Bhat B M, Wold W S
J Virol. 1986 Mar;57(3):1155-8. doi: 10.1128/JVI.57.3.1155-1158.1986.
Region E3 of adenovirus encodes about 10 overlapping mRNAs with different spliced structures. The mRNAs are 5' coterminal and form two major 3'-coterminal families termed E3A and E3B. As a group, the mRNAs have two 5' splice sites and four or five 3' splice sites. We previously described a novel class of virus mutants with deletions that enhance distant upstream and downstream 5' and 3' splice sites in region E3 (S. L. Deutscher, B. M. Bhat, M. H. Pursley, C. Cladaras, and W. S. M. Wold, Nucleic Acids Res. 13:5771-5788, 1985). We now report that two of these mutants, dl710 and dl712, are defective in RNA 3'-end formation at the E3A site. This result was surprising because the deletions in dl710 and dl712 are upstream of the putative signal for E3A RNA 3'-end formation. The explanation that we favor for this result is that the enhanced splicing activity in these mutants results in the splicing out of the E3A 3'-end site from the RNA precursor before the E3A 3' ends have a chance to form.
腺病毒的E3区域编码约10种具有不同剪接结构的重叠mRNA。这些mRNA在5'端共末端,并形成两个主要的3'端共末端家族,称为E3A和E3B。作为一个整体,这些mRNA有两个5'剪接位点和四个或五个3'剪接位点。我们之前描述了一类新型的病毒突变体,其缺失增强了E3区域中远距离上游和下游的5'和3'剪接位点(S. L. Deutscher、B. M. Bhat、M. H. Pursley、C. Cladaras和W. S. M. Wold,《核酸研究》13:5771 - 5788,1985)。我们现在报告,其中两个突变体dl710和dl712在E3A位点的RNA 3'末端形成上存在缺陷。这个结果令人惊讶,因为dl710和dl712中的缺失位于E3A RNA 3'末端形成的假定信号的上游。我们支持这个结果的解释是,这些突变体中增强的剪接活性导致在E3A 3'末端有机会形成之前,E3A 3'末端位点从RNA前体中被剪接出去。