Temperature-sensitive mutants of MH2 avian leukemia virus that map in the v-mil and the v-myc oncogene respectively.
MH2 is an avian retrovirus that contains the v-mil and v-myc oncogenes. In vitro it transforms chick macrophages that are capable of proliferation in the absence of growth factor. Earlier work showed that v-myc induces macrophage transformation and that v-mil induces the production of chicken myelomonocytic growth factor (cMGF), thus generating an autocrine system. We describe the isolation of temperature-sensitive (ts) mutants of MH2 virus. As suggested by marker rescue experiments, one mutant bears a ts lesion in v-mil, whereas the other carries a mutation in v-myc. Ts v-mil MH2-transformed macrophages become factor-dependent at the non-permissive temperature (42 degrees C), while ts-v-myc MH2-transformed macrophages cease growing and acquire a more normal macrophage phenotype at 42 degrees C irrespective of the presence of cMGF. Both phenotypes can be reversed by backshift to the permissive temperature. These results suggest that the gene products of v-mil and v-myc function independently of each other and that v-mil is necessary for the maintenance of autocrine growth, whereas v-myc is required to maintain the transformed phenotype.
D000818:Animals; D001354:Avian Leukosis Virus / Q000235:genetics*; D002455:Cell Division; D002471:Cell Transformation, Neoplastic; D002645:Chickens; D005796:Genes; D005814:Genes, Viral; D007700:Kinetics; D008264:Macrophages / Q000166:cytology; D009154:Mutation; D009856:Oncogene Proteins, Viral / Q000235:genetics; D009857:Oncogenes; D013696:Temperature
D009856:Oncogene Proteins, Viral