The retroviruses human immunodeficiency virus type 1 and Moloney murine leukemia virus adopt radically different strategies to regulate promoter-proximal polyadenylation
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Maximal gene expression in retroviruses requires that polyadenylation in the 5′ long terminal repeat (LTR) is suppressed. In human immunodeficiency virus type 1 (HIV-1) the promoter-proximal poly(A) site is blocked by interaction of U1 snRNP with the closely positioned major splice donor site (MSD) 200 nucleotides downstream. Here we investigated whether the same mechanism applies to down-regulate 5′ LTR polyadenylation in Moloney murine leukemia virus (MoMLV). Although the same molecular architecture is present in both viruses, the MoMLV poly(A) signal in the 5′ LTR is active whether or not the MSD is mutated. This surprising difference between the two retroviruses is not due to their actual poly(A) signals or MSD sequences, since exchange of either element between the two viral sequences does not alter their ability to regulate 5′ LTR poly(A) site use. Instead we demonstrate that sequence between the cap and AAUAAA is required for MSD-dependent poly(A) regulation in HIV-1, indicating a key role for this part of the LTR in poly(A) site suppression. We also show that the MoMLV poly(A) signal is an intrinsically weak RNA-processing signal. This suggests that in the absence of a poly(A) site suppression mechanism, MoMLV is forced to use a weak poly(A) signal.
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Involvement of splicing machinery influences the occlusion of the 5′ end polyA signal in HIV-1.
“Additionally, involvement of splicing machinery has also been shown to influence the occlusion of the 5′ end polyA signal in the case of HIV-1 (Furger et al. 2001).”
From Beyond reverse transcription: molecular mechanisms and emerging paradigms in retroviral replication (2026) · cites this paper as Furger et al. 2001
In MLV, suppression of the 5′ end polyA signal is not dependent on the splicing machinery and primarily relies on the weak nature of the 5′ end polyA signal.
“In the case of MLV, which also contains functional polyA signal at the 5′ end of the transcript, suppression of the 5′ end polyA signal is not dependent on the splicing machinery and primarily relies on the weak nature of the 5′ end polyA signal, thereby evading the untimely polyadenylation at the 5′ end (Furger et al. 2001).”
From Beyond reverse transcription: molecular mechanisms and emerging paradigms in retroviral replication (2026) · cites this paper as Furger et al. 2001
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Ashe, M. P., Griffin, P., James, W., & Proudfoot, N. J. (1995) · Genes & Development · doi:10.1101/gad.9.23.3008 · Cited by 125 · see citing works
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The retroviral vector family: something for everyone
Elsner, C., & Bohne, J. (2017) · Virus Genes · doi:10.1007/s11262-017-1489-0 · Cited by 36 · see citing works
Schrom, E.-M., Moschall, R., Hartl, M. J., Weitner, H., Fecher, D., Langemeier, J., Bohne, J., Wöhrl, B. M., & Bodem, J. (2013) · Retrovirology · doi:10.1186/1742-4690-10-55 · Cited by 14 · see citing works
Beyond reverse transcription: molecular mechanisms and emerging paradigms in retroviral replication
Jehad, M. A., Ali, L. M., Pillai, V. N., Prabhu, S. G., Mustafa, F., & Rizvi, T. A. (2026) · FEMS Microbiology Reviews · doi:10.1093/femsre/fuaf066 · Cited by 5 · see citing works
“Additionally, involvement of splicing machinery has also been shown to influence the occlusion of the 5 end polyA signal in the case of HIV-1 (Furger et al. 2001 ).”
- Authors
- Furger, A., Monks, J., & Proudfoot, N. J.
- Affiliations
- <!--label omitted: 1-->Sir William Dunn School of Pathology, Oxford University, Oxford OX1 3RE, United Kingdom
- University of Oxford (GB)
- Venue
- Journal of Virology
- Publisher
- American Society for Microbiology
- Published
- 2001-12
- Volume
- 75
- Issue
- 23
- Pages
- 11735-11746
- ISSN
- 0022-538X (ISSN-L)
- 1098-5514
- PMC
- PMC114759
- OpenAlex
- W2035692642
- Cited by
- 40
- References
- 1
- Citations by year
- 2025: 1 · 2023: 1 · 2022: 1 · 2021: 1 · 2019: 1 · 2017: 2 · 2013: 4
- FWCI
- 1.05
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Virology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- 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, Moloney murine leukemia virus, retroviruses, 5' long terminal repeat, U1 snRNP, RNA splicing, viral gene expression regulation
- MeSH terms
- Animals, Base Sequence, HeLa Cells, Humans, Moloney murine leukemia virus, Poly A, Promoter Regions, Genetic, Repetitive Sequences, Nucleic Acid, HIV-1, 3T3 Cells, DNA Primers, Mice
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