ANP32B Is a Nuclear Target of Henipavirus M Proteins
ANP32B Is a Nuclear Target of Henipavirus M Proteins
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DOI：
10.1371/journal.pone.0097233
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发表时间：
2014-05-13
期刊：
影响因子：
3.7
通讯作者：
Finke, Stefan
中科院分区：
文献类型：
--
作者：
Bauer, Anja;Neumann, Sebastian;Finke, Stefan
负链RNA病毒（NSV）的膜增殖和出芽主要由病毒基质蛋白（M）驱动。此外，还已知几种M蛋白参与宿主细胞操作。然而，关于细胞靶点和详细分子机制的知识对于许多M蛋白来说是贫乏的。例如，尼帕病毒（NiV）M蛋白通过细胞核的运输对于病毒释放是必不可少的，但NiV M的核靶点仍然未知。为了鉴定亨德拉病毒M蛋白的细胞相互作用物，表达了标记的亨德拉病毒（HeV）M蛋白，并分离和分析了含M的蛋白复合物。复合物中存在酸性富亮氨酸核磷蛋白32家族成员B（ANP 32 B），表明该蛋白质代表病毒基质蛋白的直接或间接相互作用物。ANP32B的过表达导致HeV M蛋白在核内的特异性聚集，从而提供了ANP32B和M蛋白之间的功能联系。在质粒驱动的HeV和NiV基质蛋白表达后以及在NiV感染的细胞中观察到ANP 32 B依赖性核积累。后者表明亨尼帕病毒M蛋白与ANP 32 B的相互作用也发生在病毒复制的背景下。从这些数据中，我们得出结论，ANP32 B是亨尼帕病毒M的核靶点，可能有助于病毒复制。ANP32 B对HeV核穿梭的潜在影响以及HeV M对ANP32 B在宿主细胞存活和基因表达调控中的功能的影响进行了讨论。
Membrane envelopment and budding of negative strand RNA viruses (NSVs) is mainly driven by viral matrix proteins (M). In addition, several M proteins are also known to be involved in host cell manipulation. Knowledge about the cellular targets and detailed molecular mechanisms, however, is poor for many M proteins. For instance, Nipah Virus (NiV) M protein trafficking through the nucleus is essential for virus release, but nuclear targets of NiV M remain unknown. To identify cellular interactors of henipavirus M proteins, tagged Hendra Virus (HeV) M proteins were expressed and M-containing protein complexes were isolated and analysed. Presence of acidic leucine-rich nuclear phosphoprotein 32 family member B (ANP32B) in the complex suggested that this protein represents a direct or indirect interactor of the viral matrix protein. Over-expression of ANP32B led to specific nuclear accumulation of HeV M, providing a functional link between ANP32B and M protein. ANP32B-dependent nuclear accumulation was observed after plasmid-driven expression of HeV and NiV matrix proteins and also in NiV infected cells. The latter indicated that an interaction of henipavirus M protein with ANP32B also occurs in the context of virus replication. From these data we conclude that ANP32B is a nuclear target of henipavirus M that may contribute to virus replication. Potential effects of ANP32B on HeV nuclear shuttling and host cell manipulation by HeV M affecting ANP32B functions in host cell survival and gene expression regulation are discussed.