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 |
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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 |
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