How do retroviral oncogenes induce transformation in avian erythroid cells?
The v-erb B oncogene, as well as other oncogenes of the src-gene family transform immature erythroid cells from chick bone marrow in vivo and in vitro. The erb B-transformed erythroid cells differ from normal late erythroid precursors (CFU-E) in that they have acquired the capacity to undergo self-renewal as well as to differentiate terminally. They also do not require the normal erythroid differentiation hormone, erythropoietin, for either process. Cooperation of v-erb B with a second oncogene, v-erb A, results in a differentiation arrest of the transformed cells, which now only use the self-renewal pathway. Studies with conditional and non-conditional mutants in both v-erb B and v-erb A will be presented to elucidate further how the transforming proteins encoded by these oncogenes, gp74erb B and gp75gag-erb A, affect the differentiation programme of the infected erythroid precursor with the outcome of hormone-independent leukaemic cells arrested at an early stage of erythroid differentiation.
Beug
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Kahn
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Vennström
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Hayman
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Graf
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D000818:Animals; D001854:Bone Marrow Cells; D002471:Cell Transformation, Neoplastic; D002645:Chickens; D006412:Hematopoietic Stem Cells / Q000166:cytology*; D008954:Models, Biological; D009154:Mutation; D009857:Oncogenes; D012190:Retroviridae / Q000235:genetics*