Jiangnan Liu, Noemi Nagy, Carlos Ayala-Torres, Solenne Bleuse, Francisco Aguilar-Alonso, Ola Larsson, Maria G Masucci
{"title":"eb病毒去泛素酶BPLF1调节应激诱导的核糖体ufmy化和网状吞噬。","authors":"Jiangnan Liu, Noemi Nagy, Carlos Ayala-Torres, Solenne Bleuse, Francisco Aguilar-Alonso, Ola Larsson, Maria G Masucci","doi":"10.1080/15548627.2024.2440846","DOIUrl":null,"url":null,"abstract":"<p><p>The synthesis of membrane and secreted proteins is safeguarded by an endoplasmic reticulum-associated ribosome quality control (ER-RQC) that promotes the disposal of defective translation products by the proteasome or via a lysosome-dependent pathway involving the degradation of portions of the ER by macroautophagy (reticulophagy). The UFMylation of RPL26 on ER-stalled ribosomes is essential for activating the ER-RQC and reticulophagy. Here, we report that the viral deubiquitinase (vDUB) encoded in the N-terminal domain of the Epstein-Barr virus (EBV) large tegument protein BPLF1 hinders the UFMylation of RPL26 on ribosomes that stall at the ER, promotes the stabilization of ER-RQC substrates, and inhibits reticulophagy. The vDUB did not act as a de-UFMylase or interfere with the UFMylation of the ER membrane protein CYB5R3 by the UFL1 ligase. Instead, it copurified with ribosomes in sucrose gradients and abrogated a ZNF598- and LTN1-independent ubiquitination event required for RPL26 UFMylation. Physiological levels of BPLF1 impaired the UFMylation of RPL26 in productively EBV-infected cells, pointing to an important role of the enzyme in regulating the translation quality control that allows the efficient synthesis of viral proteins and the production of infectious virus.<b>Abbreviation</b>: BPLF1, BamH1 P fragment left open readingframe-1; CDK5RAP3, CDK5regulatory subunit associated protein 3; ChFP, mCherry fluorescent protein; DDRGK1, DDRGKdomain containing 1; EBV, Epstein-Barr virus; eGFP, enhancedGFP; ER-RQC, endoplasmicreticulum-associated ribosome quality control; LCL, EBV-carryinglymphoblastoid cell line; GFP, green fluorescent protein; RQC, ribosome quality control; SRP, signal recognition particle; UFM1, ubiquitin fold modifier 1; UFL1, UFM1 specific ligase 1.</p>","PeriodicalId":93893,"journal":{"name":"Autophagy","volume":" ","pages":"996-1018"},"PeriodicalIF":0.0000,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12013442/pdf/","citationCount":"0","resultStr":"{\"title\":\"The Epstein-Barr virus deubiquitinase BPLF1 regulates stress-induced ribosome UFMylation and reticulophagy.\",\"authors\":\"Jiangnan Liu, Noemi Nagy, Carlos Ayala-Torres, Solenne Bleuse, Francisco Aguilar-Alonso, Ola Larsson, Maria G Masucci\",\"doi\":\"10.1080/15548627.2024.2440846\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The synthesis of membrane and secreted proteins is safeguarded by an endoplasmic reticulum-associated ribosome quality control (ER-RQC) that promotes the disposal of defective translation products by the proteasome or via a lysosome-dependent pathway involving the degradation of portions of the ER by macroautophagy (reticulophagy). The UFMylation of RPL26 on ER-stalled ribosomes is essential for activating the ER-RQC and reticulophagy. Here, we report that the viral deubiquitinase (vDUB) encoded in the N-terminal domain of the Epstein-Barr virus (EBV) large tegument protein BPLF1 hinders the UFMylation of RPL26 on ribosomes that stall at the ER, promotes the stabilization of ER-RQC substrates, and inhibits reticulophagy. The vDUB did not act as a de-UFMylase or interfere with the UFMylation of the ER membrane protein CYB5R3 by the UFL1 ligase. Instead, it copurified with ribosomes in sucrose gradients and abrogated a ZNF598- and LTN1-independent ubiquitination event required for RPL26 UFMylation. Physiological levels of BPLF1 impaired the UFMylation of RPL26 in productively EBV-infected cells, pointing to an important role of the enzyme in regulating the translation quality control that allows the efficient synthesis of viral proteins and the production of infectious virus.<b>Abbreviation</b>: BPLF1, BamH1 P fragment left open readingframe-1; CDK5RAP3, CDK5regulatory subunit associated protein 3; ChFP, mCherry fluorescent protein; DDRGK1, DDRGKdomain containing 1; EBV, Epstein-Barr virus; eGFP, enhancedGFP; ER-RQC, endoplasmicreticulum-associated ribosome quality control; LCL, EBV-carryinglymphoblastoid cell line; GFP, green fluorescent protein; RQC, ribosome quality control; SRP, signal recognition particle; UFM1, ubiquitin fold modifier 1; UFL1, UFM1 specific ligase 1.</p>\",\"PeriodicalId\":93893,\"journal\":{\"name\":\"Autophagy\",\"volume\":\" \",\"pages\":\"996-1018\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2025-05-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12013442/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Autophagy\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1080/15548627.2024.2440846\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/1/22 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Autophagy","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1080/15548627.2024.2440846","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/22 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
摘要
膜和分泌蛋白的合成受到内质网相关核糖体质量控制(ER- rqc)的保护,内质网相关核糖体质量控制促进蛋白酶体或溶酶体依赖途径处理有缺陷的翻译产物,溶酶体依赖途径涉及内质网部分通过巨噬(网状吞噬)降解。er停滞核糖体上RPL26的ufmy化对于激活ER-RQC和网状吞噬是必不可少的。在这里,我们报道了在eb病毒(EBV)大被膜蛋白BPLF1的n端区域编码的病毒去泛素酶(vDUB)阻碍了在内质网停滞的核糖体上RPL26的ufmy化,促进了ER- rqc底物的稳定,并抑制了网状吞噬。vDUB不作为去ufmylase或干扰UFL1连接酶对ER膜蛋白CYB5R3的ufmylase。相反,它在蔗糖梯度下与核糖体进行增殖,并消除了RPL26 ufmy化所需的不依赖于ZNF598和ltn1的泛素化事件。生理水平的BPLF1破坏了高产ebv感染细胞中RPL26的ufmyation,这表明该酶在调节翻译质量控制中发挥重要作用,从而使病毒蛋白的有效合成和感染性病毒的产生成为可能。简称:BPLF1, BamH1 P fragment left open readingframe-1;CDK5RAP3, cdk5调控亚基相关蛋白3;ChFP, mCherry荧光蛋白;DDRGK1, DDRGKdomain containing 1;EBV, eb病毒;eGFP enhancedGFP;内质网相关核糖体质量控制;LCL,携带ebv的淋巴母细胞样细胞系;绿色荧光蛋白;RQC,核糖体质量控制;SRP:信号识别粒子;UFM1,泛素折叠修饰因子1;UFL1, UFM1特异性连接酶1。
The Epstein-Barr virus deubiquitinase BPLF1 regulates stress-induced ribosome UFMylation and reticulophagy.
The synthesis of membrane and secreted proteins is safeguarded by an endoplasmic reticulum-associated ribosome quality control (ER-RQC) that promotes the disposal of defective translation products by the proteasome or via a lysosome-dependent pathway involving the degradation of portions of the ER by macroautophagy (reticulophagy). The UFMylation of RPL26 on ER-stalled ribosomes is essential for activating the ER-RQC and reticulophagy. Here, we report that the viral deubiquitinase (vDUB) encoded in the N-terminal domain of the Epstein-Barr virus (EBV) large tegument protein BPLF1 hinders the UFMylation of RPL26 on ribosomes that stall at the ER, promotes the stabilization of ER-RQC substrates, and inhibits reticulophagy. The vDUB did not act as a de-UFMylase or interfere with the UFMylation of the ER membrane protein CYB5R3 by the UFL1 ligase. Instead, it copurified with ribosomes in sucrose gradients and abrogated a ZNF598- and LTN1-independent ubiquitination event required for RPL26 UFMylation. Physiological levels of BPLF1 impaired the UFMylation of RPL26 in productively EBV-infected cells, pointing to an important role of the enzyme in regulating the translation quality control that allows the efficient synthesis of viral proteins and the production of infectious virus.Abbreviation: BPLF1, BamH1 P fragment left open readingframe-1; CDK5RAP3, CDK5regulatory subunit associated protein 3; ChFP, mCherry fluorescent protein; DDRGK1, DDRGKdomain containing 1; EBV, Epstein-Barr virus; eGFP, enhancedGFP; ER-RQC, endoplasmicreticulum-associated ribosome quality control; LCL, EBV-carryinglymphoblastoid cell line; GFP, green fluorescent protein; RQC, ribosome quality control; SRP, signal recognition particle; UFM1, ubiquitin fold modifier 1; UFL1, UFM1 specific ligase 1.