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

Dutta, Anindya; Wang, L H; Hanafusa, Terukiyo; Hanafusa, Hidesaburô

doi:10.1128/jvi.55.3.728-735.1985

Cited by 20 publications

(3 citation statements)

References 32 publications

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“…All acute oncogenic retroviruses lose part of their viral genes during the oncogene transduction process, thus becoming replication deficient and relying on helper viruses to replicate and assemble infectious viral particles (43). Although the Schmidt-Ruppin and Prague strains of RSV contain the v-src gene yet preserve all of the viral structural genes and are replication competent, there is evidence that the original RSV was a replication-defective transforming virus (16). The current replication-competent strains of RSV were probably produced after a second recombination event.…”

Section: Rpl30mentioning

confidence: 99%

A novel oncogene, v-ryk, encoding a truncated receptor tyrosine kinase is transduced into the RPL30 virus without loss of viral sequences

Jia

Mayer

Hanafusa

et al. 1992

J Virol

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The RPL viruses are acute oncogenic avian retroviruses isolated from chicken tumors. We carried out a genetic analysis of three of the viruses, RPL25, RPL28, and RPL3O. While RPL25 and RPL28 were shown to contain the erbB oncogene, RPL3O appeared to contain a novel protein tyrosine kinase oncogene. This gene, v-ryk, was cloned and sequenced. The v-ryk oncogene contains a 1.39-kb nonretroviral sequence that includes a tyrosine kinase domain which was inserted into the viral envelope protein gp37-coding region and fused in frame with upstream gp37 to generate a p69m,37-y fusion oncoprotein. Unlike that of other acutely transforming retroviruses, transduction of the v-ryk gene into RPL30 did not result in deletion of viral sequences. Sequence analysis suggested that v-Ryk is more homologous to receptor-type tyrosine kinases than to nonreceptor-type kinases. By reconstitution of a virus from its cDNA, the v-ryk oncogene has been shown to be fully responsible for the transforming activity of the RPL30 virus. Antibodies specific to v-Ryk immunoprecipitated the v-Ryk oncoprotein from cells transformed by the RPL30 virus. The v-Ryk protein was shown to be first synthesized as a 150-kDa precursor and then cleaved into the mature 69-kDa gp37-Ryk fusion protein, both parts of which were found to be localized to the membrane fraction. As expected from the sequence of v-Ryk, immunoprecipitates of v-Ryk from RPL3O-transformed cells were found to display a protein tyrosine kinase activity in vitro, and the levels of tyrosine-phosphorylated proteins are elevated in

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Section: Rpl30mentioning

confidence: 99%

A novel oncogene, v-ryk, encoding a truncated receptor tyrosine kinase is transduced into the RPL30 virus without loss of viral sequences

Jia

Mayer

Hanafusa

et al. 1992

J Virol

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“…However, it cannot be generalized that such sequence homology is always needed for recombination between a viral genome and c-onc sequences. For example, no similar homology is present at the recombination junctions of src in SR-A or PR-C RSV (33,41), although some homology is present between the pol-env junction of avian retroviruses and the region of c-src DNA corresponding to the 5' recombination junction of v-src in BH RSV and in RSV29 (8,21…”

Section: Resultsmentioning

confidence: 99%

Transduction of c-src coding and intron sequences by a transformation-defective deletion mutant of Rous sarcoma virus

Soong¹,

Iijima²,

Wang³

1986

J Virol

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The mechanism of cellular src (c-src) transduction by a transformation-defective deletion mutant, td109, of Rous sarcoma virus was studied by sequence analysis of the recombinational junctions in three tdlO9-derived recovered sarcoma viruses (rASVs). Our results show that two rASVs have been generated by recombination between tdlO9 and c-src at the region between exons 1 and 2 defined previously. Significant homology between td109 and c-src sequences was present at the sites of recombination. The viral and c-src sequence junction of the third rASV was formed by splicing a cryptic donor site at the 5' region of env of tdlO9 to exon 1 of c-src. Various lengths of c-src internal intron 1 sequences were incorporated into all three rASV genomes, which resulted from activation of potential splice donor and acceptor sites. The incorporated intron 1 sequences were absent in the c-src mRNA, excluding its being the precursor for recombination with l109 and implying that initial recombinations most likely took place at the DNA level. A potential splice acceptor site within the incorporated intron 1 sequences in two rASVs was activated and was used for the src mRNA synthesis in infected cells. The normal env mRNA splice acceptor site was used for src mRNA synthesis for the third rASV.

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“…The sequence analysis of replication-defective RSV29, believed to be an early passage of the original Rous isolate, suggests that this virus is a direct precursor of the Bryan high-titer strain [83]. The conclusion that this also indicates defectiveness of the original isolate is not warranted, as deletion of the env gene could have occurred and could be selected for within the presumably short passage history of RSV29 [83].…”

Section: Idle Speculationmentioning

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

Cited by 20 publications

References 32 publications

A novel oncogene, v-ryk, encoding a truncated receptor tyrosine kinase is transduced into the RPL30 virus without loss of viral sequences

A novel oncogene, v-ryk, encoding a truncated receptor tyrosine kinase is transduced into the RPL30 virus without loss of viral sequences

Transduction of c-src coding and intron sequences by a transformation-defective deletion mutant of Rous sarcoma virus

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

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