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人类免疫缺陷病毒1型启动子的反式激活受基础启动子活性和猿猴病毒40 DNA复制起点的影响。

Tat transactivation of the human immunodeficiency virus type 1 promoter is influenced by basal promoter activity and the simian virus 40 origin of DNA replication.

作者信息

Kessler M, Mathews M B

机构信息

Cold Spring Harbor Laboratory, NY 11724-2208.

出版信息

Proc Natl Acad Sci U S A. 1991 Nov 15;88(22):10018-22. doi: 10.1073/pnas.88.22.10018.

DOI:10.1073/pnas.88.22.10018
PMID:1658792
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC52858/
Abstract

We examined the activation of transcription from the human immunodeficiency virus type 1 (HIV-1) promoter by the viral Tat protein in a transient expression system. Plasmids contained a HIV-reporter gene cassette and a simian virus 40 origin of DNA replication. Run-on assays of transcription complex distribution and analysis of cytoplasmic RNA accumulation confirmed that Tat is able to activate transcription by two mechanisms: by increasing the rate of transcriptional initiation and the efficiency of transcriptional elongation. The degree to which Tat stimulated initiation is determined by the basal level of HIV-directed transcription, which is influenced by the presence [corrected] of the simian virus 40 replication origin. Tat functions primarily to increase the efficiency of elongation when the origin is present and the basal level of transcription is high [corrected]. On the other hand, Tat functions primarily to increase the rate of initiation when the origin is absent [corrected] and the basal level of transcription is 10-fold lower. These studies suggest that the site of integration of the virus into the cellular genome may significantly affect the level of expression from the HIV promoter and consequently the pathobiology of the virus.

摘要

我们在瞬时表达系统中研究了病毒Tat蛋白对人免疫缺陷病毒1型（HIV-1）启动子转录的激活作用。质粒包含一个HIV报告基因盒和一个猿猴病毒40 DNA复制起点。转录复合物分布的连续分析和细胞质RNA积累分析证实，Tat能够通过两种机制激活转录：提高转录起始速率和转录延伸效率。Tat刺激起始的程度由HIV指导转录的基础水平决定，而基础水平受猿猴病毒40复制起点的影响。当存在复制起点且转录基础水平较高时，Tat主要作用是提高延伸效率。另一方面，当不存在复制起点且转录基础水平低10倍时，Tat主要作用是提高起始速率。这些研究表明，病毒整合到细胞基因组中的位点可能会显著影响HIV启动子的表达水平，进而影响病毒的病理生物学。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d22c/52858/efd27b43e3f7/pnas01072-0122-c.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d22c/52858/efd27b43e3f7/pnas01072-0122-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d22c/52858/0a77717f1713/pnas01072-0120-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d22c/52858/561021ffed5d/pnas01072-0121-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d22c/52858/82b821a4c70b/pnas01072-0121-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d22c/52858/29bc1975ce71/pnas01072-0121-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d22c/52858/5cbe4d2a2594/pnas01072-0122-a.jpg
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