High-Frequency C-Type Virus Induction by Inhibitors of Protein Synthesis

Aaronson, Stuart A.; Dunn, Claire Y.

doi:10.1126/science.183.4123.422

Cited by 101 publications

(37 citation statements)

References 30 publications

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“…The return to the virus-restricted state following cycloheximide induction was much more rapid than has previously been shown with virus activation by another class of inducers, halogenated pyrimidines. With these latter drugs, type-C virus release from BALB/c cells begins within 24-48 hr and peaks at around 72 hr; however, the cells remain virus-activated at high frequency for several more days (12,16).…”

Section: Methodsmentioning

confidence: 99%

“…Activated sarcoma virus was measured in tissue culture fluids as previously described (16). An infectious center assay to quantitate the fraction of sarcoma virus-activated cells has also been reported (9,16 formamide, 1 mM EDTA, 15 mM Tris -HC1, pH 7.5, and 150 mM NaCl. Hybridization was assayed with nuclease S-1 (19,20).…”

Section: Methodsmentioning

confidence: 99%

“…(9,13,14,16). Activated sarcoma virus was measured in tissue culture fluids as previously described (16).…”

Section: Methodsmentioning

confidence: 99%

“…Thus, study of the mechanisms involved in cellular regulation of naturally integrated type-C viral genes may be of importance in the development of methods to prevent expression of their malignant potential. In a recent report, several chemicals that inhibit different steps in protein synthesis in eukaryotes have been demonstrated to induce type-C virus at high frequency from virus-negative mouse cells (9). In the present studies, the mechanism of action of one of these chemicals, cycloheximide, has been investigated.…”

mentioning

confidence: 99%

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Induction of Type-C RNA Virus by Cycloheximide: Increased Expression of Virus-Specific RNA

Aaronson

Anderson

Dunn

et al. 1974

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

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Mouse cells contain the genetic information for multiple endogenous type-C RNA viruses. The mechanisms by which the cell controls expression of these naturally integrated viruses are not yet known. Recently, chemicals that inhibit protein synthesis have been sl-Gwn to induce a specific type-C virus at high frequenc, f rom BALB/c mouse embryo cells. In the present studie'z. virus activation in response to a representative trans"I;inal inhibitor, cycloheximide, is demonstrated to be I i ansient, with virus release primarily occurring within the first 12-24 hr following drug exposure. Analysis of virus-specific RNA in cells by molecular hybridization revealed an absolute increase in viral RNA concentration in cycloheximide-treated cells. This was blocked by simultaneous exposure of the cells to actinomycin D. Further, inhibition of RNA synthesis during but not subsequent to cycloheximide exposure prevented virus activation. These findings show that virus induction by cycloheximide requires de novo RNA synthesis during but not after drug exposure and suggest that the required RNA species may be that of the virus itself. The present results are consistent with the hypothesis that translational inhibitors prevent synthesis of a labile protein whose normal action is to inhibit viral RNA transcription or to cause degradation of viral RNA.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

“…(9,13,14,16). Activated sarcoma virus was measured in tissue culture fluids as previously described (16).…”

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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Induction of Type-C RNA Virus by Cycloheximide: Increased Expression of Virus-Specific RNA

Aaronson

Anderson

Dunn

et al. 1974

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

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“…Because ecotropic virus spread cannot occur in mink cells, the confluent cells were next treated with mitomycin C (10 gg/ml) for 2 h, and were then trypsinized and co-cultivated with NIH/3T3 cells (passage 2). Mitomycin C prevents the mink cells from undergoing further cellular division; however, since there is only a gradual cytocidal effect, virus production (if initiated) may continue for several days (Aaronson & Dunn, 1974). The ratio of mink cells to NIH/3T3 cells could be varied and ratios of 3 : 1, 1 : 1 and 1 : 3 were equally effective (data not shown).…”

Section: Treatment Of Recipient Cells With Metaphase Chromosomes Frommentioning

confidence: 93%

Transfer of Murine Leukaemia and Murine Sarcoma Virus Genetic Information by Transfection with Isolated Metaphase Chromosomes

Levin

Hughes²,

Graeter

et al. 1982

Journal of General Virology

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SUMMARYChromosome-mediated transfer of murine leukaemia (MuLV) and murine sarcoma (MuSV) virus genetic information to uninfected recipient cells was investigated. Metaphase chromosomes from AKR MuLV-infected SC-1 mouse cells were incubated with NIH/3T3 cells. After several passages (1 to 3 weeks), infectious virions exhibiting reverse transcriptase activity and the characteristic host range of ecotropic, N-tropic AKR virus appeared in the supernatant fluids of the treated cells. Restriction endonuclease analysis of genomic DNA from transfected cells indicated that AKR proviral DNA was associated with the high molecular weight DNA of the host. These results demonstrate that the AKR MuLV genome can be stably transferred to uninfected recipient cells via isolated metaphase chromosomes. Although AKR virions are not able to infect heterologous cells, chromosomemediated transfection resulted in the establishment of productive AKR MuLV infection in mink cells. Thus, the use of chromosomes to transfer virus genes can circumvent the natural host restriction barrier. In other experiments, it was shown that normal NIH/3T3 cells were transformed after exposure to metaphase chromosomes isolated from an MuSV-infected, non-producer line. Foci were detected 14 to 21 days after chromosome treatment and were shown to contain true viral transformants since transforming virus was produced after superinfection with MuLV.

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Actinomycin‐D‐resistant in vitro mouse cell line derived from a methylcholanthrene‐induced sarcoma: Decrease of malignancy and antigenic characteristics

Belehradek

Biedler

Thonier

et al. 1974

Intl Journal of Cancer

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The tumorigenic EPO clonal cell line, derived from a methylcholanthrene-induced murine sarcoma, was exposed to increasing concentrations of actinomycin D and gave rise to a subline, resistant to 0.02 mug of actinomycin D per ml of medium, which was designated EPO/ADj. Drug resistance was accompained by a striking decrease of tumorigenic capacity as determined by the tumor take incidence and tumor growth rate in syngeneic C57BL/6 mice (normal and X-irradiated), as well as by tumor take incidence in the cheek pouch of cortisone-treated weanling Syrian hamsters. One of the tumors obtained after inoculation of EPO/ADj cells into syngeneic mice was reexplanted in culture and developed as the EPO/ADj/T subline. It was found to be relatively resistant to actinomycin D as compared to the parental EPO cells. The morphology of cells changed with actinomycin-D-resistance: EPO/ADj cells were more spread and flattened and less overlapping than the original fibroblast-like EPO cells. EPO/ADj/T cells, however, had an aspect similar to that of EPO cells. No major differences were seen between the karyotypes of EPO, EPO/ADj and EPO/ADj/T cells. Tumor-specific antigen(s), characteristic of drug-sensitive, parental EPO line, was expressed in the resistant EPO/ADj and EPO/ADj/T lines, as shown by: (a) transplantation resistance to challenge with EPO cells in syngeneic mice pretreated with EPO/ADj cells; and (b) cross-reactivity in indirect immunofluorescence tests performed with sera from syngeneic animals hyperimmunized with EPO or EPO/ADj cells. Furthermore, an additional surface antigen(s), absent from EPO cells, was demonstrated in EPO/ADj and EPO/ADj/T cells by means of immunofluorescence tests performed with specific anti-EPO/ADj syngeneic sera previously absorbed on EPO or EPO/ADj cells.

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High-Frequency C-Type Virus Induction by Inhibitors of Protein Synthesis

Cited by 101 publications

References 30 publications

Induction of Type-C RNA Virus by Cycloheximide: Increased Expression of Virus-Specific RNA

Induction of Type-C RNA Virus by Cycloheximide: Increased Expression of Virus-Specific RNA

Transfer of Murine Leukaemia and Murine Sarcoma Virus Genetic Information by Transfection with Isolated Metaphase Chromosomes

Actinomycin‐D‐resistant in vitro mouse cell line derived from a methylcholanthrene‐induced sarcoma: Decrease of malignancy and antigenic characteristics

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