Rein A, Lowy D R, Gerwin B I, Ruscetti S K, Bassin R H
J Virol. 1982 Feb;41(2):626-34. doi: 10.1128/JVI.41.2.626-634.1982.
We have described the isolation of a replication-defective murine leukemia virus from a culture of AKR lymphoma cells [Rein et al., Nature (London) 282:753-754, 1979]. To facilitate the characterization of this murine leukemia virus, we transmitted it to mink cells and analyzed its genome by restriction mapping of the mink cellular DNA. This genome resembled the Akv genome quite closely, but it had an additional KpnI cleavage site at 1.3 kilobase pairs from the 5' end of the provirus and a small (approximately 50-base-pair) deletion between 1.8 and 3.0 kilobase pairs from the 5' end. When we tested these mink cells by immune precipitation or by competition radioimmunoassay, we found that they synthesized gPr82env, but contained no detectable gag or pol proteins. It seems likely that the KpnI cleavage site at 1.3 kilobase pairs reflects an abnormal sequence at or near the beginning of the gag gene, which prevents gag or pol translation by introducing a frameshift or termination codon into this region.
我们已描述了从AKR淋巴瘤细胞培养物中分离出一种复制缺陷型鼠白血病病毒的过程[Rein等人,《自然》(伦敦)282:753 - 754,1979]。为便于对这种鼠白血病病毒进行特性分析,我们将其接种到水貂细胞中,并通过对水貂细胞DNA进行限制性图谱分析来研究其基因组。该基因组与Akv基因组非常相似,但在原病毒5'端1.3千碱基对处有一个额外的KpnI切割位点,且在5'端1.8至3.0千碱基对之间有一个小的(约50碱基对)缺失。当我们通过免疫沉淀或竞争放射免疫测定法检测这些水貂细胞时,发现它们合成了gPr82env,但未检测到gag或pol蛋白。1.3千碱基对处的KpnI切割位点似乎反映了gag基因起始处或其附近的异常序列,该异常序列通过在此区域引入移码或终止密码子来阻止gag或pol的翻译。