The mutated, myeloid cell-specific growth factor receptor v-fms transforms avian erythroid but not myeloid cells.

Abstract

In avian hematopoietic cells, transformation by tyrosine kinase oncogenes is restricted to the erythroid lineage. To study the mechanism of this striking target cell specificity, we constructed an avian retrovirus correctly expressing the feline v-fms protein, an oncogenic version of the myeloid-specific CSF-1 receptor. Similar to other tyrosine kinase oncogenes (erbB, src, fps, sea), the v-fms oncogene induced progenitor cells to self-renew in an erythropoietin-independent manner. Spontaneous differentiation of the transformed cells was arrested by v-erbA. v-fms failed to induce transformation of myeloid cells but caused myeloid cells transformed by the v-myb oncogene, as well as normal macrophages, to proliferate independent of cMGF (chicken myelomonocytic growth factor). Unlike the other tyrosine kinases, v-fms did not induce cMGF secretion in myb-myeloblasts, suggesting a nonautocrine mechanism of growth factor independence.