The invasion of tobacco mosaic virus RNA induces endoplasmic reticulum stress-related autophagy in HeLa cells
Identifieur interne : 002026 ( Main/Exploration ); précédent : 002025; suivant : 002027The invasion of tobacco mosaic virus RNA induces endoplasmic reticulum stress-related autophagy in HeLa cells
Auteurs : Li Li [République populaire de Chine] ; Li Wang [République populaire de Chine] ; Ruijing Xiao [République populaire de Chine] ; Guoguo Zhu [République populaire de Chine] ; Yan Li [République populaire de Chine] ; Changxuan Liu [République populaire de Chine] ; Ru Yang [République populaire de Chine] ; Zhiqing Tang [République populaire de Chine] ; Jie Li [République populaire de Chine] ; Wei Huang [République populaire de Chine] ; Lang Chen [République populaire de Chine] ; Xiaoling Zheng [République populaire de Chine] ; Yuling He [République populaire de Chine] ; Jinquan Tan [République populaire de Chine]Source :
- Bioscience Reports [ 0144-8463 ] ; 2011.
Descripteurs français
- KwdFr :
- MESH :
- cytologie : Cellules HeLa.
- métabolisme : ARN viral.
- physiologie : Virus de la mosaïque du tabac.
- virologie : Cellules HeLa.
- Autophagie, Humains, Interactions hôte-pathogène, Stress du réticulum endoplasmique.
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.
Url:
DOI: 10.1042/BSR20110069
PubMed: 21729006
PubMed Central: 3225954
Affiliations:
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Le document en format XML
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">The invasion of tobacco mosaic virus RNA induces endoplasmic reticulum stress-related autophagy in HeLa cells</title>
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<author><name sortKey="Xiao, Ruijing" sort="Xiao, Ruijing" uniqKey="Xiao R" first="Ruijing" last="Xiao">Ruijing Xiao</name>
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<author><name sortKey="Zhu, Guoguo" sort="Zhu, Guoguo" uniqKey="Zhu G" first="Guoguo" last="Zhu">Guoguo Zhu</name>
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<author><name sortKey="Liu, Changxuan" sort="Liu, Changxuan" uniqKey="Liu C" first="Changxuan" last="Liu">Changxuan Liu</name>
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<author><name sortKey="Chen, Lang" sort="Chen, Lang" uniqKey="Chen L" first="Lang" last="Chen">Lang Chen</name>
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</author>
<author><name sortKey="Zheng, Xiaoling" sort="Zheng, Xiaoling" uniqKey="Zheng X" first="Xiaoling" last="Zheng">Xiaoling Zheng</name>
<affiliation wicri:level="3"><nlm:aff id="A1">*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:aff>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>*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</wicri:regionArea>
<placeName><settlement type="city">Wuhan</settlement>
<region type="région">Hubei</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="He, Yuling" sort="He, Yuling" uniqKey="He Y" first="Yuling" last="He">Yuling He</name>
<affiliation wicri:level="3"><nlm:aff id="A1">*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:aff>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>*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</wicri:regionArea>
<placeName><settlement type="city">Wuhan</settlement>
<region type="région">Hubei</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Tan, Jinquan" sort="Tan, Jinquan" uniqKey="Tan J" first="Jinquan" last="Tan">Jinquan Tan</name>
<affiliation wicri:level="3"><nlm:aff id="A1">*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:aff>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>*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</wicri:regionArea>
<placeName><settlement type="city">Wuhan</settlement>
<region type="région">Hubei</region>
</placeName>
</affiliation>
</author>
</analytic>
<series><title level="j">Bioscience Reports</title>
<idno type="ISSN">0144-8463</idno>
<idno type="eISSN">1573-4935</idno>
<imprint><date when="2011">2011</date>
</imprint>
</series>
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<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="KwdFr" xml:lang="fr"><term>ARN viral (métabolisme)</term>
<term>Autophagie</term>
<term>Cellules HeLa (cytologie)</term>
<term>Cellules HeLa (virologie)</term>
<term>Humains</term>
<term>Interactions hôte-pathogène</term>
<term>Stress du réticulum endoplasmique</term>
<term>Virus de la mosaïque du tabac (physiologie)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>RNA, Viral</term>
</keywords>
<keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Cellules HeLa</term>
</keywords>
<keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>HeLa Cells</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>ARN viral</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Virus de la mosaïque du tabac</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Tobacco Mosaic Virus</term>
</keywords>
<keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Cellules HeLa</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>
<keywords scheme="MESH" xml:lang="fr"><term>Autophagie</term>
<term>Humains</term>
<term>Interactions hôte-pathogène</term>
<term>Stress du réticulum endoplasmique</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><p>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.</p>
</div>
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</div1>
</back>
</TEI>
<affiliations><list><country><li>République populaire de Chine</li>
</country>
<region><li>Anhui</li>
<li>Hubei</li>
</region>
<settlement><li>Hefei</li>
<li>Wuhan</li>
</settlement>
</list>
<tree><country name="République populaire de Chine"><region name="Hubei"><name sortKey="Li, Li" sort="Li, Li" uniqKey="Li L" first="Li" last="Li">Li Li</name>
</region>
<name sortKey="Chen, Lang" sort="Chen, Lang" uniqKey="Chen L" first="Lang" last="Chen">Lang Chen</name>
<name sortKey="He, Yuling" sort="He, Yuling" uniqKey="He Y" first="Yuling" last="He">Yuling He</name>
<name sortKey="Huang, Wei" sort="Huang, Wei" uniqKey="Huang W" first="Wei" last="Huang">Wei Huang</name>
<name sortKey="Li, Jie" sort="Li, Jie" uniqKey="Li J" first="Jie" last="Li">Jie Li</name>
<name sortKey="Li, Yan" sort="Li, Yan" uniqKey="Li Y" first="Yan" last="Li">Yan Li</name>
<name sortKey="Liu, Changxuan" sort="Liu, Changxuan" uniqKey="Liu C" first="Changxuan" last="Liu">Changxuan Liu</name>
<name sortKey="Tan, Jinquan" sort="Tan, Jinquan" uniqKey="Tan J" first="Jinquan" last="Tan">Jinquan Tan</name>
<name sortKey="Tang, Zhiqing" sort="Tang, Zhiqing" uniqKey="Tang Z" first="Zhiqing" last="Tang">Zhiqing Tang</name>
<name sortKey="Wang, Li" sort="Wang, Li" uniqKey="Wang L" first="Li" last="Wang">Li Wang</name>
<name sortKey="Xiao, Ruijing" sort="Xiao, Ruijing" uniqKey="Xiao R" first="Ruijing" last="Xiao">Ruijing Xiao</name>
<name sortKey="Yang, Ru" sort="Yang, Ru" uniqKey="Yang R" first="Ru" last="Yang">Ru Yang</name>
<name sortKey="Zheng, Xiaoling" sort="Zheng, Xiaoling" uniqKey="Zheng X" first="Xiaoling" last="Zheng">Xiaoling Zheng</name>
<name sortKey="Zhu, Guoguo" sort="Zhu, Guoguo" uniqKey="Zhu G" first="Guoguo" last="Zhu">Guoguo Zhu</name>
</country>
</tree>
</affiliations>
</record>
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