A mutation at the major phosphotyrosine in pp60v-src alters oncogenic potential.
Previously (M.A. Snyder, J.M. Bishop, W.W. Colby, and A.D. Levinson, 1983, Cell 32, 891-901) a mutant was constructed in v-src in which the major phosphotyrosine site, tyr-416, was converted to phenylalanine. This mutant has now been examined both for tumorigenicity and a number of in vitro parameters relating to the transformed state and to the known properties of pp60v-src, the product of v-src. Mouse cells transformed by this mutant gene, which are called RSV-SF1, are tumorigenic only if tested in immunodeficient mice, whereas cells transformed by the wild-type parent are tumorigenic in either syngeneic or immunodeficient animals. When examined in vitro, RSV-SF1-transformed cells are virtually indistinguishable from cells transformed by wild-type pp60v-src. These findings raise the possibility that the protein kinase activity of pp60v-src may not be fully responsible for tumorigenesis by v-src, and moreover suggest that evasion of the host immune response is a necessary step in tumorigenesis by v-src.
D000818:Animals; D001358:Avian Sarcoma Viruses / Q000235:genetics*; D002471:Cell Transformation, Neoplastic; D002478:Cells, Cultured; D004591:Electrophoresis, Polyacrylamide Gel; D051379:Mice; D008807:Mice, Inbred BALB C; D008819:Mice, Nude; D009154:Mutation; D015688:Oncogene Protein pp60(v-src); D010649:Phenylalanine; D019000:Phosphotyrosine; D011494:Protein Kinases / Q000235:genetics*; D014443:Tyrosine / Q000031:analogs & derivatives*; D014764:Viral Proteins / Q000235:genetics* / Q000302:isolation & purification
D014764:Viral Proteins; D019000:Phosphotyrosine; D014443:Tyrosine; D010649:Phenylalanine; D011494:Protein Kinases; D015688:Oncogene Protein pp60(v-src)