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植物抗病毒免疫中的翻译控制。

Translational control in plant antiviral immunity.

作者信息

Machado João Paulo B, Calil Iara P, Santos Anésia A, Fontes Elizabeth P B

机构信息

Department of Biochemistry and Molecular Biology, BIOAGRO, National Institute of Science and Technology in Plant-Pest Interactions, Universidade Federal de Viçosa, 36571.000, Viçosa, MG, Brazil.

Department of General Biology, Universidade Federal de Viçosa, 36571.000, Viçosa, MG, Brazil.

出版信息

Genet Mol Biol. 2017;40(1 suppl 1):292-304. doi: 10.1590/1678-4685-GMB-2016-0092. Epub 2017 Feb 13.

DOI:10.1590/1678-4685-GMB-2016-0092
PMID:28199446
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5452134/
Abstract

Due to the limited coding capacity of viral genomes, plant viruses depend extensively on the host cell machinery to support the viral life cycle and, thereby, interact with a large number of host proteins during infection. Within this context, as plant viruses do not harbor translation-required components, they have developed several strategies to subvert the host protein synthesis machinery to produce rapidly and efficiently the viral proteins. As a countermeasure against infection, plants have evolved defense mechanisms that impair viral infections. Among them, the host-mediated translational suppression has been characterized as an efficient mean to restrict infection. To specifically suppress translation of viral mRNAs, plants can deploy susceptible recessive resistance genes, which encode translation initiation factors from the eIF4E and eIF4G family and are required for viral mRNA translation and multiplication. Additionally, recent evidence has demonstrated that, alternatively to the cleavage of viral RNA targets, host cells can suppress viral protein translation to silence viral RNA. Finally, a novel strategy of plant antiviral defense based on suppression of host global translation, which is mediated by the transmembrane immune receptor NIK1 (nuclear shuttle protein (NSP)-Interacting Kinase1), is discussed in this review.

摘要

由于病毒基因组的编码能力有限,植物病毒在很大程度上依赖宿主细胞机制来支持病毒生命周期,因此在感染过程中会与大量宿主蛋白相互作用。在此背景下,由于植物病毒不具备翻译所需的组件,它们已开发出多种策略来颠覆宿主蛋白合成机制,以便快速高效地产生病毒蛋白。作为对抗感染的一种对策,植物进化出了损害病毒感染的防御机制。其中,宿主介导的翻译抑制已被认为是限制感染的一种有效手段。为了特异性抑制病毒mRNA的翻译,植物可以利用易感隐性抗性基因,这些基因编码来自eIF4E和eIF4G家族的翻译起始因子,是病毒mRNA翻译和增殖所必需的。此外,最近的证据表明,除了切割病毒RNA靶标外,宿主细胞还可以抑制病毒蛋白翻译以使病毒RNA沉默。最后,本文综述了一种基于跨膜免疫受体NIK1(核穿梭蛋白(NSP)相互作用激酶1)介导的抑制宿主全局翻译的植物抗病毒防御新策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/632d/5452134/9196e8a994a5/1415-4757-gmb-1678-4685-GMB-2016-0092-gf03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/632d/5452134/ee3c9afee318/1415-4757-gmb-1678-4685-GMB-2016-0092-gf01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/632d/5452134/830ea2721cda/1415-4757-gmb-1678-4685-GMB-2016-0092-gf02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/632d/5452134/9196e8a994a5/1415-4757-gmb-1678-4685-GMB-2016-0092-gf03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/632d/5452134/ee3c9afee318/1415-4757-gmb-1678-4685-GMB-2016-0092-gf01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/632d/5452134/830ea2721cda/1415-4757-gmb-1678-4685-GMB-2016-0092-gf02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/632d/5452134/9196e8a994a5/1415-4757-gmb-1678-4685-GMB-2016-0092-gf03.jpg

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