Defective v-erbB genes can be complemented by v-erbA in erythroblast and fibroblast transformation.
We have introduced 3'-terminal deletions of increasing size in the v-erbB oncogene and analysed the effects of these mutations on the transformation of fibroblasts and erythroblasts. The results show that the transforming activity of the mutants is gradually diminished, and completely abolished in those mutants that do not produce stable v-erbB proteins. The capacity to transform erythroblasts is lost before fibroblast transformation is severely affected, suggesting that a larger part of the C-terminal domain is required for mitogenic signalling in erythroid cells than in fibroblasts. In addition, the v-erbA oncogene was found to cooperate with v-erbB not only in erythroblast but also in fibroblast transformation, inducing a fully transformed phenotype in fibroblasts partially transformed by a mutant erbB oncogene.
Jansson
M
M
Differentiation Programme, European Molecular Biology Laboratory, Heidelberg, GFR.
Beug
H
H
Gray
C
C
Graf
T
T
Vennström
B
B
D001355:Alpharetrovirus; D000818:Animals; D001354:Avian Leukosis Virus; D002454:Cell Differentiation; D002472:Cell Transformation, Viral; D002642:Chick Embryo; D004252:DNA Mutational Analysis; D004900:Erythroblasts / Q000502:physiology*; D005347:Fibroblasts / Q000502:physiology*; D005816:Genetic Complementation Test; D007942:Leukemia, Experimental / Q000235:genetics*; D009856:Oncogene Proteins, Viral / Q000235:genetics / Q000378:metabolism; D009857:Oncogenes; D013696:Temperature
D009856:Oncogene Proteins, Viral