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.

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.

Induction of cellular deoxyribonucleic acid synthesis in butyrate-treated cells by simian virus 40 deoxyribonucleic acid

1981 ◽  
Vol 1 (11) ◽  
pp. 1038-1047
Author(s):  
S Kawasaki ◽  
L Diamond ◽  
R Baserga
Keyword(s):  
Ribonucleic Acid ◽  
Deoxyribonucleic Acid ◽  
Simian Virus 40 ◽  
Acid Synthesis ◽  
Simian Virus ◽  
S Phase ◽  
Temperature Sensitive ◽  
3T3 Cells ◽  
Deoxyribonucleic Acid Synthesis ◽  
G1 Cells

Sodium butyrate (3 mM) inhibited the entry into the S phase of quiescent 3T3 cells stimulated by serum, but had no effect on the accumulation of cellular ribonucleic acid. Simian virus 40 infection or manual microinjection of cloned fragments from the simian virus 40 A gene caused quiescent 3T3 cells to enter the S phase even in the presence of butyrate. NGI cells, a line of 3T3 cells transformed by simian virus 40, grew vigorously in 3 mM butyrate. Homokaryons were formed between G1 and S-phase 3T3 cells, Butyrate inhibited the induction of deoxyribonucleic acid synthesis that usually occurs in B1 nuclei when G1 cells are fused with S-phase cells. However, when G1 3T3 cells were fused with exponentially growing NGI cells, the 3T3 nuclei were induced to enter deoxyribonucleic acid synthesis. In tsAF8 cells, a ribonucleic acid polymerase II mutant that stops in the G1 phase of the cell cycle, no temporal sequence was demonstrated between the butyrate block and the temperature-sensitive block. These results confirm previous reports that certain virally coded proteins can induce cell deoxyribonucleic acid synthesis in the absence of cellular functions that are required by serum-stimulated cells. Our interpretation of these data is that butyrate inhibited cell growth by inhibiting the expression of genes required for the G0 leads to G1 leads to S transition and that the product of the simian virus 40 A gene overrode this inhibition by providing all of the necessary functions for the entry into the S phase.

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 Activation of the simian virus 40 (SV40) genome abrogates sensitivity to AVP in a rabbit collecting tubule cell line by repressing membrane expression of AVP receptors.

1991 ◽  
Vol 113 (4) ◽  
pp. 951-962 ◽  
Author(s):  
D Prié ◽  
P M Ronco ◽  
B Baudouin ◽  
M Géniteau-Legendre ◽  
M Antoine ◽  
...  
Keyword(s):  
Cell Line ◽  
Simian Virus 40 ◽  
Temperature Shift ◽  
Simian Virus ◽  
Temperature Sensitive ◽  
Membrane Expression ◽  
Cell Content ◽  
Collecting Tubule ◽  
Sv40 Genome ◽  
Transformed Cell Lines

To analyze the role of SV40 genome in the phenotypic alterations previously observed in SV40-transformed cell lines, we infected rabbit renal cortical cells with a temperature-sensitive SV40 mutant strain (tsA58) and compared the cell phenotypes at temperatures permissive (33 degrees C) and restrictive (39.5 degrees C) for SV40 genome expression. At both temperatures, the resulting cell line (RC.SVtsA58) expresses cytokeratin and uvomorulin, but epithelial differentiation is more elaborate at 39.5 degrees C as shown by the formation of a well-organized cuboidal monolayer with numerous tight junctions and desmosomes. Functional characteristics are also markedly influenced by the culture temperature: cells grown at 33 degrees C respond only to isoproterenol (ISO, 10(-6) M) by a sevenfold increase in cAMP cell content above basal values; in contrast, when transferred to 39.5 degrees C, they exhibit increased sensitivity to ISO (ISO/basal: 19.1) and a dramatic response to 10(-7) M dDarginine vasopressin (dDAVP/basal: 18.2, apparent Ka: 5 X 10(-9) M) which peaks 48 h after the temperature shift. The latter is associated with membrane expression of V2-type AVP receptors (approximately 50 fmol/10(6) cells) which are undetectable when SV40 genome is activated (33 degrees C). Clonal analysis, additivity studies, and desensitization experiments argue for the presence of a single cell type responsive to both AVP and ISO. The characteristics of the RC. SVtsA58 cell line at 39.5 degrees C (effector-stimulated cAMP profile, lack of expression of brush-border hydrolases and Tamm-Horsfall protein) suggest that it originates from the cortical collecting tubule, and probably from principal cells.

Efficient transformation of human fibroblasts by adenovirus-simian virus 40 recombinants

1984 ◽  
Vol 4 (8) ◽  
pp. 1653-1656
Author(s):  
K Van Doren ◽  
Y Gluzman
Keyword(s):  
Cell Lines ◽  
Human Fibroblasts ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
T Antigen ◽  
Origin Of Replication ◽  
Viral Dna ◽  
Early Region ◽  
Transformed Cell Lines ◽  
Sv40 Dna

The origin-defective simian virus 40 (SV40) mutant 6-1 has been useful in transforming human cells (Small et al., Nature [London] 296:671-672, 1982; Nagata et al., Nature [London] 306:597-599, 1983). However, the low efficiency of transformation achieved by DNA transfection is a major drawback of the system. To increase the efficiency of SV40-induced transformation of human fibroblasts, we used recombinant adenovirus-SV40 virions which contain a complete SV40 early region including either a wild-type or defective (6-1) origin of replication. The SV40 DNA was cloned into the adenovirus vector in place of early region 1. Cell lines transformed by viruses containing a functional origin of replication produced free SV40 DNA. These cell lines were subcloned, and some of the subclones lost the ability to produce free viral DNA. Subclones that failed to produce free viral DNA were found to possess a mutated T antigen. Cell lines transformed by viruses containing origin-defective SV40 mutants did not produce any free DNA. Because of the high efficiency of transformation, we suggest that the origin-defective chimeric virus is a convenient system for establishing SV40-transformed cell lines from any human cell type that is susceptible to infection by adenovirus type 5.

scholarly journals No activation of new initiation points for deoxyribonucleic acid replication in BALB/c 3T3 cells transformed by Kirsten sarcoma virus.

1981 ◽  
Vol 1 (8) ◽  
pp. 763-768
Author(s):  
A Oppenheim ◽  
A T Horowitz
Keyword(s):  
Deoxyribonucleic Acid ◽  
Simian Virus 40 ◽  
Soft Agar ◽  
Simian Virus ◽  
3T3 Cells ◽  
Barr Virus ◽  
Murine Sarcoma Virus ◽  
Sarcoma Virus ◽  
Epstein Barr ◽  
Transformed Cell Lines

BALB/c 3T3 cells were transformed by Kirsten sarcoma virus, and five clones were isolated in soft agar. Average replicon sizes of the transformed cell lines were estimated by the method of fiber-autoradiography (J. A. Huberman and A. D. Riggs, J. Mol. Biol.32:327-341, 1968) and found to be the same size as the nontransformed 3T3 cells, analyzed in parallel. The results indicate that, unlike simian virus 40 and Epstein-Barr virus, Kirsten sarcoma virus does not activate new initiation points for cellular deoxyribonucleic acid replication in murine sarcoma virus-transformed BALB/c 3T3 cells.

scholarly journals Induction of cellular deoxyribonucleic acid synthesis in butyrate-treated cells by simian virus 40 deoxyribonucleic acid.

1981 ◽  
Vol 1 (11) ◽  
pp. 1038-1047 ◽  
Author(s):  
S Kawasaki ◽  
L Diamond ◽  
R Baserga
Keyword(s):  
Ribonucleic Acid ◽  
Deoxyribonucleic Acid ◽  
Simian Virus 40 ◽  
Acid Synthesis ◽  
Simian Virus ◽  
S Phase ◽  
Temperature Sensitive ◽  
3T3 Cells ◽  
Deoxyribonucleic Acid Synthesis ◽  
G1 Cells

Sodium butyrate (3 mM) inhibited the entry into the S phase of quiescent 3T3 cells stimulated by serum, but had no effect on the accumulation of cellular ribonucleic acid. Simian virus 40 infection or manual microinjection of cloned fragments from the simian virus 40 A gene caused quiescent 3T3 cells to enter the S phase even in the presence of butyrate. NGI cells, a line of 3T3 cells transformed by simian virus 40, grew vigorously in 3 mM butyrate. Homokaryons were formed between G1 and S-phase 3T3 cells, Butyrate inhibited the induction of deoxyribonucleic acid synthesis that usually occurs in B1 nuclei when G1 cells are fused with S-phase cells. However, when G1 3T3 cells were fused with exponentially growing NGI cells, the 3T3 nuclei were induced to enter deoxyribonucleic acid synthesis. In tsAF8 cells, a ribonucleic acid polymerase II mutant that stops in the G1 phase of the cell cycle, no temporal sequence was demonstrated between the butyrate block and the temperature-sensitive block. These results confirm previous reports that certain virally coded proteins can induce cell deoxyribonucleic acid synthesis in the absence of cellular functions that are required by serum-stimulated cells. Our interpretation of these data is that butyrate inhibited cell growth by inhibiting the expression of genes required for the G0 leads to G1 leads to S transition and that the product of the simian virus 40 A gene overrode this inhibition by providing all of the necessary functions for the entry into the S phase.

Sign in / Sign up

Export Citation Format

Share Document