A Simplifying Concept in Tumor Virology: Virus-specific "Pleiotropic Effectors"

Weil, Roger; Salomon, Ewa; May, Evelyne; May, Pierre

doi:10.1101/sqb.1974.039.01.050

Cited by 85 publications

(65 citation statements)

References 38 publications

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“…SV40 infection and the addition of serum are known to induce cells, which have been arrested in GI by culture in low serum, to cycle and synthesize cellular DNA (54). As shown in Table 1, the overall uptake of thymidine was increased in serum-induced and lowered in SV40-induced cells, and these differences are probably due to differences in thymidine transport.…”

Section: Muntjacmentioning

confidence: 98%

“…Viral DNA replication is dependent upon the host cell cycle (25,36,42) and specifically upon an event at the very beginning of the S phase (24). T antigen, whose synthesis, like that for a cellular initiator protein(s), preceeds the onset of cellular and viral DNA synthesis (7,54), has been shown to accumulate during the prereplicative phase of the cell cycle (56). While the presence of T antigen is not sufficient to initiate the first round of cellular or viral DNA replication (24,28), a critical number of T antigen molecules, which nonpermissive cells fail to accumulate (26), appears to be required to initiate multiple rounds of viral DNA synthesis (32).…”

Section: Ca186%mentioning

confidence: 99%

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SV40‐Infected muntjac cells: Cell cycle kinetics, cell ploidy and T antigen concentration

Gershey

1980

Cytometry

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Muntjac cells in which the SV40 virus neither readily causes transformation nor replicates were used to study the effect of SV40 infection on cell ploidy and the influence of ploidy on the concentration of T antigen, which is required for the initiation of viral DNA synthesis. Both the DNA content, as measured by flow microfluorometry of propidium iodide-DNA fluorescence, and the average number of chromosomes per cell indicated that infection with SV40 did not alter the ploidy of the host cell. SV40 infection had no effect on the ploidy distribution of muntjac cells. After immunofluorescence staining with anti-T serum and fluorosceinlabeled anti-yG, infected and uninfected cultures were compared. In uninfected cells incubated with a 1:20 dilution of anti-T serum no fluorescence could be observed by fluorescence microscopy, but when examined by flow microfluorometry, fluorescence was detected after staining with as little as 1000-fold diluted antiserum. Determination of the amount of T antigen and DNA content in the same cell by simultaneous measurement of fluorescein isothiocyanate-conjugate and propidium iodide fluorescence, indicated that the cellular concentration of T antigen did not vary with the ploidy of the genome or the number of nuclei per cell. These results suggest that gene dosage is not a factor which determines the permissive environment for SV40 replication. Key terms: Flow microfluorometry, SV40, virus-host cell interactionsWe have previously reported that a viral regulatory protein, SV40 T antigen, binds to the chromosomes of muntjac cells (13). It is known that SV40 T antigen is required for the reinitiation of each round of viral DNA replication (32, 50), but the functional significance of its binding to the chromosomes of cells in which SV40 does not replicate remains unclear. By comparison with the chromosome banding pattern visualized by quinacrine staining, it appears that T antigen is binding near AT-rich regions of the DNA (14). Such bands have been associated with units of cellular DNA replication (33). AT clusters are common to sequences at or near the origins for DNA replication as has been shown by nucleotide sequencing of papovaviruses (15,22,49), adenoviruses (52), parvoviruses (2) and bacteriophages (31,39,43).

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Section: Muntjacmentioning

confidence: 98%

Section: Ca186%mentioning

confidence: 99%

SV40‐Infected muntjac cells: Cell cycle kinetics, cell ploidy and T antigen concentration

Gershey

1980

Cytometry

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“…to the S phase of the cell cycle (3,4). In addition to providing a partially synchronous cell system, the induction of cell cycle changes by polyoma virus can be related to the expression of specific viral genes (4,5).…”

mentioning

confidence: 99%

“…Infection of these resting cells induces a number of metabolic changes which cause a progression from the G1 (or Go) phase Abbreviations: ODC, L-ornithine decarboxylase; SAMD, S-adenosyl-L-methionine decarboxylase; FdUrd, 5-fluorodeoxyuridine; AMD, actinomycin D; CHI, cycloheximide; MEM, minimum essential medium; Pu, putrescine; Spd, spermidine; Sp, spermine. to the S phase of the cell cycle (3,4). In addition to providing a partially synchronous cell system, the induction of cell cycle changes by polyoma virus can be related to the expression of specific viral genes (4,5).…”

mentioning

confidence: 99%

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Biphasic stimulation of polyamine biosynthesis in primary mouse kidney cells by infection with polyoma virus:uncoupling from DNA and rRNA synthesis.

Goldstein¹,

Heby²,

Marton³

1976

Proc. Natl. Acad. Sci. U.S.A.

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Infection of primary cultures of mouse kidney cells with polyoma virus causes a biphasic increase in the activities of L-ornithine decarboxylase (ODC; L-ornithine carboxy-lyase; EC 4.1.1.17) and S-adenosyl-L-methionine decarboxylase (SAMD; S-adenosyl-L-methionine carboxy-lyase; EC 4.1.1.50), as well as in the level of the polyamines putrescine, spermidine, and spermine. An and cycloheximide suggest that the formation of ODC is subject to post-transcriptional control, whereas that of SAMD is regulated primarily at the transcriptional level. In recent years a great deal of interest has been focused on the metabolism of the polyamines during normal and neoplastic growth (1). A principal finding has been that stimulation of polyamine synthesis is associated with a shift from a quiescent to a proliferating state. In fact, the rate of polyamine synthesis shows a high correlation with the rate of cell proliferation (2). In vitro, the polyamines can stimulate cell proliferation and when added to cell-free systems they can stimulate DNA, RNA, and protein synthesis (1). Nevertheless, in vivo the precise function of the polyamines has remained for the most part obscure.In an attempt to understand the mechanisms involved in the regulation of polyamine synthesis, we have examined the rate of synthesis and the concentration of the polyamines in primary mouse kidney cell cultures infected with polyoma virus. Infection of these resting cells induces a number of metabolic changes which cause a progression from the G1 (or Go) phase Abbreviations: ODC, L-ornithine decarboxylase; SAMD, S-adenosyl-L-methionine decarboxylase; FdUrd, 5-fluorodeoxyuridine; AMD, actinomycin D; CHI, cycloheximide; MEM, minimum essential medium; Pu, putrescine; Spd, spermidine; Sp, spermine. to the S phase of the cell cycle (3, 4). In addition to providing a partially synchronous cell system, the induction of cell cycle changes by polyoma virus can be related to the expression of specific viral genes (4, 5).MATERIALS AND METHODS Primary mouse kidney cells were prepared from 9-day-old Swiss Webster Ha/ICR mice (6). Cells were plated in 100 mm plastic petri dishes and grown to confluence as monolayers in Eagle's minimum essential medium (MEM), supplemented with 10% calf serum, 40,ug/ml of Garamycin (Schering), and 1.0 ,ug/ml of Fungizone (Flow Labs). The polyoma virus inoculum was the small plaque variant derived from cultured kidney cells of infected weanling mice (6).For infection, growth medium was removed from the cell monolayer and 0.4 ml of a polyoma virus suspension (50-100 PFU per cell) was added for 2 hr at 370. After adsorption of the virus, the cells were washed and overlaid with 5 ml of Eagle's MEM containing 2% dialyzed horse serum. In some experiments the overlay medium also contained either 5-fluorodeoxyuridine (FdUrd) (15 ,g/ml), actinomycin D (AMD) (0.05 or 10 gg/ml) or cycloheximide (CHI) (15 Ig/ml). When inhibitors were added at later times after infection, 50 ,l was added to the medium from a 100 times concentrated stock soluti...

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Interspecies‐, species‐ and type‐specific T antigenic determinants of human papovaviruses (JC and BK) and of simian virus 40

Beth

Cikes

Schloen

et al. 1977

Intl Journal of Cancer

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Immunofluorescence tests, absorption studies and quantitative analysis by a very sensitive 51Cr microcomplement fixation (CF) technique were used to define the degree of relatedness between the tumor (T) antigens induced by human papovaviruses, strain JC and BK, with simian virus 40(SV40) and mouse polyoma virus (PyV). Antisera against JCV, BKV, SV40 and PyV T were raised in tumor-bearing hamsters. The data obtained indicate that T antigens of JCV, BKV and SV40 possess various subspecificities which can be distinguished and looked upon as interspecies-, species- and type-specific antigenic determinants. It was found that JCV T and BKV T synthesized in transformed hamster cells share about the same amount (20%) of interspecies cross-reacting antigen with SV40 T from H-50 cell extracts (transformed hamster cells). Although hamster cells transformed by PyV showed definite PyV T reactivity, no cross-reactivity, at least with the sera used, was found with human papovavirus and SV40 T antigens. Furthermore, degree of heterogeneity was observed within the T antigen complex derived from different SV40-transformed cells.

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A Simplifying Concept in Tumor Virology: Virus-specific "Pleiotropic Effectors"

Cited by 85 publications

References 38 publications

SV40‐Infected muntjac cells: Cell cycle kinetics, cell ploidy and T antigen concentration

SV40‐Infected muntjac cells: Cell cycle kinetics, cell ploidy and T antigen concentration

Biphasic stimulation of polyamine biosynthesis in primary mouse kidney cells by infection with polyoma virus:uncoupling from DNA and rRNA synthesis.

Interspecies‐, species‐ and type‐specific T antigenic determinants of human papovaviruses (JC and BK) and of simian virus 40

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