Huang M, Summers J
Department of Cell Biology, School of Medicine, University of New Mexico, Albuquerque 87131.
J Virol. 1994 Mar;68(3):1564-72. doi: 10.1128/JVI.68.3.1564-1572.1994.
We have found that transcription of the pregenome of an avian hepadnavirus, duck hepatitis B virus (DHBV), is dependent on the presence of a small element in the 5' transcribed region of the pregenome-encoding sequence. This element, which we have named pet (positive effector of transcription), exerts its effect in cis in a position and orientation-dependent manner, suggesting that it may function as part of the nascent pregenome transcript. The requirement for pet depends on the presence in the transcription unit of a region of the DHBV genome located upstream of the envelope promoters, which specifically suppresses transcription of templates lacking pet. In the presence of this region, deletion of pet activates transcription from downstream promoters, suggesting that pregenome transcription complexes fail to reach the downstream promoters. In vitro transcription experiments support the model that pet is required for transcription elongation on the DHBV template. We speculate that pet is required to suppress transcription termination during the first passage of pregenome transcription complexes through a viral termination region on the circular viral DNA.
我们发现,禽嗜肝DNA病毒——鸭乙型肝炎病毒(DHBV)前基因组的转录依赖于前基因组编码序列5'转录区域中一个小元件的存在。我们将这个元件命名为pet(转录阳性效应子),它以位置和方向依赖的方式顺式发挥作用,这表明它可能作为新生前基因组转录本的一部分发挥功能。对pet的需求取决于DHBV基因组转录单元中位于包膜启动子上游的一个区域的存在,该区域特异性抑制缺乏pet的模板的转录。在这个区域存在的情况下,pet的缺失会激活下游启动子的转录,这表明前基因组转录复合物无法到达下游启动子。体外转录实验支持了pet是DHBV模板转录延伸所必需的这一模型。我们推测,pet是在前基因组转录复合物首次通过环状病毒DNA上的病毒终止区域时抑制转录终止所必需的。