Reversible dependence on growth factor interleukin-3 in myeloid cells expressing temperature sensitive v-abl oncogene

Abstract

Abelson murine leukemia virus (A-MuLV) has been shown to abrogate the requirement for growth factor interleukin-3 (IL-3) in a variety of hematopoietic cell lineages by a non-autocrine mechanism. By infecting an IL-3 dependent myeloid cell line, FDC-P1, with A-MuLV containing temperature sensitive tyrosine kinase mutants of the v-abl oncogene, cell lines with temperature sensitive IL-3 independence phenotype were established. At the permissive temperature, cells expressing the ts oncogenes contained 20 fold higher levels of tyrosine-phosphorylated proteins than uninfected cells and were completely IL-3 independent. When shifted to the restrictive temperature, ts A-MuLV infected cells still contained 5 to 10 fold higher levels of phosphotyrosine but became dependent on IL-3 for growth. These results demonstrate that the maintenance of A-MuLV induced IL-3 independence requires the continuous function of the v-abl oncogene.