Chang L S, Shi Y, Shenk T
Howard Hughes Medical Institute, Department of Biology, Princeton University, New Jersey 08544-1014.
J Virol. 1989 Aug;63(8):3479-88. doi: 10.1128/JVI.63.8.3479-3488.1989.
Activity of the adeno-associated virus P5 transcriptional control region was found to be induced by adenovirus E1A gene products. A pair of adjacent sequence elements was found to mediate both basal and E1A-induced P5 activity. The first element is a binding site for the major late transcription factor (MLTF), a factor first identified on the basis of its binding to a specific sequence within the adenovirus major late promoter. The second element is a tandemly repeated 10-base-pair sequence whose relationship to previously described binding sites is unclear. Each element individually conferred E1A responsiveness on a heterologous promoter, and deletion analysis demonstrated that each contributed to the level of P5 activity in the presence of E1A products both in transfection- and infection-based assays. Although deletion of the MLTF binding site led to reduced P5 transcriptional activity in the presence of E1A proteins, the deletion generated enhanced P5 basal activity in the absence of the transcriptional activator. The negative effect of the MLTF binding site in the absence of activator and its positive effect in the presence of activator combine to enhance the magnitude of the response by the P5 control region to E1A gene products.
腺相关病毒P5转录控制区的活性被发现可由腺病毒E1A基因产物诱导。发现一对相邻的序列元件介导基础和E1A诱导的P5活性。第一个元件是主要晚期转录因子(MLTF)的结合位点,该因子最初是根据其与腺病毒主要晚期启动子内特定序列的结合而鉴定出来的。第二个元件是一个串联重复的10碱基对序列,其与先前描述的结合位点的关系尚不清楚。每个元件单独赋予异源启动子E1A反应性,缺失分析表明,在基于转染和感染的试验中,每个元件在E1A产物存在时都对P5活性水平有贡献。尽管在E1A蛋白存在的情况下,MLTF结合位点的缺失导致P5转录活性降低,但在没有转录激活剂的情况下,该缺失产生了增强的P5基础活性。MLTF结合位点在没有激活剂时的负面影响及其在有激活剂时的正面影响相结合,增强了P5控制区对E1A基因产物的反应幅度。