The myeloproliferative sarcoma virus retains transforming functions after introduction of a dominant selectable marker gene.
The dominant neomycin resistance gene (neoR) was introduced into the genome of the myeloproliferative sarcoma virus (MPSV), a replication-defective retrovirus carrying the mos oncogene. The resulting selectable neoR-MPSV virus did not lose its acute transforming property, unlike the results of attempts by other groups to insert marker genes into oncogenic viruses. NeoR-MPSV DNA was used to generate infectious virus by transfection followed by rescue with Friend or Moloney murine leukaemia virus. Infection of fibroblasts with this virus resulted in morphologically transformed cells which were resistant to the neomycin analogue G418. Segregation of the two functions (transformation and G418 resistance) was not observed in more than 500 independent viral transfers to fibroblasts. Furthermore, neoR-MPSV retained the leukaemogenesis-inducing properties of the wild-type virus. Myeloproliferation and G418-resistance transfer did not segregate after passage in mice.
D000818:Animals; D002471:Cell Transformation, Neoplastic; D002472:Cell Transformation, Viral; D004279:DNA, Viral / Q000235:genetics; D003673:Defective Viruses / Q000235:genetics* / Q000502:physiology; D004351:Drug Resistance; D005347:Fibroblasts / Q000187:drug effects / Q000382:microbiology; D005622:Friend murine leukemia virus / Q000502:physiology; D005799:Genes, Dominant; D005814:Genes, Viral; D005822:Genetic Vectors; D005839:Gentamicins / Q000494:pharmacology; D051379:Mice; D008979:Moloney murine leukemia virus / Q000502:physiology; D008980:Moloney murine sarcoma virus / Q000235:genetics* / Q000502:physiology; D009857:Oncogenes; D051381:Rats; D009053:Sarcoma Viruses, Murine / Q000235:genetics*; D012641:Selection, Genetic; D014776:Virus Cultivation
D004279:DNA, Viral; D005839:Gentamicins; C010680:antibiotic G 418