Nucleotide sequence of the large terminal repeat of two different strains of gibbon ape leukemia virus

Trainor, Cecelia D.; Scott, Martin; Josephs, Steven F.; Fry, Kirk E.; Reitz, M. S.

doi:10.1016/0042-6822(84)90025-4

Cited by 18 publications

(25 citation statements)

References 26 publications

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“…The position of homologous elements between GALV Seato, GALV San Francisco, and GALV CM9 are indicated by a, b, b', and c (b and b' are more divergent than a or c). The Seato strain is shown here to have three 48-bp repeats, whereas the published sequence has only two (27) measured by separating acetylated and nonacetylated forms by thin-layer chromatography. Spots were cut from the plates and counted by liquid scintillation.…”

mentioning

confidence: 94%

“…The GALV San Francisco strain contains only one of the repeated 48-bp sequences (27). These strains are associated with different hematopoietic malignancies in primates; GALV Seato is associated with granulocytic leukemia, and GALV San Francisco with lymphocytic leukemia (27). There is also a GALV LTR variant (CM9), which was recovered from the GALVcontaining, transformed gibbon T-cell line MLA144 (3).…”

mentioning

confidence: 98%

“…The GALV Seato and San Francisco strains possess a homologous element which displays strong enhancer activity in a variety of cell types (15). The GALV San Francisco strain contains only one of the repeated 48-bp sequences (27). These strains are associated with different hematopoietic malignancies in primates; GALV Seato is associated with granulocytic leukemia, and GALV San Francisco with lymphocytic leukemia (27).…”

mentioning

confidence: 99%

“…The similar behavior of each of the three extract-specific exonuclease stops and their separation by 48 bp prompted us to resequence the probe. Previously, two tandem repeats were reported (27), and we wanted to determine the nature of the third protected site. Direct sequence analysis (23) repressor-f3-galactosidase fusion protein.…”

mentioning

confidence: 99%

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Binding of a cellular protein to the gibbon ape leukemia virus enhancer.

Quinn¹,

Holbrook²,

Levens³

1987

Mol. Cell. Biol.

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The gibbon ape leukemia virus (GALV) contains enhancer activity within its long terminal repeat. In the GALV Seato strain this activity resides in a 48-base-pair (bp) repeated element. We demonstrate the existence of a cellular protein which binds in this region of the Seato strain. A sensitive method for enriching protein-DNA complexes from crude extracts coupled with exonuclease and DNase footprint analysis revealed the specific binding of this protein to a 21-bp region within each repeated element. A 22-bp oligonucleotide fragment defined solely by the 21-bp footprint binds a protein in vitro and displays enhancer activity in vivo, suggesting that this protein is a major determinant of GALV enhancer activity. The protein is present in three cell lines which are positive for enhancer activity and is not detected in Jurkat cells, which are negative for enhancer activity. Only GALV long-terminal-repeat variants which support high levels of enhancer activity in vivo compete with this protein for specific binding in vitro, suggesting a potential role for the protein in determining enhancer activity. This protein binding is not inhibited by competition with heterologous retroviral enhancers, demonstrating that it is not a ubiquitous retroviral enhancer binding protein.Viruses have proven to be excellent models for eucaryotic transcription because of their relatively small size and ease of genetic manipulation. The existence of important cisacting regulatory regions such as enhancers (16), as well as the nature of the few well-characterized mammalian mRNA transcription factors, was discovered by studying viral gene regulation (1,4,22). The enhancer element of the gibbon ape leukemia virus (GALV) is suitable for such a study. Holbrook et al. (15) recently demonstrated that the GALV enhancer element is active in several uninfected cell lines. We have sought to identify the cellular products which trans-activate this enhancer. The enhancer activity of the GALV Seato strain has been shown to reside in a 155-basepair (bp) region within the U3 region of the long terminal repeat (LTR). The enhancer element is bounded by Apal and BanI restriction endonuclease cleavage sites and includes tandem, direct, and perfect repeats of a 48-bp sequence (15).Several viral variants of the GALV enhancer element exist which exhibit different levels of enhancer activity in vivo. The GALV Seato and San Francisco strains possess a homologous element which displays strong enhancer activity in a variety of cell types (15). The GALV San Francisco strain contains only one of the repeated 48-bp sequences (27). These strains are associated with different hematopoietic malignancies in primates; GALV Seato is associated with granulocytic leukemia, and GALV San Francisco with lymphocytic leukemia (27). There is also a GALV LTR variant (CM9), which was recovered from the GALVcontaining, transformed gibbon T-cell line MLA144 (3). This variant contains a 94-bp direct repeat which has very weak but detectable enhancer activity (N. Holbrook, A. Gulino, ...

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mentioning

confidence: 94%

mentioning

confidence: 98%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Binding of a cellular protein to the gibbon ape leukemia virus enhancer.

Quinn¹,

Holbrook²,

Levens³

1987

Mol. Cell. Biol.

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“…The beginning of the R region is marked by the cap site, a G nucleotide. As a rule, the R region also contains a poly A signal, although this signal seems to be dispensable for LTR function in some cases [64], and a poly A addition site (CA) which marks the end of the R region. The remaining sequence, including the 3' inverted repeat counterpart, makes up the U 5 region.…”

Section: Hlm-2 Mosaic Provirusmentioning

confidence: 99%

Human Endogenous Retrovirus-like Sequences

Brack‐Werner¹,

Leib-Mösch²,

Werner

et al. 1989

Haematology and Blood Transfusion / Hämatologie Und Bluttransfusion

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Lentiviral Vectors for Enhanced Gene Expression in Human Hematopoietic Cells

Ramezani¹,

2000

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Accumulated data indicate that current generation lentiviral vectors, which generally utilize an internal human cytomegalovirus (CMV) immediate early region enhancer-promoter to transcribe the gene of interest, are not yet optimized for efficient expression in human hematopoietic stem/progenitor cells (HSPCs). As a first step toward this goal, we constructed self-inactivating derivatives of the HIV-1-based transfer vector pHR' containing the enhanced green fluorescent protein (GFP) gene as reporter and the Woodchuck hepatitis virus posttranscriptional regulatory element (WPRE). GFP expression was driven by a variety of strong viral and cellular promoters, including the murine stem cell virus (MSCV) long terminal repeat (LTR), a Gibbon ape leukemia virus (GALV) LTR, the human elongation factor 1alpha (EF1alpha) promoter, the composite CAG promoter (consisting of the CMV immediate early enhancer and the chicken beta-actin promoter), and the human phosphoglycerate kinase 1 (PGK) promoter. In contrast to results obtained in human embryonic kidney 293T cells and fibrosarcoma HT1080 cells, in which the CMV promoter expressed GFP at the highest levels, significantly higher levels of GFP expression (3- to 5-fold) were achieved with the MSCV LTR, the EF1alpha promoter, and the CAG promoter in the human HSPC line KG1a. Removal of the WPRE indicated that it stimulated GFP expression from all of the vectors in KG1a cells (up to 3-fold), although it only marginally improved the performance of the intron-containing EF1alpha and CAG promoters (<1.5-fold stimulation). The vectors using the MSCV LTR, the GALV LTR, and the PGK promoter were the most efficient at transducing primary human CD34+ cord blood progenitors under the conditions employed. High-level GFP expression in the NOD/SCID xenograft model was demonstrated with the pHR' derivative bearing the MSCV LTR. These new lentiviral vector backbones provide a basis for the rational design of improved delivery vehicles for human HSPC gene transfer applications.

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Nucleotide sequence of the large terminal repeat of two different strains of gibbon ape leukemia virus

Cited by 18 publications

References 26 publications

Binding of a cellular protein to the gibbon ape leukemia virus enhancer.

Binding of a cellular protein to the gibbon ape leukemia virus enhancer.

Human Endogenous Retrovirus-like Sequences

Lentiviral Vectors for Enhanced Gene Expression in Human Hematopoietic Cells

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