Regulation of Expression of the Integrated Retrovirus Genome

Weinberg, Robert A.; Steffen, David L.

doi:10.1099/0022-1317-54-1-1

Cited by 9 publications

(4 citation statements)

References 27 publications

(32 reference statements)

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“…All transformed nonproducer cells were found to express high levels of both viral RNA and p21 transforming protein (at least 10to 30-fold higher than endogenous mouse ras expression) with little variation between cell lines. This lack of variation was somewhat unexpected and contrasts markedly with results of studies on the expression of other retrovirus proviruses (5,17,41). We can envisage two explanations to account for this observation.…”

Section: Discussioncontrasting

confidence: 60%

Expression of Kirsten murine sarcoma virus in transformed nonproducer and revertant NIH/3T3 cells: evidence for cell-mediated resistance to a viral oncogene in phenotypic reversion

Norton¹,

Cook²,

Roberts³

et al. 1984

J Virol

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Expression of the provirus in a clonally related series of Kirsten murine sarcoma virus-transformed NIH/ 3T3 nonproducer cell lines was examined at both the transcriptional and translational levels. All cells expressed high levels of genome-sized viral RNA with little variation between cell lines despite differences in provirus integration site and copy number. Expression of K-ratis RNA was estimated to be at least 10to 20-fold higher than that of the mouse cellular homolog of the viral transforming gene. Levels of the viruscoded transforming protein, p21, were similarly elevated, with little variation between nonproducer cells. In two revertant cell lines containing a normal provirus and a rescuable transforming gene, no impairment in expression at either the transcriptional or translational level was found. After superinfection with Kirsten murine sarcoma virus, one revertant became more tumorigenic. whereas the other remained nontumorigenic. These results show that cell transformation by Kirsten murine sarcoma virus is invariably associated with elevated expression of the virus-coded oncogene and that one of the revertants is resistant to the action of the viral transforming gene.

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Section: Discussioncontrasting

confidence: 60%

Expression of Kirsten murine sarcoma virus in transformed nonproducer and revertant NIH/3T3 cells: evidence for cell-mediated resistance to a viral oncogene in phenotypic reversion

Norton¹,

Cook²,

Roberts³

et al. 1984

J Virol

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“…It is generally found that actively transcribing genes are undermethylated compared to inactive genes (for review, see Doerfler, 1981) and the same appears to be true for retrovirus proviruses (Guntaka et al, 1980;Weinberg & Steffen, 1981 ;Montandon et al, 1982;Hoffmann et aL, •982). However, it is not known to what extent the site of integration can influence the methylation status of proviral DNA.…”

Section: Discussionmentioning

confidence: 99%

Integration of Proviral DNA in Kirsten Murine Sarcoma Virus-infected Mouse Fibroblasts

Norton

Avery

1984

Journal of General Virology

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SUMMARYThe structure and sites of integration of proviral DNA were studied in 19 clonally related Kirsten murine sarcoma virus-transformed non-producer NIH/3T3 cell lines. The majority of these cell lines contained a single provirus, inserted colinearly with respect to unintegrated linear viral DNA, and lacking detectable methylation at MspI/HpaII sites. Although all proviruses were located at distinct integration sites in the host cell genome, the possible existence of similarities between some adjacent host flanking sequences, suggested from restriction mapping data, could not be ruled out. In three phenotypically reverted cell lines no change in either proviral DNA or adjacent host flanking sequences was detectable. In addition, the revertant proviruses lacked detectable methylation at Mspl/HpaII sites. These findings suggest that changes in cellular function(s) may be responsible for loss of transformed phenotype in these cells.

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“…Expression of the viral proteins coded by the endogenous virus is under the control of many host factors including the differentiated state of the cell and hormonal factors (Weinberg & Steffen, 1981). It is, however, possible to induce the production of this endogenous virus by treatment of cells with various nucleotide analogues.…”

Section: Use Of Host Cell Fabricmentioning

confidence: 99%

Viruses–exploiters or dependants of the host?

Newton

1982

Parasitology

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Viruses are frequently referred to as the supreme parasites and yet it is now more than 20 years since any paper on this topic was published inParasitology. This deficiency probably reflects the great emphasis placed during the last two decades on those aspects of virology christened by Sir Christopher Andrewes ‘dream virology’ (Andrewes, 1973), namely the molecular and genetic properties of viruses, in contrast to the more clinical and biological aspects of ‘steam’ virology. Many modern virologists select a virus as a convenient model system with which to investigate such things as genetic organization or control of transcription, with little regard for the interaction with the host cell that supports its replication. Paradoxically, it is this very emphasis on the detailed molecular mechanisms of virus replication that has now put us in a better position to understand the relationships between these highly specialized parasites and their host systems than for any other type of parasite. Recent advances in cell biology coupled with an understanding of the molecular basis of viral replicative mechanisms mean that new insight is possible into the interactions of a virus with its host. For example, we are just beginning to appreciate why a virus should infect one individual and not another, or why it should multiply only in certain tissues at certain stages of development of a multicellular organism. Indeed, study of such tropisms may frequently tell us as much about the host cell as about the virus.

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Regulation of Expression of the Integrated Retrovirus Genome

Cited by 9 publications

References 27 publications

Expression of Kirsten murine sarcoma virus in transformed nonproducer and revertant NIH/3T3 cells: evidence for cell-mediated resistance to a viral oncogene in phenotypic reversion

Expression of Kirsten murine sarcoma virus in transformed nonproducer and revertant NIH/3T3 cells: evidence for cell-mediated resistance to a viral oncogene in phenotypic reversion

Integration of Proviral DNA in Kirsten Murine Sarcoma Virus-infected Mouse Fibroblasts

Viruses–exploiters or dependants of the host?

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