Genetics of RNA Tumor Viruses

Vogt, Peter K.

doi:10.1007/978-1-4684-2718-9_8

Cited by 105 publications

(83 citation statements)

References 446 publications

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“…The first such oncogene to be identified and characterized was the src gene of Rous sarcoma virus (RSV); convincing evidence has accumulated which indicates that src is responsible for the oncogenicity of RSV (38). It has more recently become clear that the avian acute or defective leukemia viruses (DLVs) also possess oncogenes (25,28,29).…”

mentioning

confidence: 99%

Transcripts from the Cellular Homologs of Retroviral Oncogenes: Distribution Among Chicken Tissues

1982

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The oncogenes (v-oncgenes) of rapidly transforming retroviruses have homologs (c-oncgenes) in the genomes of normal cells. In this study, we characterized and quantitated transcription from four c-oncgenes, c-myb, c-myc, c-erb, and c-src, in a variety of chicken cells and tissues. Electrophoretic analysis of polyadenylated RNA, followed by transfer to nitrocellulose and hybridization to clonedoncprobes showed that c-myb, c-myc, and c-srceach give rise to a single mature transcript, whereas c-erbgives rise to multiple transcripts (B. Vennstrom and J. M. Bishop, Cell, in press) which vary in abundance among different cells and tissues. Transcription from c-myb, c-myc, c-erb, and c-srcwas quantitated by a “dot-blot” hybridization assay. We found that c-myc, c-erb, and c-srctranscription could be detected in nearly all cells and tissues examined, whereas c-mybtranscription was detected only in some hemopoietic cells; these cells, however, belong to several different lineages. Thus, in no case was expression of a c-oncgene restricted to a single cell lineage. There appeared to be a correlation between levels of c-mybexpression and hemopoietic activity of the tissues and cells examined, which suggests that c-mybmay be expressed primarily in immature hemopoietic cells. An examination of c-oncRNA levels in target cells and tissues for viruses carrying the corresponding v-oncgenes revealed no obvious correlation, direct or inverse, between susceptibility to transformation by a given v-oncgene and expression of the homologous c-oncgene.

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confidence: 99%

Transcripts from the Cellular Homologs of Retroviral Oncogenes: Distribution Among Chicken Tissues

1982

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“…There are a large number of murine and avian retroviruses which are capable of cellular transformation and oncogenesis (26). Most of these viruses exercise their oncogenic action by means of a single, transformation-specific protein encoded by the viral genome (14).…”

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confidence: 99%

Mouse cells contain two distinct ras gene mRNA species that can be translated into a p21 onc protein.

Ellis¹,

DeFeo²,

Furth³

et al. 1982

Mol. Cell. Biol.

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The Kirsten (Ki) and Harvey (Ha) strains of murine sarcoma virus encode a 21,000-dalton protein (p21 ras) which is the product of the transforming gene of these viruses. Normal cells express low levels of p21 ras encoded by cellular genes (Ki-ras and Ha-ras) homologous to the Ki and Ha murine sarcoma virus transformation genes. A bone marrow-derived mouse cell line, 416B, has been shown to express unusually high levels of p21 ras. In this manuscript, we investigated the molecular biology of p21 ras gene expression in 416B and other normal mouse cells. We identified four distinct polyadenylated and polysomeassociated RNAs, two related to Ki-ras and two to Ha-ras. The levels in 416B cells of the two Ki-ras RNAs, sized 5.2 and 2.0 kilobases, were both elevated approximately 25-fold over levels found in normal mouse cells; there was no corresponding change in 416B cells in the levels of the two Ha-ras RNAs. We partially purified the two Ki-ras mRNAs and separated them by velocity sedimentation in sucrose density gradients. Both the 5.2-and 2.0-kilobase mRNAs could be translated in vitro into p21 ras. These results show that a cellular onc protein can be translated from two distinct cellular mRNA species.

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“…Collectively, these changes are termed "the transformed phenotype." The establishment and maintenance of all these transformation parameters require the activity of pp6(Yrc, a phosphoprotein which possesses a protein kinase activity (3,6,10,14,15,19,21).…”

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confidence: 99%

Phosphorylation of a 36,000 Mr cellular protein in cells infected with partial transformation mutants of rous sarcoma virus.

Nakamura¹,

Weber²

1982

Mol. Cell. Biol.

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We have isolated and characterized mutants of Rous sarcoma virus which induce some parameters of transformation but fail to fully induce other parameters. We believe these mutants code for a pp60src which phosphorylates some targets well but phosphorylates others poorly. Using these mutants, we examined the phosphorylation of a 36,000 Mr protein which is phosphorylated on a tyrosine in cells transformed by Rous sarcoma virus, in an attempt to correlate this phosphorylation with the expression of specific transformation parameters. We found that phosphorylation of the 36,000 Mr protein was neither necessary nor sufficient for loss of fibronectin or for loss of density-dependent inhibition of growth. Phosphorylation of the protein was not sufficient for morphological alterations, increased hexose transport, or loss of adhesiveness. For the parameters measured, the best correlation was with increased plasminogen activator. In addition, it is noteworthy that cells infected with the mutant CU2 displayed low levels of phosphorylation of the 36,000 Mr protein and also were deficient in anchorage-independent growth and tumorigenicity, raising the possibility that the phosphorylation of the 35,000 Mr protein may be required for malignant growth properties.

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Genetics of RNA Tumor Viruses

Cited by 105 publications

References 446 publications

Transcripts from the Cellular Homologs of Retroviral Oncogenes: Distribution Among Chicken Tissues

Transcripts from the Cellular Homologs of Retroviral Oncogenes: Distribution Among Chicken Tissues

Mouse cells contain two distinct ras gene mRNA species that can be translated into a p21 onc protein.

Phosphorylation of a 36,000 Mr cellular protein in cells infected with partial transformation mutants of rous sarcoma virus.

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