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人博卡病毒 1 NP1 蛋白是一种多功能的病毒 RNA 加工调节因子。

The Human Bocavirus 1 NP1 Protein Is a Multifunctional Regulator of Viral RNA Processing.

机构信息

Department of Molecular Microbiology and Immunology, University of Missouri-Columbia, School of Medicine, Bond Life Sciences Center, Columbia, Missouri, USA.

Department of Molecular Microbiology and Immunology, University of Missouri-Columbia, School of Medicine, Bond Life Sciences Center, Columbia, Missouri, USA

出版信息

J Virol. 2018 Oct 29;92(22). doi: 10.1128/JVI.01187-18. Print 2018 Nov 15.

DOI:10.1128/JVI.01187-18
PMID:30135129
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6206480/
Abstract

Human bocavirus 1 (HBoV1) encodes a genus-specific protein, NP1, which regulates viral alternative pre-mRNA processing. Similar to NP1 of the related bocavirus minute virus of canine (MVC), HBoV1 NP1 suppressed cleavage and polyadenylation of RNAs at the viral internal polyadenylation site (pA)p. HBoV1 (pA)p is a complex region. It contains 5 significant cleavage and polyadenylation sites, and NP1 was found to regulate only the three of these sites that are governed by canonical AAUAAA hexamer signals. HBoV1 NP1 also facilitated splicing of the upstream intron adjacent to (pA)p. Alternative polyadenylation and splicing of the upstream intron were independent of each other, functioned efficiently within an isolated transcription unit, and were responsive independent of NP1. Characterization of HBoV1 NP1 generalizes its function within the genus , uncovers important differences, and provides important comparisons with MVC NP1 for mechanistic and evolutionary considerations. The are small nonenveloped icosahedral viruses that are important pathogens in many animal species, including humans. The NP1 protein of human bocavirus 1 (HBoV1), similar to NP1 of the bocavirus minute virus of canine (MVC), regulates viral alternative RNA processing by both suppressing polyadenylation at an internal site, (pA)p, and facilitating splicing of an upstream adjacent intron. These effects allow both extension into the capsid gene and splicing of the viral pre-mRNA that correctly registers the capsid gene open reading frame. Characterization of HBoV1 NP1 generalizes this central mode of parvovirus gene regulation to another member of the bocavirus genus and uncovers both important similarities and differences in function compared to MVC NP1 that will be important for future comparative studies.

摘要

人博卡病毒 1(HBoV1)编码一种属特异性蛋白 NP1,该蛋白调节病毒的替代前体 mRNA 加工。与相关博卡病毒犬微小病毒(MVC)的 NP1 相似,HBoV1 NP1 抑制了病毒内部 poly(A)位点(pA)p 处的 RNA 切割和多聚腺苷酸化。HBoV1(pA)p 是一个复杂的区域。它包含 5 个重要的切割和多聚腺苷酸化位点,研究发现 NP1 仅调节这 3 个受典型 AAUAAA 六聚体信号控制的位点。HBoV1 NP1 还促进了紧邻(pA)p 的上游内含子的剪接。上游内含子的可变剪接和多聚腺苷酸化彼此独立,在分离的转录单位中高效发挥作用,并且独立于 NP1 响应。HBoV1 NP1 的特征概括了其在属内的功能,揭示了重要的差异,并为机制和进化考虑提供了与 MVC NP1 的重要比较。博卡病毒属是小型无包膜二十面体病毒,是许多动物物种(包括人类)的重要病原体。人博卡病毒 1(HBoV1)的 NP1 蛋白与犬博卡病毒微小病毒(MVC)的 NP1 相似,通过抑制内部位点(pA)p 的多聚腺苷酸化和促进上游相邻内含子的剪接来调节病毒的替代 RNA 加工。这些作用允许延伸到衣壳基因并剪接正确注册衣壳基因开放阅读框的病毒前体 mRNA。HBoV1 NP1 的特征概括了这种细小病毒基因调控的中心模式,适用于博卡病毒属的另一个成员,并揭示了与 MVC NP1 相比,在功能上的重要相似性和差异,这对于未来的比较研究将非常重要。

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本文引用的文献

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Minute Virus of Canines NP1 Protein Governs the Expression of a Subset of Essential Nonstructural Proteins via Its Role in RNA Processing.犬微小病毒NP1蛋白通过其在RNA加工中的作用调控一组必需非结构蛋白的表达。
J Virol. 2017 May 26;91(12). doi: 10.1128/JVI.00260-17. Print 2017 Jun 15.
2
Parvovirus Expresses a Small Noncoding RNA That Plays an Essential Role in Virus Replication.细小病毒表达一种在病毒复制中起关键作用的小非编码RNA。
J Virol. 2017 Mar 29;91(8). doi: 10.1128/JVI.02375-16. Print 2017 Apr 15.
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DNA Damage Signaling Is Required for Replication of Human Bocavirus 1 DNA in Dividing HEK293 Cells.DNA损伤信号传导是人类博卡病毒1 DNA在分裂的HEK293细胞中复制所必需的。
J Virol. 2016 Dec 16;91(1). doi: 10.1128/JVI.01831-16. Print 2017 Jan 1.
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Analysis of cis and trans Requirements for DNA Replication at the Right-End Hairpin of the Human Bocavirus 1 Genome.人博卡病毒1型基因组右端发夹结构处DNA复制的顺式和反式需求分析
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Nonstructural Protein NP1 of Human Bocavirus 1 Plays a Critical Role in the Expression of Viral Capsid Proteins.人博卡病毒1型的非结构蛋白NP1在病毒衣壳蛋白的表达中起关键作用。
J Virol. 2016 Apr 14;90(9):4658-4669. doi: 10.1128/JVI.02964-15. Print 2016 May.
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