Characterization of a rearrangement in viral DNA: Mapping of the circular simian virus 40-like DNA containing a triplication of a specific one-third of the viral genome

1974 ◽  
Vol 87 (2) ◽  
pp. 289-301 ◽  
Author(s):  
George Khoury ◽  
George C. Fareed ◽  
Karen Berry ◽  
Malcolm A. Martin ◽  
Theresa N.H. Lee ◽  
...  
Keyword(s):  
Viral Genome ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Viral Dna ◽  
Dna Mapping

scholarly journals Rat cells transformed by simian virus 40 give rise to tumor cells which contain no viral proteins and often no viral DNA.

1983 ◽  
Vol 3 (6) ◽  
pp. 1138-1145 ◽  
Author(s):  
R Seif ◽  
I Seif ◽  
J Wantyghem
Keyword(s):  
Tumor Cells ◽  
Viral Genome ◽  
Simian Virus 40 ◽  
Viral Proteins ◽  
Simian Virus ◽  
Tumor Formation ◽  
Temperature Sensitive ◽  
3T3 Cells ◽  
Viral Dna ◽  
Transformed Cell Lines

Rat 3T3 cells transformed by simian virus 40 were injected into rats to examine their capacity to develop into tumors. Both large T-dependent (N) transformants and large T-independent (A) transformants were used. All the transformed cell lines contained large T and small t and could multiply efficiently in agar. Only some transformants could develop into tumors. All tumor cells examined had lost both large T and small t. Tumor cells in which the viral genome could still be detected were found together with tumor cells in which the simian virus 40 DNA could no longer be detected. N transformants which displayed the transformed phenotype in a temperature-sensitive manner became temperature insensitive during tumor formation.

Characterization of simian virus 40 DNA component II during viral DNA replication

1973 ◽  
Vol 74 (2) ◽  
pp. 95-111 ◽  
Author(s):  
George C. Fareed ◽  
M.Louese McKerlie ◽  
Norman P. Salzman
Keyword(s):  
Dna Replication ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Viral Dna ◽  
Viral Dna Replication

The structure and expression of the integrated viral DNA in mouse cells transformed by simian virus 40

1980 ◽  
Vol 210 (1180) ◽  
pp. 437-450 ◽  
Keyword(s):  
Molecular Cloning ◽  
Viral Genome ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Transformed Cells ◽  
Chromosomal Dna ◽  
Viral Dna ◽  
Dna Templates ◽  
Transcription Pattern ◽  
Mouse Cells

Mouse cells stably transformed by simian virus 40 (SV40) contain viral DNA covalently integrated into their chromosomal DNA. We have used molecular cloning techniques to isolate and characterize the integrated viral DNA, together with the flanking cellular sequences, from several lines of transformed cells. We have identified in SV40-infected mouse cells a novel form of viral DNA, which we believe to be the precursor to the integrated DNA. The mRNAs transcribed from the integrated viral DNA templates have been characterized. Integrating the viral genome into the cellular chromosome can significantly alter its transcription pattern and in several cases the altered mRNAs encode novel forms of viral tumour antigen.

Rat cells transformed by simian virus 40 give rise to tumor cells which contain no viral proteins and often no viral DNA

1983 ◽  
Vol 3 (6) ◽  
pp. 1138-1145
Author(s):  
R Seif ◽  
I Seif ◽  
J Wantyghem
Keyword(s):  
Tumor Cells ◽  
Viral Genome ◽  
Simian Virus 40 ◽  
Viral Proteins ◽  
Simian Virus ◽  
Tumor Formation ◽  
Temperature Sensitive ◽  
3T3 Cells ◽  
Viral Dna ◽  
Transformed Cell Lines

Rat 3T3 cells transformed by simian virus 40 were injected into rats to examine their capacity to develop into tumors. Both large T-dependent (N) transformants and large T-independent (A) transformants were used. All the transformed cell lines contained large T and small t and could multiply efficiently in agar. Only some transformants could develop into tumors. All tumor cells examined had lost both large T and small t. Tumor cells in which the viral genome could still be detected were found together with tumor cells in which the simian virus 40 DNA could no longer be detected. N transformants which displayed the transformed phenotype in a temperature-sensitive manner became temperature insensitive during tumor formation.

scholarly journals Regulation of simian virus 40 gene expression in Xenopus laevis oocytes.

1985 ◽  
Vol 5 (8) ◽  
pp. 2019-2028 ◽  
Author(s):  
T Michaeli ◽  
C Prives
Keyword(s):  
Xenopus Laevis ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
T Antigen ◽  
Oocyte Nucleus ◽  
Xenopus Laevis Oocytes ◽  
Large T Antigen ◽  
Viral Dna ◽  
Infected Monkey ◽  
Sv40 Dna

Expression of the simian virus 40 (SV40) early and late regions was examined in Xenopus laevis oocytes microinjected with viral DNA. In contrast to the situation in monkey cells, both late-strand-specific (L-strand) RNA and early-strand-specific (E-strand) RNA could be detected as early as 2 h after injection. At all time points tested thereafter, L-strand RNA was synthesized in excess over E-strand RNA. Significantly greater quantities of L-strand, relative to E-strand, RNA were detected over a 100-fold range of DNA concentrations injected. Analysis of the subcellular distribution of [35S]methionine-labeled viral proteins revealed that while the majority of the VP-1 and all detectable small t antigen were found in the oocyte cytoplasm, most of the large T antigen was located in the oocyte nucleus. The presence of the large T antigen in the nucleus led us to investigate whether this viral product influences the relative synthesis of late or early RNA in the oocyte as it does in infected monkey cells. Microinjection of either mutant C6 SV40 DNA, which encodes a large T antigen unable to bind specifically to viral regulatory sequences, or deleted viral DNA lacking part of the large T antigen coding sequences yielded ratios of L-strand to E-strand RNA that were similar to those observed with wild-type SV40 DNA. Taken together, these observations suggest that the regulation of SV40 RNA synthesis in X. laevis oocytes occurs by a fundamentally different mechanism than that observed in infected monkey cells. This notion was further supported by the observation that the major 5' ends of L-strand RNA synthesized in oocytes were different from those detected in infected cells. Furthermore, only a subset of those L-strand RNAs were polyadenylated.

Molecular analysis of enhanced replication of UV-damaged simian virus 40 DNA in UV-treated mammalian cells

1988 ◽  
Vol 8 (6) ◽  
pp. 2428-2434
Author(s):  
J M Treger ◽  
J Hauser ◽  
K Dixon
Keyword(s):  
Uv Radiation ◽  
Uv Irradiation ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
Viral Dna ◽  
Repair Capacity ◽  
Pyrimidine Dimers ◽  
Infected Cells ◽  
Replicative Intermediates ◽  
Kinetics Of

Irradiation of simian virus 40 (SV40)-infected cells with low fluences of UV light (20 to 60 J/m2, inducing one to three pyrimidine dimers per SV40 genome) causes a dramatic inhibition of viral DNA replication. However, treatment of cells with UV radiation (20 J/m2) before infection with SV40 virus enhances the replication of UV-damaged viral DNA. To investigate the mechanism of this enhancement of replication, we analyzed the kinetics of synthesis and interconversion of viral replicative intermediates synthesized after UV irradiation of SV40-infected cells that had been pretreated with UV radiation. This enhancement did not appear to be due to an expansion of the size of the pool of replicative intermediates after irradiation of pretreated infected cells; the kinetics of incorporation of labeled thymidine into replicative intermediates were very similar after irradiation of infected control and pretreated cells. The major products of replication of SV40 DNA after UV irradiation at the low UV fluences used here were form II molecules with single-stranded gaps (relaxed circular intermediates). There did not appear to be a change in the proportion of these molecules synthesized when cells were pretreated with UV radiation. Thus, it is unlikely that a substantial amount of DNA synthesis occurs past pyrimidine dimers without leaving gaps. This conclusion is supported by the observation that the proportion of newly synthesized SV40 form I molecules that contain pyrimidine dimers was not increased in pretreated cells. Pulse-chase experiments suggested that there is a more efficient conversion of replicative intermediates into form I molecules in pretreated cells. This could be due to more efficient gap filling in relaxed circular intermediate molecules or to the release of blocked replication forks. Alternatively, the enhanced replication observed here may be due to an increase in the excision repair capacity of the pretreated cells.

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