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Murine gammaherpesvirus-68 ORF38 encodes a tegument protein and is packaged into virions during secondary envelopment

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Protein & Cell 2014年第2期5卷 141-150页

作者： Sheng Shen Haitao Guo hongyu deng Chinese Academy of Sciences Key Laboratory of Infection and Immunity Institute of Biophysics Chinese Academy of Sciences Beijing 100101 China University of Chi'nese Academy of Sciences Beijing 100049 China

Tegument is the unique structure of a herpesvirion which occupies the space between nucleocapsid and envelope. Accumulating data have indicated that inter- actions among tegument proteins play a key role in virion morphogenesis. Morphogenesis of gam- maherpesviruses including Kaposi＇s sarcoma-associ- ated herpesvirus （KSHV） and Epstein-Barr virus （EBV） is poorly understood due to the lack of efficient de novo lytic replication in cell culture. Murine gammaherpesvi- rus-68 （MHV-68） is genetically related to these two human herpesviruses and serves as an effective model to study the lytic replication of gammaherpesviruses. We previously showed that ORF33 of MHV-68 encodes a tegument protein and plays an essential role in virion maturation in the cytoplasm. However, the molecular mechanism of how ORF33 participates in virion mor- phogenesis has not been elucidated. In this study we demonstrated that ORF38 of MHV-68 is also a tegument protein and is localized to cytoplasmic compartments during both transient transfection and viral infection. Immuno-gold labeling assay showed that ORF38 is only present on virions that have entered the cytoplasmic vesicles, indicating that ORF38 is packaged into virions during secondary envelopment. We further showed that ORF38 co-localizes with ORF33 during viral infection; therefore, the interaction between ORF38 and ORF33 is conserved among herpesviruses. Notably, we found that although ORF33 by itself is distributed in both the nucleus and the cytoplasm, in the presence of ORF38, ORF33 is co-localized to trans-Golgi network （TGN）, a site where secondary envelopment takes place.

关键词： gammaherpesvirus tegument protein,ORF38 ORF33 TGN

CCAAT/enhancer binding proteins play a role in oriLyt-dependent genome replication during MHV-68 de novo infection

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Protein & Cell 2011年第6期2卷 463-469页

作者： Jing Qi Danyang Gong hongyu deng CAS Key Laboratory of Infection and Immunity Institute of BiophysicsChinese Academy of SciencesBeijing 100101China Graduate School of the Chinese Academy of Sciences Beijing 100080China

Murine gammaherpesvirus 68(MHV-68),a member of the gammaherpesvirus family,replicates robustly in permissive cell lines and is able to infect laboratory ***-68 has emerged as a model for studying the basic aspects of viral replication and host–virus interactions of its human *** genome replication is mediated through a cis-element in the viral genome called the origin of lytic replication(oriLyt).A family of transcription factors,CCAAT/enhancer binding proteins(C/EBPs),assists in oriLyt-mediated DNA replication during gammaherpesvirus *** this study,we examined the role of C/EBPs in gammaherpesvirus DNA replication during de novo infection,using MHV-68 as a *** found that C/EBP α and β bind to the CCAAT boxes in the MHV-68 oriLyt core region both in vitro and in vivo,as demonstrated by electrophoretic mobility shift assay and chromatin immunoprecipitation assay.A dominant negative form of C/EBPs significantly impaired the lytic replication efficiency of MHV-68 on both the plasmid and genome levels in a replication assay,indicating that functional C/EBPs are required for maximal MHV-68 genome DNA ***,our data demonstrate that C/EBPs interact with the oriLyt core region and play an important role in MHV-68 lytic DNA replication during de novo infection.

关键词： C/EBPs murine gammaherpesvirus 68 oriLyt lytic replication

Remodeling of host membranes during herpesvirus assembly and egress

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Protein & Cell 2019年第5期10卷 315-326页

作者： Ying Lv Sheng Zhou Shengyan Gao hongyu deng CAS Key Laboratory of Infection and Immunity Institute of BiophysicsChinese Academy of SciencesBeijing 100101China University of Chinese Academy of Sciences Beijing 100049China CAS Center for Excellence in Biomacromolecules Institute of BiophysicsChinese Academy of SciencesBeijing 100101China

Many viruses,enveloped or non-enveloped,remodel host membrane structures for their replication,assembly and escape from host *** are important human pathogens and cause many *** large enveloped DNA viruses,herpesviruses undergo several complex steps to complete their life cycles and produce infectious ***,herpesvirus assembly initiates in the nucleus,producing nucleocapsids that are too large to cross through the nuclear *** nucleocapsids instead bud at the inner nuclear membrane to form primary enveloped virions in the perinuclear space followed by fusion of the primary envelopes with the outer nuclear membrane,to translocate the nucleocapsids into the ***,nucleocapsids obtain a series of tegument proteins in the cytoplasm and bud into vesicles derived from host organelles to acquire viral *** vesicles are then transported to and fuse with the plasma membrane to release the mature virions to the extracellular ***,at least two budding and fusion events take place at cellular membrane structures during herpesviruses assembly and egress,which induce membrane *** this review,we describe and discuss how herpesviruses exploit and remodel host membrane structures to assemble and escape from the host cell.

关键词： herpesviruses assembly egress budding fusion membrane deformations

Role of tegument proteins in herpesvirus assembly and egress

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Protein & Cell 2010年第11期1卷 987-998页

作者： Haitao Guo Sheng Shen Lili Wang hongyu deng CAS Key Laboratory of Infection and Immunity Institute of BiophysicsChinese Academy of SciencesBeijing 100101China Graduate School of the Chinese Academy of Sciences Beijing 100080China

Morphogenesis and maturation of viral particles is an essential step of viral *** infectious herpesviral particle has a multilayered architecture,and contains a large DNA genome,a capsid shell,a tegument and an envelope spiked with *** to herpesviruses,tegument is a structure that occupies the space between the nucleocapsid and the envelope and contains many virus encoded proteins called tegument *** the tegument has been described as an amorphous structure,but increasing evidence supports the notion that there is an ordered addition of tegument during virion assembly,which is consistent with the important roles of tegument proteins in the assembly and egress of herpesviral *** this review we first give an overview of the herpesvirus assembly and egress *** then discuss the roles of selected tegument proteins in each step of the process,i.e.,primary envelopment,deenvelopment,secondary envelopment and transport of viral *** also suggest key issues that should be addressed in the near future.

关键词： herpesvirus tegument assembly egress transport

Crystal structure and functional implication of the RUN domain of human NESCA

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Protein & Cell 2012年第8期3卷 609-617页

作者： Qifan Sun Chuanhui Han Lan Liu Yizhi Wang hongyu deng Lin Bai Tao Jiang National Laboratory of Biomacromolecules Institute of BiophysicsChinese Academy of SciencesBeijing 100101China Graduate University of Chinese Academy of Sciences Beijing 100039China Chinese Academy of Sciences Key Laboratory of Infection and Immunity Institute of BiophysicsChinese Academy of SciencesBeijing 100101China

NESCA,a newly discovered signaling adapter protein in the NGF-pathway,contains a RUN domain at its *** we report the crystal structure of the NESCA RUN domain determined at 2.0-Å*** overall fold of the NESCA RUN domain comprises nine helices,resembling the RUN domain of RPIPx and the RUN1 domain of ***,compared to the other RUN domains,the RUN domain of NESCA has significantly different surface electrostatic distributions at the putative GTPase-interacting *** demonstrate that the RUN domain of NESCA can bind H-Ras,a downstream signaling molecule of TrkA,with high ***,NESCA RUN can directly interact with *** results provide new insights into how NESCA participates in the NGF-TrkA signaling pathway.

关键词： NESCA RUN domain crystal structure TrkA Ras

Identification of new type I interferon- stimulated genes and investigation of their involvement in IFN-β activation

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Protein & Cell 2018年第9期9卷 799-807页

作者： Xiaolin Zhang Wei Yang Xinlu Wang Xuyuan Zhang Huabin Tian hongyu deng Liguo Zhang Guangxia Gao CAS Key Laboratory of Infection and Immunity CAS Center for Excellence in Biomacromolecules Institute of Biophysics Chinese Academy of Sciences Beijing 100101 China University of Chinese Academy of Sciences Beijing 100049 China

Virus infection induces the production of type I interferons （IFNs）. IFNs bind to their heterodimeric receptors to initiate downstream cascade of signaling, leading to the up-regulation of interferon-stimulated genes （ISGs）. ISGs play very important roles in innate immunity through a variety of mechanisms. Although hundreds of ISGs have been identified, it is commonly recognized that more ISGs await to be discovered. The aim of this study was to identify new ISGs and to probe their roles in regulating virus-induced type I IFN production. We used consensus interferon （Con-IFN）, an artificial alpha IFN that was shown to be more potent than naturally existing type I IFN, to treat three human immune cell lines, CEM, U937 and Daudi cells. Microarray analysis was employed to identify those genes whose expres- sions were up-regulated. Six hundred and seventeen genes were up-regulated more than 3-fold. Out of these 617 genes, 138 were not previously reported as ISGs and thus were further pursued. Validation of these 138 genes using quantitative reverse transcription PCR （qRT-PCR） confirmed 91 genes. We screened 89 genes for those involved in Sendal virus （SeV）-induced IFN-13 promoter activation, and PIM1 was identified as one whose expression inhibited SeV-mediated IFN-β activation. We provide evidence indicating that PIM1 specifically inhibits RIG-I- and MDA5-mediated IFN-β signaling. Our results expand the ISG library and iden- tify PIM1 as an ISG that participates in the regulation of virus-induced type I interferon production.

关键词： interferon-stimulated genes IFN-β signaling PIM1 RIG-I MDA5

Ferroptosis:a critical mechanism of N^(6)-methyladenosine modification involved in carcinogenesis and tumor progression

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Science China(Life Sciences) 2024年第6期67卷 1119-1132页

作者： Qingqing Wei Changning Xue Mengna Li Jianxia Wei Lemei Zheng Shipeng Chen Yumei Duan hongyu deng Faqing Tang Wei Xiong Ming Zhou NHC Key Laboratory of Carcinogenesis Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of MedicineCentral South UniversityChangsha 410013China Cancer Research Institute and School of Basic Medical Sciences Central South UniversityChangsha 410078China The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education Central South UniversityChangsha 410078China Hunan Key Laboratory of Oncotarget Gene Hunan Key Laboratory of Cancer MetabolismHunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of MedicineCentral South UniversityChangsha 410013China

Ferroptosis is an iron-dependent regulatory cell necrosis induced by iron overload and lipid *** occurs when multiple redoxactive enzymes are ectopically expressed or show abnormal ***,the precise regulation of ferroptosis-related molecules is mediated across multiple levels,including transcriptional,posttranscriptional,translational,and epigenetic levels.N^(6)-methyladenosine(m^(6)A)is a highly evolutionarily conserved epigenetic modification in *** m^(6)A modification is commonly linked to tumor proliferation,progression,and therapy resistance because it is involved in RNA metabolic ***,accumulating evidence suggests that dysregulated ferroptosis caused by the m^(6)A modification drives tumor *** this review,we summarized the roles of m^(6)A regulators in ferroptosis-mediated malignant tumor progression and outlined the m^(6)A regulatory mechanism involved in ferroptosis *** also analyzed the potential value and application strategies of targeting m^(6)A/ferroptosis pathway in the clinical diagnosis and therapy of tumors.

关键词： ferroptosis m6A modification RNA methylation m^(6)A regulator tumor progression

Phase separation in herpesvirus assembly

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Phase separation in herpesvirus assembly

2021年全国生物相分离和相变学术研讨会

作者： hongyu deng CAS Key Laboratory of Infection and Immunity CAS Center for Excellence in BiomacromoleculesInstitute of BiophysicsChinese Academy of Sciences University of Chinese Academy of Sciences

A mature herpesvirus particle consists of four distinct structures:a large double-stranded DNA genome,a capsid enclosing the genome,a tegument layer and an *** morphogenesis is a complicated event that takes place in the late phase of herpesvirus lytic life *** viral genome is first packaged into a preformed capsid in the *** nucleocapsid then translocates into the cytoplasm,undergoes tegumentation to acquire a series of tegument proteins,and buds into a glycoproteins-decorated vesicle to form a mature ***,mature virions are released from the cell through *** the dozens of virally-encoded structural proteins are assembled into a mature virion and how this process is regulated temporally and spatially remain poorly *** this talk,I will describe our work on functional identification and characterization of several viral proteins which are essential for virion morphogenesis,and reveal how phase separation plays a critical role in mediating the assembly of a herpesvirus.

关键词： herpesvirus assembly morphogenesis phase separation

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局部平均刚度比对底框结构抗震性能的影响

哈尔滨工程大学学报 2015年第12期36卷 1571-1577页

作者：邓宏宇孙柏涛哈尔滨工程大学航天与建筑工程学院黑龙江哈尔滨150001 中国地震局工程力学研究所地震工程与工程振动重点实验室黑龙江哈尔滨150080

为了研究平面内刚度不均匀性对底框结构抗震性能的影响,提出了局部平均刚度比的概念。建立具有不同局部平均刚度比的ABAQUS有限元模型,并进行弹塑性时程分析。分析结果表明：平面内刚度分布不均匀会导致局部墙体严重破坏,从而影响结构... 详细信息

为了研究平面内刚度不均匀性对底框结构抗震性能的影响,提出了局部平均刚度比的概念。建立具有不同局部平均刚度比的ABAQUS有限元模型,并进行弹塑性时程分析。分析结果表明：平面内刚度分布不均匀会导致局部墙体严重破坏,从而影响结构整体的安全性。局部平均刚度比作为衡量同一楼层平面内局部区域刚度大小的指标,其值过低时会造成该区域抗侧刚度不足,墙体破坏严重;过高时会造成薄弱部位转移,对平面内其他区域的墙体产生不利影响。综合分析以上结果,建议底框结构的局部平均刚度比控制在0.66-1.30,该结论可作为我国抗震规范平面内刚度分布的补充规定,为结构设计提供参考。

关键词：局部平均刚度比底框结构扭转效应抗震能力有限元模拟 ABAQUS 弹塑性时程分析