Murine leukemia virus long terminal repeat sequences can enhance gene activity in a cell-type-specific manner

1985 ◽  
Vol 5 (10) ◽  
pp. 2832-2835 ◽  
Author(s):  
F K Yoshimura ◽  
B Davison ◽  
K Chaffin
Keyword(s):  
Long Terminal Repeat ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Cell Type ◽  
Specific Manner ◽  
A Cell ◽  
Cell Type Specific ◽  
Murine Leukemia

We tested the ability of sequences in the long terminal repeat (LTR) of a mink cell focus-forming (MCF) murine leukemia virus to function as an enhancer in a cell-type-specific manner. In a stable transformation assay, the MCF or Akv LTR and the simian virus 40 enhancer had similar activities in murine fibroblasts. In contrast, the MCF LTR had a significantly greater activity in murine T lymphoid cells than did either the simian virus 40 enhancer or the Akv LTR.

scholarly journals Murine leukemia virus long terminal repeat sequences can enhance gene activity in a cell-type-specific manner.

1985 ◽  
Vol 5 (10) ◽  
pp. 2832-2835 ◽  
Author(s):  
F K Yoshimura ◽  
B Davison ◽  
K Chaffin
Keyword(s):  
Long Terminal Repeat ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Cell Type ◽  
Specific Manner ◽  
A Cell ◽  
Cell Type Specific ◽  
Murine Leukemia

We tested the ability of sequences in the long terminal repeat (LTR) of a mink cell focus-forming (MCF) murine leukemia virus to function as an enhancer in a cell-type-specific manner. In a stable transformation assay, the MCF or Akv LTR and the simian virus 40 enhancer had similar activities in murine fibroblasts. In contrast, the MCF LTR had a significantly greater activity in murine T lymphoid cells than did either the simian virus 40 enhancer or the Akv LTR.

scholarly journals Retrovirus transduction: generation of infectious retroviruses expressing dominant and selectable genes is associated with in vivo recombination and deletion events.

1983 ◽  
Vol 3 (12) ◽  
pp. 2180-2190 ◽  
Author(s):  
A L Joyner ◽  
A Bernstein
Keyword(s):  
Long Terminal Repeat ◽  
Thymidine Kinase ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Terminal Repeat ◽  
Moloney Murine Leukemia Virus ◽  
Murine Leukemia

We describe the generation of infectious retroviruses containing foreign genes by an in vivo recombination-deletion mechanism. Cotransfection into mouse cells of chimeric plasmids carrying a murine retrovirus 5' long terminal repeat and either the thymidine kinase (tk) gene of herpesvirus or the dominant selectable bacterial gene for neomycin resistance (neo), along with a clone of Moloney murine leukemia virus, results in the generation of infectious thymidine kinase or neomycin-resistant viruses. Expression of the selectable marker in these viruses can be regulated by the homologous transcriptional promoter of the gene, by the promoter contained within the Friend spleen focus-forming virus long terminal repeat, or by the simian virus 40 early region promoter. In all cases, the rescued viruses appeared to arise by recombination in vivo with Moloney murine leukemia virus sequences, resulting in the acquisition of the Moloney 3' long terminal repeat and variable amounts of the 3' adjacent Moloney genome. In two of the thymidine kinase constructs where tk was inserted 200 base pairs downstream from the long terminal repeat, the rescued viruses acquired a large part of the murine leukemia virus genome, including the region involved in packaging genomic RNA into virions. The generation of infectious neomycin-resistant virus is associated with deletions of simian virus 40 splicing and polyadenylation sequences. These results demonstrate that nonhomologous recombination and deletion events can take place in animal cells, resulting in the acquisition or removal of cis-acting sequences required for, or inhibitory to, retrovirus infectivity.

Retrovirus transduction: generation of infectious retroviruses expressing dominant and selectable genes is associated with in vivo recombination and deletion events

1983 ◽  
Vol 3 (12) ◽  
pp. 2180-2190
Author(s):  
A L Joyner ◽  
A Bernstein
Keyword(s):  
Long Terminal Repeat ◽  
Thymidine Kinase ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Terminal Repeat ◽  
Moloney Murine Leukemia Virus ◽  
Murine Leukemia

We describe the generation of infectious retroviruses containing foreign genes by an in vivo recombination-deletion mechanism. Cotransfection into mouse cells of chimeric plasmids carrying a murine retrovirus 5' long terminal repeat and either the thymidine kinase (tk) gene of herpesvirus or the dominant selectable bacterial gene for neomycin resistance (neo), along with a clone of Moloney murine leukemia virus, results in the generation of infectious thymidine kinase or neomycin-resistant viruses. Expression of the selectable marker in these viruses can be regulated by the homologous transcriptional promoter of the gene, by the promoter contained within the Friend spleen focus-forming virus long terminal repeat, or by the simian virus 40 early region promoter. In all cases, the rescued viruses appeared to arise by recombination in vivo with Moloney murine leukemia virus sequences, resulting in the acquisition of the Moloney 3' long terminal repeat and variable amounts of the 3' adjacent Moloney genome. In two of the thymidine kinase constructs where tk was inserted 200 base pairs downstream from the long terminal repeat, the rescued viruses acquired a large part of the murine leukemia virus genome, including the region involved in packaging genomic RNA into virions. The generation of infectious neomycin-resistant virus is associated with deletions of simian virus 40 splicing and polyadenylation sequences. These results demonstrate that nonhomologous recombination and deletion events can take place in animal cells, resulting in the acquisition or removal of cis-acting sequences required for, or inhibitory to, retrovirus infectivity.

Lymphoid and other tissue-specific phenotypes of polyomavirus enhancer recombinants: positive and negative combinational effects on enhancer specificity and activity

1986 ◽  
Vol 6 (6) ◽  
pp. 2068-2079
Author(s):  
B A Campbell ◽  
L P Villarreal
Keyword(s):  
Cell Lines ◽  
Heavy Chain ◽  
Murine Leukemia Virus ◽  
Tissue Specificity ◽  
Leukemia Virus ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Lymphoid Cells ◽  
B Lymphoid ◽  
Murine Leukemia

Heterologous enhancer recombinants and deletions of the polyomavirus (Py) noncoding region were constructed and analyzed for tissue specificity of DNA replication and transcription in a number of lymphoid and other cell lines. The simian virus 40 72-base-pair repeat, mouse immunoglobulin heavy-chain enhancer, and Moloney murine leukemia virus enhancer were inserted into the PvuII-D locus (nucleotides 5128 through 5265) of Py. The ability of these recombinants and the parental PvuII-D deletion mutant to replicate in permissive 3T6 cells and MOP-6 cells as well as in nonpermissive mouse B lymphoid, T lymphoid, mastocyte, and embryonal carcinoma cells was determined. Wild-type Py DNA was not permissive for replication in most lymphoid cell lines, except one hybridoma line. Simply deleting the Py PvuII-D region, however, gave Py an expanded host range, allowing high-level replication in some T lymphoid and mastocytoma cell lines, indicating that this element can be a tissue-specific negative as well as positive element. Substitution of the murine leukemia virus enhancer for Py PvuII-D yielded a Py genome which retained the ability to replicate in 3T6 cells but also replicated well in B lymphoid cells. Substitution with the immunoglobulin heavy-chain enhancer allowed replication in B lymphoid cells but interfered with replication in 3T6 cells and mastocytomas. Surprisingly, substitution with the simian virus 40 72-base-pair enhancer repeat gave a recombinant which would not replicate in any cell line tried, including MOP-6 cells, even though other recombinants with this enhancer would replicate. Thus, we observed both cooperation and interference in these combinations between enhancer components and the Py genome and that these combined activities were cell specific. These results are presented as evidence that there may be a positional dependence, or syntax, for the recognition of genetic elements controlling Py tissue specificity.

Bovine leukemia virus long terminal repeat: a cell type-specific promoter

Science ◽  
1985 ◽  
Vol 227 (4684) ◽  
pp. 317-320 ◽  
Author(s):  
D Derse ◽  
S. Caradonna ◽  
J. Casey
Keyword(s):  
Long Terminal Repeat ◽  
Bovine Leukemia Virus ◽  
Leukemia Virus ◽  
Terminal Repeat ◽  
Cell Type ◽  
A Cell ◽  
Cell Type Specific

scholarly journals Induced expression from the Moloney murine leukemia virus long terminal repeat during differentiation of human myeloid cells is mediated through its transcriptional enhancer.

1989 ◽  
Vol 9 (8) ◽  
pp. 3571-3575 ◽  
Author(s):  
D Reisman ◽  
V Rotter
Keyword(s):  
Long Terminal Repeat ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Myeloid Cells ◽  
Simian Virus 40 ◽  
Terminal Repeat ◽  
Moloney Murine Leukemia Virus ◽  
Transcriptional Enhancer ◽  
Sv40 Promoter ◽  
Murine Leukemia

Transcription from the Moloney murine leukemia virus (Mo-MuLV) long terminal repeat (LTR) is inhibited in murine stem cells and induced during maturation of these cells. We have investigated whether alterations in the activity of this viral regulatory element also occur during differentiation of human myeloid leukemia cells. The Mo-MuLV LTR and the simian virus 40 (SV40) early promoter were introduced into HL-60 promyelocytes on Epstein-Barr virus-derived chloramphenicol acetyltransferase expression vectors. When these cells were induced to terminally differentiate, transcription from the Mo-MuLV LTR was induced approximately 10-fold. Expression from the SV40 promoter remained constant during differentiation of these cells. Replacing the SV40 transcriptional enhancer with the Mo-MuLV LTR transcriptional enhancer rendered the SV40 promoter inducible during differentiation. We conclude that sequences within the transcriptional enhancer of the Mo-MuLV LTR contain cis-acting elements responsible for induction of gene expression during differentiation of human myeloid cells.

scholarly journals Fibroblast surface antigen produced but not retained by virus-transformed human cells.

1975 ◽  
Vol 142 (2) ◽  
pp. 530-535 ◽  
Author(s):  
A Vaheri ◽  
E Ruoslahti
Keyword(s):  
Human Serum ◽  
Human Fibroblasts ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Malignant Cells ◽  
Cell Type ◽  
Glycoprotein Antigen ◽  
A Cell ◽  
Normal Human ◽  
Cell Type Specific

Normal human fibroblasts contain a cell type-specific glycoprotein antigen (SF) that is known to be slowly shed into the medium and to be present also in human serum. Immunofluorescence with anti-SF antibodies showed that SF antigen has a highly nonrandom fibrillar distribution in surface of normal fibroblasts. Simian virus 40-transformed fibroblasts also produced the SF antigen, as shown by radioimmunoassay or immunodiffusion tests, but it was not retained by the surface of these cells. This creates a major difference between the surfaces of normal and malignant cells.

Induced expression from the Moloney murine leukemia virus long terminal repeat during differentiation of human myeloid cells is mediated through its transcriptional enhancer

1989 ◽  
Vol 9 (8) ◽  
pp. 3571-3575
Author(s):  
D Reisman ◽  
V Rotter
Keyword(s):  
Long Terminal Repeat ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Myeloid Cells ◽  
Simian Virus 40 ◽  
Terminal Repeat ◽  
Moloney Murine Leukemia Virus ◽  
Transcriptional Enhancer ◽  
Sv40 Promoter ◽  
Murine Leukemia

Transcription from the Moloney murine leukemia virus (Mo-MuLV) long terminal repeat (LTR) is inhibited in murine stem cells and induced during maturation of these cells. We have investigated whether alterations in the activity of this viral regulatory element also occur during differentiation of human myeloid leukemia cells. The Mo-MuLV LTR and the simian virus 40 (SV40) early promoter were introduced into HL-60 promyelocytes on Epstein-Barr virus-derived chloramphenicol acetyltransferase expression vectors. When these cells were induced to terminally differentiate, transcription from the Mo-MuLV LTR was induced approximately 10-fold. Expression from the SV40 promoter remained constant during differentiation of these cells. Replacing the SV40 transcriptional enhancer with the Mo-MuLV LTR transcriptional enhancer rendered the SV40 promoter inducible during differentiation. We conclude that sequences within the transcriptional enhancer of the Mo-MuLV LTR contain cis-acting elements responsible for induction of gene expression during differentiation of human myeloid cells.

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