Transforming capacities and defectiveness of avian leukemia viruses OK10 and E26

Graf, Thomas; Oker-Blom, N; Тодоров, Т.; Beug, Hartmut

doi:10.1016/0042-6822(79)90024-2

Cited by 72 publications

(31 citation statements)

References 12 publications

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“…1A). By comparison, medium of a culture infected with nondefective OKAV (5,8) and labeled in the same way as the nonproducer culture produced a sharp peak of OKAV 32P-labeled virions at a density of 1.18 g/ml that contained about 10-fold more radioactivity per isotope added to the culture than the peak obtained from medium of nonThe publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisment" in accordance with 18 (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…DVP production by OK10-transformed quail nonproducer cells (5,8) was monitored by subjecting the growth media of cultures labeled with 32P043-for 6 hr to standard procedures used for the purification of infectious avian tumor viruses (9,21,22). 32P-Labeled material banding between 1.15 and 1.19 g/ml with a broad peak at 1.17 g/ml was released by OK10-transformed nonproducer cells (Fig.…”

Section: Resultsmentioning

confidence: 99%

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OK10, an avian acute leukemia virus of the MC29 subgroup with a unique genetic structure

Bister

Ramsay

Hayman

et al. 1980

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

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The RNA of defective avian acute leukemia virus OK1O was isolated from a defective virus particle, released by OK10-transformed nonproducer avian fibroblasts, as a 60S complex consisting of 8.6-kilobase subunits. Oligonucleotide fingerprinting and RNA cDNA hybridization identified two sets of sequences in OK1O RNA: group-specific sequences, which are related to all nondefective members of the avian tumor virus group, and a sequence closely related to the subgroup-specific sequences (mcv) of the myelocytomatosis virus (MC29) subgoup of avian acute leukemia viruses. Hence, OK1O is classified as a member of the MC29 subgroup of avian tumor viruses, in agreement with classification based on its oncogenic spectrum. The group-specific sequences of OK1O RNA include partial (A) pol and env genes, a c-region, and, unlike those of all other members of the MC29 subgroup, a complete gag gene. Oligonucleotide mapping revealed 5'-gag-Apol-mcv-Aenv-c-3' as the order of the subgroup-specific and group-specific elements of OK1O RNA. The genetic unit gag-Apol-mcv, measuring ;6.4 kilobases, codes for the nonstructural, presumably transforming,

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

OK10, an avian acute leukemia virus of the MC29 subgroup with a unique genetic structure

Bister

Ramsay

Hayman

et al. 1980

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

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“…Furthermore, 'blood smear analysis shows a preponderance of immature cells of erythroid origin (5,6). Cells from the buffy coat were cultured in vitro and grew within a period of [3][4][5][6][7][8] electrophoresis and RNA fractions were hybridized to cloned AMV-specific proviral DNA. Specific hybridization was observed with the 5.7-kb RNA component and smaller degradation products but not with the 8.5-kb E26AV RNA (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Subsequently, on the basis of in vitro transformation assays and in vivo studies it was proposed to reclassify E26 as a myeloblastosis virus (2)(3)(4). However, recent analyses of differentiation parameters of leukemic cells from chicken and quail clearly indicated that, in vivo, the primary hematopoietic target cell for E26 belongs to the erythroid lineage but also includes some myeloid cells (5,6).…”

mentioning

confidence: 99%

Acute leukemia viruses E26 and avian myeloblastosis virus have related transformation-specific RNA sequences but different genetic structures, gene products, and oncogenic properties

Bister

Nunn

Moscovici

et al. 1982

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

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Replication-defective acute leukemia viruses E26 and myeloblastosis virus (AMV) cause distinct leukemias although they belong to the same subgroup of oncogenic avian tumor viruses based on shared transformation-specific (onc) RNA sequences. E26 causes predominantly erythroblastosis in chicken and in quail, whereas AMV induces a myeloid leukemia. However, upon cultivation in vitro for >1 month, a majority of surviving hemopoietic cells of E26-infected animals bear myeloid markers similar to those of AMV-transformed cells. We have analyzed the genetic structure and gene products of E26 virus for a comparison with those of AMV. An E26/helper virus complex was found to contain two RNA species: a 5.7-kilobase (kb) RNA that hybridizes with cloned AMV-specific proviral DNA and hence is probably the E26 genome; and an 8.5-kb RNA that is unrelated to AMV and represents helper virus RNA. Thus, E26 RNA is smaller than 7.5-kb AMV RNA. Hybridization of size-selected poly(A)-terminating E26 RNA fragments with AMV-specific DNA indicated that the shared specific sequences are located in the 5' half of the E26 genome as opposed to a 3' location in AMV RNA. In nonproducer cells transformed in vitro by E26, a gag-related nonstructural 135,000-dalton protein (p135) was found. No gag (Pr76) or gag-pol (Prl80) precursors of essential virion proteins, which are present in AMV nonproducer cells, were observed. pl35 was also found in cultured E26 virus producing cells of several leukemic chickens, and its intracellular concentration relative to that of the essential virion proteins encoded by the helper virus correlates with the ratio of E26 to helper RNA in virions released by these cells. p135 is phosphorylated but not glycosylated; antigenically it is not related to the pol or env gene products. It appears to be coded for by a partial gag gene and by E26-specific RNA sequences, presumably including those shared with AMV. Hence, AMV and E26 appear to use different strategies for the expression of related onc sequences: AMV is thought to encode a transforming protein via a subgenomic mRNA, whereas E26 codes for a gag-related polyprotein via genomic RNA. It is speculated that differences in the oncogenic properties of E26 and AMV are due to differences in their genetic structures and gene products.

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“…E26 induced an erythroblast (Sotirov, 1981) that exhibited a more dierentiated phenotype than those seen in erythroid disease induced by the previously identi®ed Avian Erythroblastosis virus (AEV). However, like another virus, AMV (Avian Myeloblastosis virus), the E26 virus could also transform myeloblasts in vivo and in vitro (Graf et al, 1978;1979;Moscovici et al, 1981;Radke et al, 1982). In addition, E26 could transform quail ®broblasts in tissue culture (Graf et al, 1979) and this property, together with its ability to induce a novel erythroid disease, suggested the E26 virus represented a unique isolate dierent from AMV or the erythroblastosis-inducing AEV.…”

Section: The Avian Erythroleukemia Virus E26 Identi®es the ®Rst Ets Genementioning

confidence: 99%

Ets and retroviruses–transduction and activation of members of the Ets oncogene family in viral oncogenesis

Blair

Athanasiou

2000

Oncogene

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Transforming capacities and defectiveness of avian leukemia viruses OK10 and E26

Cited by 72 publications

References 12 publications

OK10, an avian acute leukemia virus of the MC29 subgroup with a unique genetic structure

OK10, an avian acute leukemia virus of the MC29 subgroup with a unique genetic structure

Acute leukemia viruses E26 and avian myeloblastosis virus have related transformation-specific RNA sequences but different genetic structures, gene products, and oncogenic properties

Ets and retroviruses–transduction and activation of members of the Ets oncogene family in viral oncogenesis

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