Boeuf H, Jansen-Durr P, Kédinger C
Laboratoire de Génétique Moléculaire des Eucaryotes du CNRS, Faculté de Médecina, Strasbourg, France.
Oncogene. 1990 May;5(5):691-9.
The murine embryonal carcinoma (EC) F9 cells express an adenovirus EIa-like activity which is abolished after differentiation of these cells. We have examined the ability of the adenovirus EIa gene products to transactivate the viral early EIIa (EIIaE) promoter in this cell system. Surprisingly, as shown both by infection and transfection experiments, the EIIaE promoter was refractory to viral EIa-mediated activation in the undifferentiated F9 EC cells, EIa-responsiveness being recovered only after differentiation of these cells. This EC-cell-specific restriction did not correspond to a lack of EIa gene expression, nor to a deficiency of any of the major transcription factors involved in EIIaE basal promoter activity. In these differentiated F9 cells, EIIaE promoter activation correlates with a modification of E2F resulting in its ability to cooperatively interact with the promoter. Our observation that such a modification neither occurs in uninfected F9 EC cells (Jansen-Durr et al., 1989, EMBO J., 8, 3365), nor at early times after infection of these cells suggests that a viral product is required together with the EIa-like activity to induce this modification of E2F. The implication of an EIV gene product in this effect is discussed.
小鼠胚胎癌（EC）F9细胞表达一种腺病毒EIa样活性，这种活性在这些细胞分化后会消失。我们已经在这个细胞系统中检测了腺病毒EIa基因产物反式激活病毒早期EIIa（EIIaE）启动子的能力。令人惊讶的是，正如感染和转染实验所显示的那样，在未分化的F9 EC细胞中，EIIaE启动子对病毒EIa介导的激活具有抗性，只有在这些细胞分化后，EIa反应性才得以恢复。这种EC细胞特异性限制既不对应于EIa基因表达的缺乏，也不对应于参与EIIaE基础启动子活性的任何主要转录因子的缺陷。在这些分化的F9细胞中，EIIaE启动子激活与E2F的修饰相关，导致其能够与启动子协同相互作用。我们观察到这种修饰既不在未感染的F9 EC细胞中发生（Jansen-Durr等人，1989年，《欧洲分子生物学组织杂志》，8，3365），也不在这些细胞感染后的早期发生，这表明需要一种病毒产物与EIa样活性一起诱导E2F的这种修饰。本文讨论了EIV基因产物在这种效应中的作用。
