Continuous production of rous sarcoma virus free of transformation defective virus in clones of established RSV-transformed quail cells

Marx, Maria; Cerutt, Pierre; Hill, M.; Carloni, Guido; Sergeant, Alain; Kaczorek, Michel

doi:10.1016/0042-6822(81)90084-2

Cited by 10 publications

(5 citation statements)

References 29 publications

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“…The Schmidt-Ruppin strain of RSV, subgroup E, was used as the wild-type virus (45). The isolation and characterization of RSV mutants tsNY68 (41) and tsPA101 (11) have been reported previously.…”

Section: Materuils and Methodsmentioning

confidence: 99%

Transcriptional downregulation of the retina-specific QR1 gene by pp60v-src and identification of a novel v-src-responsive unit.

Pierani¹,

Pouponnot²,

Calothy³

1993

Mol. Cell. Biol.

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The embryonic avian neuroretina (NR) is part of the central nervous system and is composed of various cell types: photoreceptors and neuronal and Muller (glial) inactivation. Cl is also a target for regulation during development. We have identified the DNA binding site for the Cl complex, a repeated GCTGAC sequence, and shown that mutations in this element abolish binding of this factor as well as transcription of the gene at the nonpermissive temperature. Neither formation of Cl nor that of C2 seems to involve factors known to be targeted in the pp60v" cascade. Our data suggest that Cl could be a novel target for both developmental control and oncogene-induced cell growth regulation.

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Section: Materuils and Methodsmentioning

confidence: 99%

Transcriptional downregulation of the retina-specific QR1 gene by pp60v-src and identification of a novel v-src-responsive unit.

Pierani¹,

Pouponnot²,

Calothy³

1993

Mol. Cell. Biol.

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“…dlPA105 was isolated during a study of a complex td viral stock produced by Q3B cells, an established line of QEF (M. Hill, personal communication) chronically infected with SRE. These cells were initially infected with virus produced by Q56/3B cells, a clone of QEF transformed by SRE found to continuously release sarcoma virus free of td particles (42). However, 3 weeks after infection, Q3B cells were releasing a large excess of td particles in addition to the original transforming virus (M. Marx, unpublished results).…”

Section: Resultsmentioning

confidence: 99%

“…Q56/3B is a clone of QEF established in culture after transformation with SRE. These cells continuously produce sarcoma virus free of transformationdefective (td) particles (42).…”

Section: Methodsmentioning

confidence: 99%

“…Analysis of viral RNA. Virions were pelleted from 200 ml of clarified culture medium at 100,000 x g. Viral RNA was extracted and purified as previously described (42). After denaturation by the glyoxal-dimethyl sulfoxide method (43) and electrophoresis in 1% agarose gel, RNA was transferred on diazobenzyl-oxymethyl paper (1) and hybridized to virusspecific probes.…”

Section: Edtamentioning

confidence: 99%

“…Digestion with restriction enzymes was carried out at 37°C for 4 h in 40-pI mixtures containing 8 to 10 jig of DNA, buffers recommended by the supplier, and 60 U of restriction enzyme. Digested DNAs were electrophoresed in 1% agarose gels and transferred to nitrocellulose filters by the method of Southern (56) as described previously (42). Hybridization was performed by the method of Wahl et al (59) by using virus-specific probes radioactively labeled by nick translation (52).…”

Section: Edtamentioning

confidence: 99%

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N-terminal deletion in the src gene of Rous sarcoma virus results in synthesis of a 45,000-Mr protein with mitogenic activity

Laugier¹,

Marx²,

Barnier³

et al. 1987

J Virol

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Expression of the v-src gene of Rous sarcoma virus in avian embryo neuroretina cells results in transformation and sustained proliferation of these normally resting cells. Transformed neuroretina cells are also tumorigenic upon inoculation into immunodeficient hosts. We have previously described conditional mutants of Rous sarcoma virus encoding p6Ov-sr proteins which induce proliferation of neuroretina cells in the absence of transformation and tumorigenicity. These results suggest that p6oVSrC is composed of functionally distinct domains which may interact with multiple cellular targets. In this study, we describe a spontaneous variant of Rous sarcoma virus, subgroup E, which carries a deletion of 278 base pairs in the 5' portion of the v-src gene but which has retained the ability to induce proliferation of quail neuroretina cells. The deleted v-src gene encodes a 45,000-molecular-weight phosphoprotein which contains both phosphoserine and phosphotyrosine, is myristylated, and possesses tyrosine kinase activity indistinguishable from that of wild-type p60VSrC. Molecular cloning and sequence analysis of the mutant v-src gene have shown that this deletion extends from amino acid 33 to 126 of the wild-type p60vr-s. Therefore, this portion of the v-src protein is dispensable for the mitogenic activity of Rous sarcoma virus in neuroretina cells.

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Isolation of proteins with kinase activity and related to pp60 src from human cells

Pavloff

Biquard

Hanania

et al. 1984

Biochemical and Biophysical Research Communications

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Continuous production of rous sarcoma virus free of transformation defective virus in clones of established RSV-transformed quail cells

Cited by 10 publications

References 29 publications

Transcriptional downregulation of the retina-specific QR1 gene by pp60v-src and identification of a novel v-src-responsive unit.

Transcriptional downregulation of the retina-specific QR1 gene by pp60v-src and identification of a novel v-src-responsive unit.

N-terminal deletion in the src gene of Rous sarcoma virus results in synthesis of a 45,000-Mr protein with mitogenic activity

Isolation of proteins with kinase activity and related to pp60 src from human cells

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