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Cited by 125RNA Research and SplicingHIV Research and TreatmentRNA and protein synthesis mechanisms

The DOI matches its Crossref record; 62 of the 62 references it cites were found in a registry or an index.

Poly(A) site selection in the HIV-1 provirus: inhibition of promoter-proximal polyadenylation by the downstream major splice donor site

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Ashe, M P, Griffin, P, James, W, Proudfoot, N J·1995·Genes & Development
DOI 10.1101/gad.9.23.3008
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Abstract

In common with all retroviruses, the human immunodeficiency virus type 1 (HIV-1) contains duplicated long terminal repeat (LTR) sequences flanking the proviral genome. These LTRs contain identical poly(A) signals, which are both transcribed into RNA. Therefore, to allow efficient viral expression, a mechanism must exist to either restrict promoter-proximal poly(A) site use or enhance the activity of the promoter-distal poly(A) site. We have examined the use of both poly(A) sites using proviral clones. Mutation of the previously defined upstream activatory sequences of the 3' LTR poly(A) site decreases the efficiency of polyadenylation when placed in competition with an efficient downstream processing signal. However, in the absence of competition, these mutations have no effect on HIV-1 polyadenylation. In addition, the 5' LTR poly(A) site is inactive, whereas a heterologous poly(A) site positioned in its place is utilized efficiently. Furthermore, transcription initiating from the 3' LTR promoter utilizes the 3' LTR poly(A) signal efficiently. Therefore, the main determinant of the differential poly(A) site use appears to be neither proximity to a promoter element in the 5' LTR nor the presence of upstream activating sequences at the 3' LTR. Instead, we show that the major splice donor site that is immediately downstream of the 5' LTR inhibits cleavage and polyadenylation at the promoter-proximal site. The fact that this poly(A) site is active in a proviral clone when the major splice donor site is mutated suggests that the selective use of poly(A) signals in HIV-1 is mediated by a direct inhibition of the HIV-1 poly(A) site by downstream splicing events or factors involved in splicing.

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Research works printed but not linked: 2

  1. 1988, Synthesis of a gene for the HIV transactivation protein TAT by a novel single stranded approach involving in vivo gap repair., Nucleic Acids Res., 16, 4278
  2. 1992, Multiple Sp1 binding sites confer enhancer-independent, replication-activated transcription of HIV-1 and globin promoters., New Biol., 4, 369

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Metadata

Authors
Ashe, M. P., Griffin, P., James, W., & Proudfoot, N. J.
Affiliations
University of Oxford (GB)
ORCID
Venue
Genes & Development
Publisher
Cold Spring Harbor Laboratory
Published
1995-12-01
Volume
9
Issue
23
Pages
3008-3025
ISSN
  • 0890-9369 (ISSN-L)
  • 1549-5477
DOI
10.1101/gad.9.23.3008
OpenAlex
W2108413560
Cited by
125
References
62
Citations by year
2026: 1 · 2025: 4 · 2024: 4 · 2023: 5 · 2022: 4 · 2021: 2 · 2019: 3 · 2018: 5 · 2017: 2 · 2016: 5 · 2015: 2 · 2014: 5 · 2013: 5 · 2012: 4
Type
posted content
Language
en
Open access
Locations
  • Genes & Development (publishedVersion)
  • PubMed (publishedVersion)
  • Research Explorer (The University of Manchester) (submittedVersion)
Funders
  • Wellcome Trust
  • Medical Research Council
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA Research and Splicing
  • Life Sciences › Immunology and Microbiology › Virology › HIV Research and Treatment
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA and protein synthesis mechanisms
Keywords
HIV-1, polyadenylation site selection, long terminal repeat, upstream activator sequence, 5' LTR, 3' LTR, retroviral transcription, polyadenylation signal
MeSH terms
Base Sequence, Binding, Competitive, Gene Expression Regulation, Humans, Molecular Sequence Data, Mutation, Poly A, Promoter Regions, Genetic, Proviruses, RNA Splicing, RNA, Messenger, Transcription, Genetic, HIV-1, HIV Long Terminal Repeat

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