单纯疱疹病毒 (HSV-1) 启动子控制的标记基因表达的影响。一种方法使用来自病毒基因组短重复区域的 HSV-1 DNA 复制起点 (HSV-1oris),并允许质粒携带的模板同时复制和转录激活。另一种方法是使用猿猴病毒 40 复制起点 (SV40ori),允许在 HSV-1 感染激活转录之前进行质粒模板复制。两种方案对 HSV-1 重复感染诱导的报告基因活性水平具有显着不同的影响。当细胞用 HSV-1 重复感染时,使用 SV40 复制报告质粒,产生的报告基因活性水平与质粒拷贝数成正比。相反,我们的结果表明,含有或接近HSV-1orisin报告质粒的序列对所有病毒启动子的表达具有显着的抑制作用,无论该质粒是否允许复制。尽管如此,早期 (β) 启动子控制的报告酶活性在后期下降,而在 HSV-1oris 介导的模板复制后,由严格的晚期 (γ) 启动子控制的报告酶活性显着升高。
We have used two methods to induce template replication in order to assess the effect on expression of marker genes controlled by herpes simplex virus type 1 (HSV-1) promoters. One method used the HSV-1 origin of DNA replication from the short repeat region of the viral genome (HSV-1oris), and allowed simultaneous replication and transcriptional activation of the plasmid-borne template. The other, using the simian virus 40 origin of replication (SV40ori) allowed plasmid template replication prior to activation of transcription by HSV-1 infection. The two regimes had markedly different effects upon the levels of reporter gene activity induced by HSV-1 superinfection. Replication of reporter plasmids using the SV40oriyielded levels of reporter gene activity proportional to plasmid copy number when cells were superinfected with HSV-1. In contrast, our results indicated that sequences containing, or in close proximity to, the HSV-1orisin the reporter plasmid had a significant inhibitory effect on expression from all viral promoters whether or not the plasmid was allowed to replicate. Still, the early (β) promoter-controlled reporter enzyme activity declined at late times while that controlled by the strict late (γ) promoter was significantly higher following HSV-1oris-mediated template replication.