Mutations in v- myb alter the differentiation of myelomonocytic cells transformed by the oncogene
Identifieur interne : 004A24 ( Main/Exploration ); précédent : 004A23; suivant : 004A25Mutations in v- myb alter the differentiation of myelomonocytic cells transformed by the oncogene
Auteurs : Martino Introna [Allemagne] ; Josée Golay [Allemagne] ; Jon Frampton [Allemagne] ; Toru Nakano [Allemagne] ; Scott A. Ness [Allemagne] ; Thomas Graf [Allemagne]Source :
- Cell [ 0092-8674 ] ; 1990.
English descriptors
- Teeft :
- Acad, Amino, Amino acid substitutions, Amino acids, Antigen expression, Avian, Avian erythroblastosis virus, Avian graf, Avian leukemia virus, Avian leukemia viruses, Avian myeloblastosis virus, Beug, Binding domain, Blood smears, Bone marrow, Bone marrow cells, Ceils, Cell surface antigen, Cell type, Chick, Clone, Different forms, Different phenotypes, Differentiation phenotype, Ecorl site, Erythroid, Fibroblast, Fusion protein, Gene, Gene expression, Gene product, Genome, Genome structure, Golay, Graf, Granule, Granule expression, Helper phage, Helper virus, Hematopoietic, Hematopoietic cells, Histograms show, Homeodomain proteins, Hybrid viruses, Indirect immunofluorescence, Leukemia, Leukemia virus, Leukemic, Leukemic ceils, Leukemic cells, Long terminal, Lowest granule positivity, Ltrs, Lysozyme, Macrophage, Mature macrophages, Monoblast, Monoclonal antibody, Monocytic cells, Monocytic pathway, Moscovici, Mutant, Mutation, Myeioid cells, Myeloid, Myeloid ceils, Myeloid cells, Myeloid differentiation, Myeloid target cells, Myelomonocytic, Myelomonocytic cells, Natl, Ness, Normal counterparts, Nunn, Oncogene, Outer face, Parental viruses, Phenotype, Plasmid, Point mutants, Point mutations, Proc, Promyelocyte phenotype, Promyelocytes, Protein expression, Pvm2 plasmid, Recombinant, Recombinant virus, Recombinant viruses, Results show, Single point mutations, Specific point mutations, Standard proteins, Target cells, Unpublished data, Various forms, Viral, Virus, Virus stocks.
Abstract
Abstract: Chick myelomonocytic cells transformed by the v-myb oncogene-containing viruses E26 and AMV differ in that the former resemble myeloblasts and express the v-myb-regulated granulocyte-specific mim-1 gene, while the latter resemble monoblasts and are mim-1 negative. We constructed a series of AMV-E26 chimeras and localized the critical differences between these viruses to three point mutations within the second repeat of the v-myb DNA binding domain. These three positions are altered in the v-myb protein of AMV relative to the proteins encoded by c-myb or E26 v-myb. Back mutating AMV v-myb at any of these three sites restored the oncogene's ability to activate the mim-1 gene. Surprisingly, two of these changes led to the transformation, in vitro and in vivo, of cells having a promyelocyte-like phenotype. These results indicate that different forms of v-myb impose alternate phenotypes of differentiation on transformed myeloid cells, probably by regulating unique sets of differentiation-specific genes.
Url:
DOI: 10.1016/0092-8674(90)90424-D
Affiliations:
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Le document en format XML
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<term>Antigen expression</term>
<term>Avian</term>
<term>Avian erythroblastosis virus</term>
<term>Avian graf</term>
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<term>Avian leukemia viruses</term>
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<term>Clone</term>
<term>Different forms</term>
<term>Different phenotypes</term>
<term>Differentiation phenotype</term>
<term>Ecorl site</term>
<term>Erythroid</term>
<term>Fibroblast</term>
<term>Fusion protein</term>
<term>Gene</term>
<term>Gene expression</term>
<term>Gene product</term>
<term>Genome</term>
<term>Genome structure</term>
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<term>Graf</term>
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<term>Granule expression</term>
<term>Helper phage</term>
<term>Helper virus</term>
<term>Hematopoietic</term>
<term>Hematopoietic cells</term>
<term>Histograms show</term>
<term>Homeodomain proteins</term>
<term>Hybrid viruses</term>
<term>Indirect immunofluorescence</term>
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<term>Leukemia virus</term>
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<term>Leukemic cells</term>
<term>Long terminal</term>
<term>Lowest granule positivity</term>
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<term>Lysozyme</term>
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<term>Monoclonal antibody</term>
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<term>Moscovici</term>
<term>Mutant</term>
<term>Mutation</term>
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<term>Myeloid</term>
<term>Myeloid ceils</term>
<term>Myeloid cells</term>
<term>Myeloid differentiation</term>
<term>Myeloid target cells</term>
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<term>Ness</term>
<term>Normal counterparts</term>
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<term>Oncogene</term>
<term>Outer face</term>
<term>Parental viruses</term>
<term>Phenotype</term>
<term>Plasmid</term>
<term>Point mutants</term>
<term>Point mutations</term>
<term>Proc</term>
<term>Promyelocyte phenotype</term>
<term>Promyelocytes</term>
<term>Protein expression</term>
<term>Pvm2 plasmid</term>
<term>Recombinant</term>
<term>Recombinant virus</term>
<term>Recombinant viruses</term>
<term>Results show</term>
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<term>Specific point mutations</term>
<term>Standard proteins</term>
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<front><div type="abstract" xml:lang="en">Abstract: Chick myelomonocytic cells transformed by the v-myb oncogene-containing viruses E26 and AMV differ in that the former resemble myeloblasts and express the v-myb-regulated granulocyte-specific mim-1 gene, while the latter resemble monoblasts and are mim-1 negative. We constructed a series of AMV-E26 chimeras and localized the critical differences between these viruses to three point mutations within the second repeat of the v-myb DNA binding domain. These three positions are altered in the v-myb protein of AMV relative to the proteins encoded by c-myb or E26 v-myb. Back mutating AMV v-myb at any of these three sites restored the oncogene's ability to activate the mim-1 gene. Surprisingly, two of these changes led to the transformation, in vitro and in vivo, of cells having a promyelocyte-like phenotype. These results indicate that different forms of v-myb impose alternate phenotypes of differentiation on transformed myeloid cells, probably by regulating unique sets of differentiation-specific genes.</div>
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<name sortKey="Ness, Scott A" sort="Ness, Scott A" uniqKey="Ness S" first="Scott A." last="Ness">Scott A. Ness</name>
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