Hilberg F, Stocking C, Ostertag W, Grez M
Proc Natl Acad Sci U S A. 1987 Aug;84(15):5232-6. doi: 10.1073/pnas.84.15.5232.
A retroviral host-range neomycin-resistant myeloproliferative sarcoma virus mutant, which is expressed in the embryonal carcinoma cell lines F9 and PCC4aza1R, was molecularly cloned and analyzed. This mutant virus, PCMV, differs from myeloproliferative sarcoma virus by two major deletions, one of which spans exactly a 75-base-pair repeat of the long terminal repeat. Functional analysis of recombinant viruses shows that the host-range expansion of PCMV is a property of nucleotide changes within the U3 region of the long terminal repeat. Furthermore, expression assays of chimeric long terminal repeats show that the enhancer region of PCMV joined to the promoter region of Moloney murine leukemia virus is sufficient to direct the synthesis of chloramphenicol acetyltransferase in F9 and PCC4 cells.
一种在胚胎癌细胞系F9和PCC4aza1R中表达的逆转录病毒宿主范围新霉素抗性骨髓增殖性肉瘤病毒突变体被进行了分子克隆和分析。这种突变病毒，即PCMV，与骨髓增殖性肉瘤病毒有两个主要缺失不同，其中一个缺失恰好跨越了长末端重复序列的一个75碱基对的重复序列。重组病毒的功能分析表明，PCMV的宿主范围扩展是长末端重复序列U3区域内核苷酸变化的特性。此外，嵌合长末端重复序列的表达分析表明，与莫洛尼鼠白血病病毒启动子区域相连的PCMV增强子区域足以指导F9和PCC4细胞中氯霉素乙酰转移酶的合成。
