Hatzoglou M, Bosch F, Park E A, Hanson R W
Pew Center for Molecular Nutrition, Case Western Reserve University, School of Medicine, Cleveland, Ohio 44106.
J Biol Chem. 1991 May 5;266(13):8416-25.
The interaction of promoters contained in a Moloney murine leukemia virus (MoMLV)-based retroviral vector was studied after infection of FTO-2B rat hepatoma and NIH 3T3 mouse fibroblast cells. Segments of the phosphoenolpyruvate carboxykinase (PEPCK) promoter-regulatory region, which are known from previous studies to confer responsiveness to hormones, were linked to the structural genes for bovine growth hormone, amino-3'-glycosyl phosphotransferase (neo), and herpes-virus thymidine kinase and inserted into a MoMLV-based retroviral vector. In vectors in which PEPCK was the only internal promoter, it was the major site of gene transcription. This dominant effect was independent of the orientation of the PEPCK promoter relative to the 5' long terminal repeat of the provirus and was noted with as little as -174 base pairs of the 5'-flanking sequence. NIH 3T3 cells, which do not express the endogenous PEPCK gene, transcribed the transduced PEPCK-chimeric genes at the same high levels as was observed in hepatoma cells. When two promoters were present in the provirus, the expression of chimeric structural genes depended on the relative position and orientation of these genes as well as the type of cell infected by the retrovirus. Differential responses of proviral promoters in infected cells were also observed in the presence of hormones. Dibutyryl cyclic AMP increased the expression of genes linked to the PEPCK promoter in FTO-2B and NIH 3T3 cells, whereas glucocorticoids stimulated transcription from both the PEPCK promoter and the long terminal repeat in FTO-2B cells. The effect of these hormones on transcription of proviral promoters depended on their position relative to the 5' long terminal repeat. In contrast, insulin uniformly inhibited transcription from the PEPCK promoter in a position-independent manner but only in hepatoma cells and not in fibroblasts. In clonally isolated FTO-2B cells infected with a retrovirus, the site of proviral integration was also a major factor determining the expression and hormonal regulation from the internal promoters. The data suggest that the hormonal regulation of the expression of genes contained in retroviral vectors depends on the type and position of the regulatory elements present in the provirus and the lineage of the infected cell.
在感染FTO - 2B大鼠肝癌细胞和NIH 3T3小鼠成纤维细胞后,对基于莫洛尼鼠白血病病毒(MoMLV)的逆转录病毒载体中所含启动子的相互作用进行了研究。磷酸烯醇式丙酮酸羧激酶(PEPCK)启动子调控区的片段,先前的研究已知其可赋予对激素的反应性,与牛生长激素、氨基 - 3'-糖基磷酸转移酶(neo)和疱疹病毒胸苷激酶的结构基因相连,并插入到基于MoMLV的逆转录病毒载体中。在PEPCK是唯一内部启动子的载体中,它是基因转录的主要位点。这种主导效应与PEPCK启动子相对于前病毒5'长末端重复序列的方向无关,并且在5'侧翼序列仅有 - 174个碱基对时就已观察到。不表达内源性PEPCK基因的NIH 3T3细胞,转录转导的PEPCK嵌合基因的水平与在肝癌细胞中观察到的一样高。当前病毒中存在两个启动子时,嵌合结构基因的表达取决于这些基因的相对位置和方向以及逆转录病毒感染的细胞类型。在存在激素的情况下,也观察到了感染细胞中前病毒启动子的不同反应。二丁酰环磷腺苷(dibutyryl cyclic AMP)增加了FTO - 2B和NIH 3T3细胞中与PEPCK启动子相连的基因的表达,而糖皮质激素刺激了FTO - 2B细胞中PEPCK启动子和长末端重复序列的转录。这些激素对前病毒启动子转录的影响取决于它们相对于5'长末端重复序列的位置。相反,胰岛素以位置无关的方式均匀抑制PEPCK启动子的转录,但仅在肝癌细胞中而非成纤维细胞中。在感染逆转录病毒的克隆分离的FTO - 2B细胞中,前病毒整合位点也是决定内部启动子表达和激素调节的主要因素。数据表明,逆转录病毒载体中所含基因表达的激素调节取决于前病毒中存在的调控元件的类型和位置以及感染细胞的谱系。