Heterotransplantation of Rous Sarcoma and Rous Sarcoma Virus to Mammals

Schmidt-Ruppin, K. H.

doi:10.1159/000224235

Cited by 16 publications

(6 citation statements)

References 18 publications

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“…(A) Comparison of the 3' ends of pol in RSV-29 no. 1.2 and in PR-RSV-C (22). A * indicates the same base as RSV-29, and a blank space indicates the absence of that base in PR-RSV-C. Al, A2 and Bi, B2 are pairs of direct repeats present in the PR-RSV-C sequence.…”

Section: Discussionmentioning

confidence: 99%

“…As a result, these viruses are usually replication defective (11,17,24). The common strains of Rous sarcoma virus (RSV), Schmidt-Ruppin (SR-RSV) (22) and Prague (PR-RSV) (12), are anomalous in that they contain an oncogene and yet preserve all the genes for replication (34). However, the Bryan high-titer strain of RSV (BH-RSV) has been found to lack the env gene, rendering the virus replication defective (4,8,21).…”

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confidence: 99%

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Partial nucleotide sequence of Rous sarcoma virus-29 provides evidence that the original Rous sarcoma virus was replication defective

Dutta¹,

Wang²,

Hanafusa³

et al. 1985

J Virol

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Rous sarcoma virus-29 (RSV-29) is the strain of RSV that has the least number of passages beyond its isolation from chicken tumor no. 1 among all current strains of RSV. Biological characterization indicated that it was replication defective. RNA analysis of nonproducer clones of RSV-29-infected chicken embryonic fibroblasts showed the presence of a subgenomic message of 2.6 kilobases containing src and a genomic RNA of 7.7 kilobases that contains gag, pol, and src, but not env. The src-containing EcoRI fragment of RSV-29 proviral DNA was molecularly cloned. Sequence analysis of the regions flanking src revealed that the env gene was completely deleted in RSV-29 and that the sequence across the deletion was exactly the same as the Bryan high-titer strain of RSV. The sequence immediately 3' to src in RSV-29 was closely related to that of the Prague strain of RSV. The fact that the strain of RSV which has the minimal number of passages beyond its isolation is replication defective supports the hypothesis of Lerner and Hanafusa (J. Virol. 49:549-556, 1984) that the original RSV is a defective transforming virus. This defective transforming virus is postulated to be the precursor to other defective RSVs like the Bryan high-titer strain and to nondefective RSVs like the Prague strain. The particular clone of RSV-29 that we studied also had a short stretch of sequence duplication at the 3' end of the pol gene, which was presumably created by an error of reverse transcription.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Partial nucleotide sequence of Rous sarcoma virus-29 provides evidence that the original Rous sarcoma virus was replication defective

Dutta¹,

Wang²,

Hanafusa³

et al. 1985

J Virol

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“…Chicken embryo fibroblasts and chicken cell lines producing four different avian retroviruses were obtained from H. Hanafusa (The Rockefeller University, New York, N.Y.) and grown in DMEM supplemented with 5% newborn calf serum and 10% tryptone phosphate broth. The four avian viruses consisted of two nontransforming viruses, Rous-associated virus 1 (44) and Fujinami-associated virus, a subgroup C virus (23), and two transforming viruses, the Bryan high-titer strain of Rous sarcoma virus (RSV) (4) and the Schmidt-Ruppin strain of RSV (46). Enzymatic manipulations of DNA.…”

Section: Methodsmentioning

confidence: 99%

Analysis of retroviral pol gene products with antisera raised against fusion proteins produced in Escherichia coli

Tanese

Roth

Goff

1986

J Virol

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Portions of the pol gene of Moloney murine leukemia virus (MuLV) were expressed as fusion proteins in Escherichia coli, and the purified proteins were used to elicit antibodies in rabbits. The sera were used to examine the mature pol gene products contained in virion particles and identified the reverse transcriptase and a second protein, P46Po', encoded by the 3' portion of the gene. The P46 protein was not phosphorylated and was present at the same molar abundance as the reverse transcriptase. The sera were also used to detect the Pr2009agPol intracellular precursor protein and to analyze its processing to the mature forms. The proteins formed by several Moloney MuLV mutants were analyzed. Further tests revealed cross-reactivity with Friend MuLV and feline leukemia virus proteins, but not with avian retrovirus proteins.

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“…However, there were other strains of avian sarcoma in circulation, notably in Europe. These included the Prague strain of RSV [26], the Carr–Zilber and Schmidt–Ruppin strains [27,28] and the independently isolated avian sarcoma virus referred to as Bratislava 77 (B77) [29]. Several of these strains were studied for their activity in mammals [27,28,30,31,32,33,34].…”

Section: Non-defective Avian Sarcoma Virusesmentioning

confidence: 99%

“…These included the Prague strain of RSV [26], the Carr–Zilber and Schmidt–Ruppin strains [27,28] and the independently isolated avian sarcoma virus referred to as Bratislava 77 (B77) [29]. Several of these strains were studied for their activity in mammals [27,28,30,31,32,33,34]. In contrast to the Bryan high-titer strain, they showed significant ability to induce tumors in rodents and other laboratory animals and to transform mammalian cells in culture.…”

Section: Non-defective Avian Sarcoma Virusesmentioning

confidence: 99%

The Importance of Being Non-Defective: A Mini Review Dedicated to the Memory of Jan Svoboda

Vogt

2019

Viruses

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Jan Svoboda triggered investigations on non-defective avian sarcoma viruses. These viruses were a critical factor in the genetic understanding of retroviruses. They provided the single and unique access to the field and facilitated the discovery of the first oncogene src and of the cellular origin of retroviral oncogenes. They continue to be of importance as singularly effective expression vectors that have provided insights into the molecular functions of numerous oncogenes. Combined with the contributions to the validation of the provirus hypothesis, Jan Svoboda’s investigations of non-defective avian sarcoma viruses have shaped a large and important part of retrovirology.

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Heterotransplantation of Rous Sarcoma and Rous Sarcoma Virus to Mammals

Cited by 16 publications

References 18 publications

Partial nucleotide sequence of Rous sarcoma virus-29 provides evidence that the original Rous sarcoma virus was replication defective

Partial nucleotide sequence of Rous sarcoma virus-29 provides evidence that the original Rous sarcoma virus was replication defective

Analysis of retroviral pol gene products with antisera raised against fusion proteins produced in Escherichia coli

The Importance of Being Non-Defective: A Mini Review Dedicated to the Memory of Jan Svoboda

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