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首页> 外文学位 >Cellular protein interactions with a picornavirus RNA intermediate affects positive-strand RNA synthesis.
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Cellular protein interactions with a picornavirus RNA intermediate affects positive-strand RNA synthesis.

机译：细胞蛋白与微小RNA病毒RNA中间体的相互作用影响正链RNA的合成。

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摘要

Poliovirus is a member of a group of small, single-stranded positive-sense RNA viruses that replicate in the cytoplasm of the infected cell. Due to the limited coding capacity of the viral genome, poliovirus relies on sequestration and binding of host cell proteins, in addition to the non-structural proteins encoded by the single open reading frame of the viral RNA, to productively produce progeny positive-strand RNAs that will be incorporated into infectious virions. Association of host cell and viral non-structural proteins occurs on the regions of the viral RNA that do not code for protein, and allows for a local concentration of the protein components required for the necessary processes through extensive base-pairing to form stable RNA secondary structures. Examples of important viral non-coding regions (NCRs) interacting with cellular and/or viral proteins include the internal ribosome entry site or IRES located at the 5' end of the poliovirus genome, which allows for initiation of cap-independent RNA translation of the RNA genome and the cis-acting element or cre, which is required for uridylylation of the RNA polymerase protein primer VPg. In our studies we have investigated the importance of the 3' NCR and its function in poliovirus replication. Previous studies had determined that a viral mutant lacking the 3' NCR was still capable of replicating in vitro and in cell culture, albeit with a positive-strand RNA synthesis defect compared to wild type. We report here that the cellular protein hnRNP C, previously identified as binding to the 3' end of the poliovirus negative-strand RNA intermediate, also binds at the 5' end of negative-strand RNA. We demonstrate that the addition of hnRNP C proteins can stimulate viral RNA synthesis in vitro, as well as increase the production of infectious virus progeny in cell culture. Conversely, we show that removal of hnRNP C results in decreased virus yields and positive-strand RNA synthesis, suggesting that hnRNP C binding to the RNA termini of the poliovirus negative-strand may allow efficient RNA replication. Based upon these observations and the observation that the 5' end of poliovirus negative-strand RNA also binds poliovirus replication proteins, we conclude that the 3' NCR of poliovirus has an important role in positive-strand RNA synthesis via the interaction of its negative-strand RNA complement with hnRNP C and other viral and/or cellular factors.
机译：脊髓灰质炎病毒是在感染细胞的细胞质中复制的一组小型单链正义RNA病毒的成员。由于病毒基因组的编码能力有限，脊髓灰质炎病毒除了通过病毒RNA的单个开放阅读框编码的非结构蛋白之外，还依赖于宿主细胞蛋白的固存和结合，以有效地产生子代正链RNA并将其整合到传染性病毒粒子中。宿主细胞和病毒非结构蛋白的缔合发生在病毒RNA的不编码蛋白质的区域上，并通过广泛的碱基配对形成稳定的RNA二级，从而使必要过程所需的蛋白质成分局部浓缩。结构。与细胞和/或病毒蛋白相互作用的重要病毒非编码区（NCR）的例子包括位于脊髓灰质炎病毒基因组5'端的内部核糖体进入位点或IRES，这可启动非依赖于帽的RNA翻译RNA基因组和顺式作用元件或cre，这是RNA聚合酶蛋白引物VPg的尿苷酸化所必需的。在我们的研究中，我们研究了3'NCR的重要性及其在脊髓灰质炎病毒复制中的功能。先前的研究已经确定，缺乏3'NCR的病毒突变体仍然能够在体外和细胞培养中复制，尽管与野生型相比具有正链RNA合成缺陷。我们在这里报告说，以前被鉴定为与脊髓灰质炎病毒负链RNA中间体的3'末端结合的细胞蛋白hnRNP C，也在负链RNA的5'末端结合。我们证明，hnRNP C蛋白的添加可以刺激体外病毒RNA的合成，以及增加细胞培养中传染性病毒后代的产生。相反，我们显示去除hnRNP C会导致病毒产量降低和正链RNA合成减少，这表明hnRNP C与脊髓灰质炎病毒负链的RNA末端结合可能允许有效的RNA复制。根据这些观察结果以及脊髓灰质炎病毒负链RNA的5'末端也结合脊髓灰质炎病毒复制蛋白的观察，我们得出结论，脊髓灰质炎病毒的3'NCR通过其负-核苷酸的相互作用在正链RNA合成中具有重要作用。链RNA与hnRNP C和其他病毒和/或细胞因子互补。

著录项

  • 作者

    Ertel, Kenneth James.;

  • 作者单位

    University of California, Irvine.;

  • 授予单位 University of California, Irvine.;
  • 学科 Biology Virology.
  • 学位 Ph.D.
  • 年度 2009
  • 页码 213 p.
  • 总页数 213
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

  • 入库时间 2022-08-17 11:38:26

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