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SARS-CoV-2破坏剪接、翻译和蛋白质运输以抑制宿主防御
作者:小柯机器人 发布时间:2020/10/11 21:44:03

美国加州理工学院Mitchell Guttman、佛蒙特大学Devdoot Majumdar等研究人员合作发现,SARS-CoV-2破坏剪接、翻译和蛋白质运输以抑制宿主防御。相关论文于2020年10月8日在线发表于国际学术期刊《细胞》。

研究人员全面定义了SARS-CoV-2蛋白与人类RNA之间的相互作用。NSP16与U1和U2剪接RNA的mRNA识别域结合,并起抑制SARS-CoV-2感染后整体剪接mRNA的作用。NSP1在核糖体的mRNA进入通道中与18S核糖体RNA结合,并在感染后导致mRNA翻译的整体抑制。
 
最后,NSP8和NSP9与信号识别颗粒中的7SL RNA结合,并在感染后干扰蛋白质向细胞膜的运输。这些基本细胞功能中每一个的破坏都起着抑制干扰素对病毒感染的反应的作用。这些结果揭示了SARS-CoV-2利用多管齐下的策略来拮抗必需的细胞过程,从而抑制宿主防御。
 
据悉,SARS-CoV-2是最近发现的一种冠状病毒,可引起呼吸道疾病,称为COVID-19。尽管有迫切需求,但人们仍不完全了解SARS-CoV-2发病机理的分子基础。
 
附:英文原文

Title: SARS-CoV-2 disrupts splicing, translation, and protein trafficking to suppress host defenses

Author: Abhik K. Banerjee, Mario R. Blanco, Emily A. Bruce, Drew D. Honson, Linlin M. Chen, Amy Chow, Prashant Bhat, Noah Ollikainen, Sofia A. Quinodoz, Colin Loney, Jasmine Thai, Zachary D. Miller, Aaron E. Lin, Madaline M. Schmidt, Douglas G. Stewart, Daniel Goldfarb, Giuditta De Lorenzo, Suzannah J. Rihn, Rebecca Voorhees, Jason W. Botten, Devdoot Majumdar, Mitchell Guttman

Issue&Volume: 2020-10-08

Abstract: SARS-CoV-2 is a recently identified coronavirus that causes the respiratory disease known as COVID-19. Despite the urgent need, we still do not fully understand the molecular basis of SARS-CoV-2 pathogenesis. Here, we comprehensively define the interactions between SARS-CoV-2 proteins and human RNAs. NSP16 binds to the mRNA recognition domains of the U1 and U2 splicing RNAs and acts to suppress global mRNA splicing upon SARS-CoV-2 infection. NSP1 binds to 18S ribosomal RNA in the mRNA entry channel of the ribosome and leads to global inhibition of mRNA translation upon infection. Finally, NSP8 and NSP9 bind to the 7SL RNA in the Signal Recognition Particle and interfere with protein trafficking to the cell membrane upon infection. Disruption of each of these essential cellular functions acts to suppress the interferon response to viral infection. Our results uncover a multipronged strategy utilized by SARS-CoV-2 to antagonize essential cellular processes to suppress host defenses.

DOI: 10.1016/j.cell.2020.10.004

Source: https://www.cell.com/cell/fulltext/S0092-8674(20)31310-6

期刊信息
Cell:《细胞》,创刊于1974年。隶属于细胞出版社,最新IF:36.216
官方网址:https://www.cell.com/