Bridge E, Xia D X, Carmo-Fonseca M, Cardinali B, Lamond A I, Pettersson U
Department of Medical Genetics, Uppsala University, Sweden.
J Virol. 1995 Jan;69(1):281-90. doi: 10.1128/JVI.69.1.281-290.1995.
Adenovirus infection affects the nuclear distribution of host splicing factors. Late phase-infected cells contain discrete clusters of small nuclear ribonucleoproteins (snRNPs) that are separate from centers containing the viral 72-kilodalton DNA-binding protein (72K protein). In the present study, we demonstrate that these snRNP clusters also contain splicing factors from the SR protein family. We show that a previously described monoclonal antibody, 3C5, detects SR proteins. Furthermore, we demonstrate that late region 3 transcription occurs at a maximal rate in infected cultures in which greater than 90% of the cells contain the snRNP clusters, indicating that such cells are actively transcribing their late genes. During the onset of the late phase, the intranuclear distribution of splicing factors is very different from that seen after the late phase is established. When late viral transcription commences, cells with snRNP clusters are less prevalent than in cultures that are maintaining maximum levels of late transcription. Instead, a cell type which shows snRNPs, concentrated in foci that also contain the viral 72K DNA-binding protein is detected. This cell type disappears from cultures by 18 to 20 h after a high-multiplicity infection. These results suggest a dynamic organization of splicing factors in infected cells that can be correlated to the status of viral gene expression. Our work also provides an explanation for the differing results that have been published concerning the organization of splicing factors in the adenovirus-infected cell nucleus (L. F. Jiménez-García and D. L. Spector, Cell 73:47-59, 1993). During the present study we observed that a monoclonal antibody against the SC-35 protein, which was used by Jiménez-García and Spector to study the localization of the SC-35 splicing factor in adenovirus-infected cells, cross-reacts with the adenovirus 72K DNA-binding protein and is thus unsuitable for this type of study.
腺病毒感染会影响宿主剪接因子的核分布。晚期感染的细胞含有离散的小核核糖核蛋白(snRNP)簇,这些簇与含有病毒72千道尔顿DNA结合蛋白(72K蛋白)的中心区域是分开的。在本研究中,我们证明这些snRNP簇还包含SR蛋白家族的剪接因子。我们表明,先前描述的单克隆抗体3C5可检测到SR蛋白。此外,我们证明晚期区域3转录在感染培养物中以最大速率发生,其中超过90%的细胞含有snRNP簇,这表明此类细胞正在积极转录其晚期基因。在晚期开始时,剪接因子的核内分布与晚期建立后所见的分布非常不同。当晚期病毒转录开始时,具有snRNP簇的细胞比维持晚期转录最大水平的培养物中更为少见。相反,检测到一种细胞类型,其snRNP集中在也含有病毒72K DNA结合蛋白的病灶中。在高倍感染后18至20小时,这种细胞类型从培养物中消失。这些结果表明感染细胞中剪接因子的动态组织与病毒基因表达状态相关。我们的工作也为已发表的关于腺病毒感染细胞核中剪接因子组织的不同结果提供了解释(L.F.希门尼斯 - 加西亚和D.L.斯佩克特,《细胞》73:47 - 59,1993)。在本研究过程中,我们观察到希门尼斯 - 加西亚和斯佩克特用于研究腺病毒感染细胞中SC - 35剪接因子定位的抗SC - 35蛋白单克隆抗体与腺病毒72K DNA结合蛋白发生交叉反应,因此不适用于此类研究。