Ostertag W, Seliger B, Kollek R, Stocking C, Bergholz U, Smadja-Joffe F
J Gen Virol. 1986 Jul;67 ( Pt 7):1361-71. doi: 10.1099/0022-1317-67-7-1361.
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.
将显性新霉素抗性基因（neoR）导入骨髓增殖性肉瘤病毒（MPSV）的基因组中，MPSV是一种携带mos癌基因的复制缺陷型逆转录病毒。与其他研究小组将标记基因插入致癌病毒的尝试结果不同，所得的可选择neoR-MPSV病毒并未丧失其急性转化特性。通过转染随后用Friend或莫洛尼氏鼠白血病病毒拯救，利用neoR-MPSV DNA产生感染性病毒。用这种病毒感染成纤维细胞会产生形态学上转化的细胞，这些细胞对新霉素类似物G418具有抗性。在对成纤维细胞进行的500多次独立病毒传代中，未观察到两种功能（转化和G418抗性）的分离。此外，neoR-MPSV保留了野生型病毒诱导白血病发生的特性。在小鼠体内传代后，骨髓增殖和G418抗性转移并未分离。
