The invasion of tobacco mosaic virus RNA induces endoplasmic reticulum stress-related autophagy in HeLa cells.
Identifieur interne : 001501 ( PubMed/Corpus ); précédent : 001500; suivant : 001502The invasion of tobacco mosaic virus RNA induces endoplasmic reticulum stress-related autophagy in HeLa cells.
Auteurs : Li Li ; Li Wang ; Ruijing Xiao ; Guoguo Zhu ; Yan Li ; Changxuan Liu ; Ru Yang ; Zhiqing Tang ; Jie Li ; Wei Huang ; Lang Chen ; Xiaoling Zheng ; Yuling He ; Jinquan TanSource :
- Bioscience reports [ 1573-4935 ] ; 2012.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : RNA, Viral.
- cytology : HeLa Cells.
- physiology : Tobacco Mosaic Virus.
- virology : HeLa Cells.
- Autophagy, Endoplasmic Reticulum Stress, Host-Pathogen Interactions, Humans.
Abstract
The ability of human cells to defend against viruses originating from distant species has long been ignored. Owing to the pressure of natural evolution and human exploration, some of these viruses may be able to invade human beings. If their 'fresh' host had no defences, the viruses could cause a serious pandemic, as seen with HIV, SARS (severe acute respiratory syndrome) and avian influenza virus that originated from chimpanzees, the common palm civet and birds, respectively. It is unknown whether the human immune system could tolerate invasion with a plant virus. To model such an alien virus invasion, we chose TMV (tobacco mosaic virus) and used human epithelial carcinoma cells (HeLa cells) as its 'fresh' host. We established a reliable system for transfecting TMV-RNA into HeLa cells and found that TMV-RNA triggered autophagy in HeLa cells as shown by the appearance of autophagic vacuoles, the conversion of LC3-I (light chain protein 3-I) to LC3-II, the up-regulated expression of Beclin1 and the accumulation of TMV protein on autophagosomal membranes. We observed suspected TMV virions in HeLa cells by TEM (transmission electron microscopy). Furthermore, we found that TMV-RNA was translated into CP (coat protein) in the ER (endoplasmic reticulum) and that TMV-positive RNA translocated from the cytoplasm to the nucleolus. Finally, we detected greatly increased expression of GRP78 (78 kDa glucose-regulated protein), a typical marker of ERS (ER stress) and found that the formation of autophagosomes was closely related to the expanded ER membrane. Taken together, our data indicate that HeLa cells used ERS and ERS-related autophagy to defend against TMV-RNA.
DOI: 10.1042/BSR20110069
PubMed: 21729006
Links to Exploration step
pubmed:21729006Le document en format XML
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last="He">Yuling He</name></author><author><name sortKey="Tan, Jinquan" sort="Tan, Jinquan" uniqKey="Tan J" first="Jinquan" last="Tan">Jinquan Tan</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2012">2012</date><idno type="RBID">pubmed:21729006</idno><idno type="pmid">21729006</idno><idno type="doi">10.1042/BSR20110069</idno><idno type="wicri:Area/PubMed/Corpus">001501</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001501</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">The invasion of tobacco mosaic virus RNA induces endoplasmic reticulum stress-related autophagy in HeLa cells.</title><author><name sortKey="Li, Li" sort="Li, Li" uniqKey="Li L" first="Li" last="Li">Li Li</name><affiliation><nlm:affiliation>Laboratory of Allergy and Clinical Immunology, Department of Immunology, Institute of Allergy and Immune-related Diseases, Centre for Medical Research, Wuhan University School of Medicine, Wuhan, People's Republic of China.</nlm:affiliation></affiliation></author><author><name sortKey="Wang, Li" sort="Wang, Li" uniqKey="Wang L" first="Li" last="Wang">Li Wang</name></author><author><name sortKey="Xiao, Ruijing" sort="Xiao, Ruijing" uniqKey="Xiao R" first="Ruijing" last="Xiao">Ruijing Xiao</name></author><author><name sortKey="Zhu, Guoguo" sort="Zhu, Guoguo" uniqKey="Zhu G" first="Guoguo" last="Zhu">Guoguo Zhu</name></author><author><name sortKey="Li, Yan" sort="Li, Yan" uniqKey="Li Y" first="Yan" last="Li">Yan Li</name></author><author><name sortKey="Liu, Changxuan" sort="Liu, Changxuan" uniqKey="Liu C" first="Changxuan" last="Liu">Changxuan Liu</name></author><author><name sortKey="Yang, Ru" sort="Yang, Ru" uniqKey="Yang R" first="Ru" last="Yang">Ru Yang</name></author><author><name sortKey="Tang, Zhiqing" sort="Tang, Zhiqing" uniqKey="Tang Z" first="Zhiqing" last="Tang">Zhiqing Tang</name></author><author><name sortKey="Li, Jie" sort="Li, Jie" uniqKey="Li J" first="Jie" last="Li">Jie Li</name></author><author><name sortKey="Huang, Wei" sort="Huang, Wei" uniqKey="Huang W" first="Wei" last="Huang">Wei Huang</name></author><author><name sortKey="Chen, Lang" sort="Chen, Lang" uniqKey="Chen L" first="Lang" last="Chen">Lang Chen</name></author><author><name sortKey="Zheng, Xiaoling" sort="Zheng, Xiaoling" uniqKey="Zheng X" first="Xiaoling" last="Zheng">Xiaoling Zheng</name></author><author><name sortKey="He, Yuling" sort="He, Yuling" uniqKey="He Y" first="Yuling" last="He">Yuling He</name></author><author><name sortKey="Tan, Jinquan" sort="Tan, Jinquan" uniqKey="Tan J" first="Jinquan" last="Tan">Jinquan Tan</name></author></analytic><series><title level="j">Bioscience reports</title><idno type="eISSN">1573-4935</idno><imprint><date when="2012" type="published">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Autophagy</term><term>Endoplasmic Reticulum Stress</term><term>HeLa Cells (cytology)</term><term>HeLa Cells (virology)</term><term>Host-Pathogen Interactions</term><term>Humans</term><term>RNA, Viral (metabolism)</term><term>Tobacco Mosaic Virus (physiology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>RNA, Viral</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>HeLa Cells</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Tobacco Mosaic Virus</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>HeLa Cells</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Autophagy</term><term>Endoplasmic Reticulum Stress</term><term>Host-Pathogen Interactions</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The ability of human cells to defend against viruses originating from distant species has long been ignored. Owing to the pressure of natural evolution and human exploration, some of these viruses may be able to invade human beings. If their 'fresh' host had no defences, the viruses could cause a serious pandemic, as seen with HIV, SARS (severe acute respiratory syndrome) and avian influenza virus that originated from chimpanzees, the common palm civet and birds, respectively. It is unknown whether the human immune system could tolerate invasion with a plant virus. To model such an alien virus invasion, we chose TMV (tobacco mosaic virus) and used human epithelial carcinoma cells (HeLa cells) as its 'fresh' host. We established a reliable system for transfecting TMV-RNA into HeLa cells and found that TMV-RNA triggered autophagy in HeLa cells as shown by the appearance of autophagic vacuoles, the conversion of LC3-I (light chain protein 3-I) to LC3-II, the up-regulated expression of Beclin1 and the accumulation of TMV protein on autophagosomal membranes. We observed suspected TMV virions in HeLa cells by TEM (transmission electron microscopy). Furthermore, we found that TMV-RNA was translated into CP (coat protein) in the ER (endoplasmic reticulum) and that TMV-positive RNA translocated from the cytoplasm to the nucleolus. Finally, we detected greatly increased expression of GRP78 (78 kDa glucose-regulated protein), a typical marker of ERS (ER stress) and found that the formation of autophagosomes was closely related to the expanded ER membrane. Taken together, our data indicate that HeLa cells used ERS and ERS-related autophagy to defend against TMV-RNA.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">21729006</PMID><DateCompleted><Year>2012</Year><Month>03</Month><Day>13</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1573-4935</ISSN><JournalIssue CitedMedium="Internet"><Volume>32</Volume><Issue>2</Issue><PubDate><Year>2012</Year><Month>Apr</Month><Day>01</Day></PubDate></JournalIssue><Title>Bioscience reports</Title><ISOAbbreviation>Biosci. Rep.</ISOAbbreviation></Journal><ArticleTitle>The invasion of tobacco mosaic virus RNA induces endoplasmic reticulum stress-related autophagy in HeLa cells.</ArticleTitle><Pagination><MedlinePgn>171-86</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1042/BSR20110069</ELocationID><Abstract><AbstractText>The ability of human cells to defend against viruses originating from distant species has long been ignored. Owing to the pressure of natural evolution and human exploration, some of these viruses may be able to invade human beings. If their 'fresh' host had no defences, the viruses could cause a serious pandemic, as seen with HIV, SARS (severe acute respiratory syndrome) and avian influenza virus that originated from chimpanzees, the common palm civet and birds, respectively. It is unknown whether the human immune system could tolerate invasion with a plant virus. To model such an alien virus invasion, we chose TMV (tobacco mosaic virus) and used human epithelial carcinoma cells (HeLa cells) as its 'fresh' host. We established a reliable system for transfecting TMV-RNA into HeLa cells and found that TMV-RNA triggered autophagy in HeLa cells as shown by the appearance of autophagic vacuoles, the conversion of LC3-I (light chain protein 3-I) to LC3-II, the up-regulated expression of Beclin1 and the accumulation of TMV protein on autophagosomal membranes. We observed suspected TMV virions in HeLa cells by TEM (transmission electron microscopy). Furthermore, we found that TMV-RNA was translated into CP (coat protein) in the ER (endoplasmic reticulum) and that TMV-positive RNA translocated from the cytoplasm to the nucleolus. Finally, we detected greatly increased expression of GRP78 (78 kDa glucose-regulated protein), a typical marker of ERS (ER stress) and found that the formation of autophagosomes was closely related to the expanded ER membrane. Taken together, our data indicate that HeLa cells used ERS and ERS-related autophagy to defend against TMV-RNA.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Li</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Laboratory of Allergy and Clinical Immunology, Department of Immunology, Institute of Allergy and Immune-related Diseases, Centre for Medical Research, Wuhan University School of Medicine, Wuhan, People's Republic of China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Li</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Xiao</LastName><ForeName>Ruijing</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Zhu</LastName><ForeName>Guoguo</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Yan</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Changxuan</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Ru</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Tang</LastName><ForeName>Zhiqing</ForeName><Initials>Z</Initials></Author><Author ValidYN="Y"><LastName>Li</LastName><ForeName>Jie</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Huang</LastName><ForeName>Wei</ForeName><Initials>W</Initials></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Lang</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Zheng</LastName><ForeName>Xiaoling</ForeName><Initials>X</Initials></Author><Author ValidYN="Y"><LastName>He</LastName><ForeName>Yuling</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Tan</LastName><ForeName>Jinquan</ForeName><Initials>J</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType 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