对病毒许可与敌对细胞状态的多组学分析揭示了控制病毒感染的蛋白质网络

Honglin Chen, Philip D Charles, Quan Gu, Sabrina Liberatori, David L Robertson, Massimo Palmarini, Sam J Wilson, Shabaz Mohammed, Alfredo Castello
{"title":"对病毒许可与敌对细胞状态的多组学分析揭示了控制病毒感染的蛋白质网络","authors":"Honglin Chen, Philip D Charles, Quan Gu, Sabrina Liberatori, David L Robertson, Massimo Palmarini, Sam J Wilson, Shabaz Mohammed, Alfredo Castello","doi":"10.1101/2024.08.29.610331","DOIUrl":null,"url":null,"abstract":"The capacity of host cells to sustain or restrict virus infection is influenced by their proteome. Understanding the compendium of proteins defining cellular permissiveness is key to many questions in fundamental virology. Here, we apply a multiomic approach to determine the proteins that are associated with highly permissive, intermediate, and hostile cellular states. We observed two groups of differentially regulated genes: i) with robust changes in mRNA and protein levels, and ii) with protein/RNA discordances. Many of the latter are classified as interferon stimulated genes (ISGs) but have no reported antiviral activity. This suggests that IFN-dependent changes in mRNA levels do not imply antiviral function. Phosphoproteomics revealed an additional regulatory layer involving non-signalling proteins with altered phosphorylation. Indeed, we confirmed that several permissiveness-associated proteins with changes in abundance or phosphorylation regulate infection fitness. Altogether, our study provides a comprehensive and systematic map of the cellular alterations driving virus susceptibility.","PeriodicalId":501471,"journal":{"name":"bioRxiv - Pathology","volume":"173 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Multi-omics analysis of virus-permissive versus hostile cellular states reveals protein networks controlling virus infection\",\"authors\":\"Honglin Chen, Philip D Charles, Quan Gu, Sabrina Liberatori, David L Robertson, Massimo Palmarini, Sam J Wilson, Shabaz Mohammed, Alfredo Castello\",\"doi\":\"10.1101/2024.08.29.610331\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"The capacity of host cells to sustain or restrict virus infection is influenced by their proteome. Understanding the compendium of proteins defining cellular permissiveness is key to many questions in fundamental virology. Here, we apply a multiomic approach to determine the proteins that are associated with highly permissive, intermediate, and hostile cellular states. We observed two groups of differentially regulated genes: i) with robust changes in mRNA and protein levels, and ii) with protein/RNA discordances. Many of the latter are classified as interferon stimulated genes (ISGs) but have no reported antiviral activity. This suggests that IFN-dependent changes in mRNA levels do not imply antiviral function. Phosphoproteomics revealed an additional regulatory layer involving non-signalling proteins with altered phosphorylation. Indeed, we confirmed that several permissiveness-associated proteins with changes in abundance or phosphorylation regulate infection fitness. Altogether, our study provides a comprehensive and systematic map of the cellular alterations driving virus susceptibility.\",\"PeriodicalId\":501471,\"journal\":{\"name\":\"bioRxiv - Pathology\",\"volume\":\"173 1\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-08-30\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"bioRxiv - Pathology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1101/2024.08.29.610331\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"bioRxiv - Pathology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1101/2024.08.29.610331","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

摘要

宿主细胞维持或限制病毒感染的能力受其蛋白质组的影响。了解定义细胞允许性的蛋白质大全是基础病毒学中许多问题的关键。在这里,我们采用多组学方法来确定与细胞的高度允许性、中间状态和敌对状态相关的蛋白质。我们观察到两组差异调控基因:i) mRNA 和蛋白质水平变化强劲;ii) 蛋白质/RNA 不一致。后者中有许多被归类为干扰素刺激基因(ISGs),但没有抗病毒活性的报道。这表明,依赖于 IFN 的 mRNA 水平变化并不意味着具有抗病毒功能。磷酸化蛋白质组学揭示了另一个调控层,其中涉及磷酸化改变的非信号蛋白。事实上,我们证实了几种与允许性相关的蛋白的丰度或磷酸化的变化会调节感染的适应性。总之,我们的研究为驱动病毒易感性的细胞变化提供了一个全面而系统的图谱。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Multi-omics analysis of virus-permissive versus hostile cellular states reveals protein networks controlling virus infection
The capacity of host cells to sustain or restrict virus infection is influenced by their proteome. Understanding the compendium of proteins defining cellular permissiveness is key to many questions in fundamental virology. Here, we apply a multiomic approach to determine the proteins that are associated with highly permissive, intermediate, and hostile cellular states. We observed two groups of differentially regulated genes: i) with robust changes in mRNA and protein levels, and ii) with protein/RNA discordances. Many of the latter are classified as interferon stimulated genes (ISGs) but have no reported antiviral activity. This suggests that IFN-dependent changes in mRNA levels do not imply antiviral function. Phosphoproteomics revealed an additional regulatory layer involving non-signalling proteins with altered phosphorylation. Indeed, we confirmed that several permissiveness-associated proteins with changes in abundance or phosphorylation regulate infection fitness. Altogether, our study provides a comprehensive and systematic map of the cellular alterations driving virus susceptibility.
求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信