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人类免疫缺陷病毒中5'和3'长末端重复序列启动子功能的比较

Comparison of 5' and 3' long terminal repeat promoter function in human immunodeficiency virus.

作者信息

Klaver B, Berkhout B

机构信息

Department of Virology, Academic Medical Center, University of Amsterdam, The Netherlands.

出版信息

J Virol. 1994 Jun;68(6):3830-40. doi: 10.1128/JVI.68.6.3830-3840.1994.

DOI:10.1128/JVI.68.6.3830-3840.1994
PMID:8189520
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC236888/
Abstract

The architecture of a retroviral genome presents some unusual features for transcriptional regulation because of duplication of the transcriptional control sequences in the 5' and 3' long terminal repeats (LTRs). We have studied the transcriptional activity of the 5' and 3' LTRs of human immunodeficiency virus type 1 (HIV-1) vectors. Using full-length HIV molecular clones, we demonstrate that both LTRs function as Tat-inducible promoters. However, the absolute levels of transcription were found to be much higher for the 5' LTR than for the 3' LTR promoter. When transcription was assayed for an integrated HIV-1 provirus, we also found that the upstream 5' LTR element was the major transcriptional promoter. 3' LTR transcription, however, can be triggered by inactivation of the 5' LTR promoter. Likewise, 5' LTR transcription is induced in constructs lacking a functional 3' LTR promoter. This phenomenon of promoter suppression may have important implications for the design of HIV-based retrovirus vectors.

摘要

由于逆转录病毒基因组的转录控制序列在5'和3'长末端重复序列（LTRs）中存在重复，其基因组结构在转录调控方面呈现出一些不同寻常的特征。我们研究了1型人类免疫缺陷病毒（HIV-1）载体的5'和3' LTR的转录活性。利用全长HIV分子克隆，我们证明两个LTR均作为Tat诱导型启动子发挥作用。然而，发现5' LTR的绝对转录水平比3' LTR启动子高得多。当对整合的HIV-1原病毒进行转录检测时，我们还发现上游的5' LTR元件是主要的转录启动子。然而，3' LTR转录可由5' LTR启动子失活触发。同样，在缺乏功能性3' LTR启动子的构建体中，5' LTR转录被诱导。这种启动子抑制现象可能对基于HIV的逆转录病毒载体的设计具有重要意义。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d7d7/236888/3c83ca14b833/jvirol00015-0395-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d7d7/236888/fd76dd0bee4d/jvirol00015-0390-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d7d7/236888/d247fc0a6ff8/jvirol00015-0391-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d7d7/236888/21bf883b0fea/jvirol00015-0392-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d7d7/236888/764b1d0d81e7/jvirol00015-0392-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d7d7/236888/24d832e99523/jvirol00015-0395-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d7d7/236888/3c83ca14b833/jvirol00015-0395-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d7d7/236888/fd76dd0bee4d/jvirol00015-0390-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d7d7/236888/d247fc0a6ff8/jvirol00015-0391-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d7d7/236888/21bf883b0fea/jvirol00015-0392-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d7d7/236888/764b1d0d81e7/jvirol00015-0392-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d7d7/236888/24d832e99523/jvirol00015-0395-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d7d7/236888/3c83ca14b833/jvirol00015-0395-b.jpg

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