Anti-termination of transcription within the long terminal repeat of HIV-1 by tat gene product

Human immunodeficiency virus-1 (HIV-1) gene expression is controlled by cellular transcription factors and by virally encoded trans-activation proteins of the HIV-1 tat and art/trs genes, which are essential for viral replication. Tat trans-activates HIV-1 gene expression by interacting with the tra...

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Bibliographic Details
Published in:Nature (London) 1987-12, Vol.330 (6147), p.489-493
Main Authors: Kao, Shaw-Yi, Calman, Andrew F, Luciw, Paul A, Peterlin, B. Matija
Format: Article
Language:English
Subjects:
Acetyltransferases - genetics
Acquired immune deficiency syndrome
AIDS
AIDS/HIV
Biological and medical sciences
Cell Line
Cellular biology
Chloramphenicol O-Acetyltransferase
Fundamental and applied biological sciences. Psychology
Gene Products, tat
Genes, Viral
Genetics
HIV - genetics
Human immunodeficiency virus 1
Microbiology
Nucleic Acid Hybridization
Oncogene Proteins, Viral - genetics
Plasmids
Protein Biosynthesis
Proteins
Repetitive Sequences, Nucleic Acid
RNA, Messenger - genetics
RNA, Viral - genetics
tat Gene Products, Human Immunodeficiency Virus
Transcription Factors - genetics
Transcription, Genetic
Transfection
Virology
Virus Replication
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Summary:Human immunodeficiency virus-1 (HIV-1) gene expression is controlled by cellular transcription factors and by virally encoded trans-activation proteins of the HIV-1 tat and art/trs genes, which are essential for viral replication. Tat trans-activates HIV-1 gene expression by interacting with the trans-acting response element (TAR) located within the HIV-1 long terminal repeat (LTR) (ref. 2). In transient expression assays, tat mediates its effects largely by increasing the steady-state levels of messenger RNA species that contain the TAR sequence at or near their 5' ends, suggesting a function for tat either in transcription or in subsequent RNA processing. The tat gene could also facilitate translation of mRNA containing the TAR sequence. To determine the mechanism of trans-activation by tat, we analysed the structure and rate of synthesis of RNA species directed by the HIV-1 LTR in transient expression assays both in the presence and absence of tat. Although the rate of HIV-1 transcription initiation was not affected by tat, transcriptional elongation beyond position +59 was seen only in the presence of tat. Thus, tat trans-activates HIV-1 transcription by relieving a specific block to transcriptional elongation within the TAR sequence.
ISSN:0028-0836
1476-4687
DOI:10.1038/330489a0