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The v-myb oncogene of avian myeloblastosis virus transforms myeloid cells exclusively, both in vivo and in vitro. The c-myb proto-oncogene from which v-myb arose is expressed at relatively high levels in immature hematopoietic cells of the lymphoid, erythroid, and myeloid lineages but not in myeloblasts transformed by v-myb. This finding suggested that the nuclear v-myb gene product p48v-myb might act directly to inhibit the normal expression of the c-myb gene. I have therefore used a selectable avian retroviral vector to express p48v-myb in avian erythroblasts which normally express high levels of the c-myb gene product p75c-myb. The results demonstrate that p48v-myb and p75c-myb can be coexpressed in the nuclei of cloned cells. Therefore, p48v-myb does not invariably prevent the expression of p75c-myb.

Avian erythroblastosis virus (AEV) induces both erythroblastosis and fibrosarcomas in susceptible birds. A locus, v-erbB, within the viral genome has been implicated in AEV-mediated oncogenesis. We report here the detection and partial characterization of the protein product of the v-erbB oncogene in AEV-transformed cells. We obtained the antisera necessary for our analysis by expressing a portion of the molecularly cloned v-erbB locus in Escherichia coli and immunizing rabbits with the resulting bacterial erbB polypeptide. Antisera directed against the bacterial polypeptide reacted with v-erbB proteins obtained from virus-infected avian cells. By three criteria--tunicamycin inhibition, lectin binding and metabolic labeling with radioactive sugar precursors--the product of the v-erbB gene appears to be a glycoprotein.

Avian erythroblastosis virus (AEV) induces a fatal erythroblastosis within 2 weeks of intravenous injection in chicks in virtually 100% of cases. In chicks injected intramuscularly, sarcomas frequently develop at the site of injection before the animals die from erythroblastosis. In vitro, AEV transforms both erythroblasts, derived from bone marrow cultures, and fibroblasts. These effects have been shown to be a general property of AEV and not of separate leukaemia- and sarcoma-inducing forms of the virus. AEV is defective for replication and can be propagated only in the prewence of helper virus. Its transformation specificity is independent of the helper virus used. It is not clear whether AEV has two different genes controlling transformation of the two types of target cell or whether it has only one gene coding for both. To investigate this question, we looked for mutants of AEV unable to transform one of the two types of target cell. We now describe such a mutant, which is defective for erythroblast transformation but which can still transform fibroblasts.