Transformation-defective mutants with 5′ deletions of the src gene are frequently generated during replication of rous sarcoma virus in established quail fibroblasts

Autor: F Poirier, Philippe Dezélée, Maria Marx, Georges Calothy, Miroslav Hill, Jana Hillova, Jean-Vianney Barnier, D Laugier
Přispěvatelé: CNRS UMR 146 - Institut Curie - Developmental Genetics of Melanocytes (CNRS), Centre National de la Recherche Scientifique (CNRS), Institut Jacques Monod (IJM (UMR_7592)), Université Paris Diderot - Paris 7 (UPD7)-Centre National de la Recherche Scientifique (CNRS), Equipe 148 CNRS & Institut de Cancérologie et d'Immunogénétique
Rok vydání: 1990
Předmět:
Embryo
Nonmammalian

MESH: Oncogenes
[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology
viruses
Restriction Mapping
Mutant
MESH: Base Sequence
Virus Replication
MESH: Animals
MESH: Coturnix
Cells
Cultured

MESH: Restriction Mapping
MESH: Turkeys
0303 health sciences
Rous sarcoma virus
[SDV.NEU.PC]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Psychology and behavior
biology
MESH: Avian Sarcoma Viruses
Single-Strand Specific DNA and RNA Endonucleases
MESH: Single-Strand Specific DNA and RNA Endonucleases
030302 biochemistry & molecular biology
[SDV.NEU.SC]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Cognitive Sciences
Quail
MESH: Cell Transformation
Viral

Chromosome Deletion
MESH: Cells
Cultured

Turkeys
MESH: Mutation
MESH: Oncogene Protein pp60(v-src)
MESH: Chromosome Deletion
Molecular Sequence Data
Coturnix
Virus
Oncogene Protein pp60(v-src)
03 medical and health sciences
Virology
biology.animal
Animals
Gene
030304 developmental biology
MESH: Molecular Sequence Data
Base Sequence
MESH: Virus Replication
MESH: Embryo
Nonmammalian

Oncogenes
Cell Transformation
Viral

biology.organism_classification
Molecular biology
MESH: DNA
Viral

Avian Sarcoma Viruses
Viral replication
Cell culture
DNA
Viral

Mutation
Zdroj: Virology
Virology, Elsevier, 1990, 177 (2), pp.505-514. ⟨10.1016/0042-6822(90)90515-s⟩
ISSN: 0042-6822
1096-0341
DOI: 10.1016/0042-6822(90)90515-s
Popis: International audience; Replication of Rous sarcoma virus (RSV) in avian fibroblasts leads to the generation of replication-competent variants that are defective for cell transformation (td virus). These td variants contain deletions affecting various portions of the v-src gene. We compared the rate of td virus production in Q3B cells, a quail cell line established by mutagen treatment, and in normal quail fibroblasts. Twenty-five days after infection with an RSV stock containing only transforming virions, Q3B cells harbor similar amounts of v-src-containing and v-src-deleted proviruses. However, these cells synthesize very low levels of p60v-src and generate large excess of td variants, as determined by biological assays. Unlike Q3B cells, normal quail fibroblasts infected with the same virus stock produce td variants only after multiple passages of undiluted virus on fresh cells. Restriction analysis showed that the td virus produced by Q3B cells is composed of two types of genomes: one lacking the entire v-src gene and the other carrying partial deletions of this gene predominantly located in the amino-terminal portion of the coding region of v-src. To study the mechanisms of these partial deletions, we molecularly cloned and sequenced the v-src genes of several td proviruses. We show that these mutants carry single or multiple v-src deletions of limited size, presumably generated by multiple mechanisms. Two deletions of 170 and 112 bp located in the 5' portion of v-src are frequently generated during RSV replication in Q3B cells and may represent preferential sites for v-src deletion in these cells.
Databáze: OpenAIRE