Weiher H, Barklis E, Ostertag W, Jaenisch R
J Virol. 1987 Sep;61(9):2742-6. doi: 10.1128/JVI.61.9.2742-2746.1987.
Moloney murine leukemia virus (M-MuLV) and M-MuLV-derived retroviral vectors are not expressed in early mouse embryos or in embryonal carcinoma cells. M-MuLV-derived mutants or M-MuLV-related variants which transduce the neomycin phosphotransferase gene can, however, induce drug resistance in embryonal carcinoma cells with high efficiency. In this study we investigated the sequences critical for retroviral gene expression in two different embryonal carcinoma cell lines, F9 and PCC4. We show that two synergistically acting sequence elements mediate expression in embryonal carcinoma cells. One of these is located within the U3 region of the viral long terminal repeat, and the second one is in the 5' untranslated region of the retrovirus. The latter element, characterized by a single point mutation, affects the level of stable RNA in infected cells, suggesting a regulatory mechanism similar to that of human immunodeficiency virus in human T cells.
莫洛尼鼠白血病病毒（M-MuLV）以及源自M-MuLV的逆转录病毒载体在早期小鼠胚胎或胚胎癌细胞中不表达。然而，转导新霉素磷酸转移酶基因的源自M-MuLV的突变体或与M-MuLV相关的变体能够高效诱导胚胎癌细胞产生耐药性。在本研究中，我们调查了在两种不同的胚胎癌细胞系F9和PCC4中逆转录病毒基因表达的关键序列。我们发现，两个协同作用的序列元件介导胚胎癌细胞中的表达。其中一个位于病毒长末端重复序列的U3区域内，另一个位于逆转录病毒的5'非翻译区。后一个元件通过单点突变来表征，影响受感染细胞中稳定RNA的水平，提示其调控机制类似于人类免疫缺陷病毒在人类T细胞中的调控机制。
