Contribution of trafficking signals in the cytoplasmic tail of the infectious bronchitis virus spike protein to virus infection.
Identifieur interne : 004887 ( Main/Exploration ); précédent : 004886; suivant : 004888Contribution of trafficking signals in the cytoplasmic tail of the infectious bronchitis virus spike protein to virus infection.
Auteurs : Soonjeon Youn [États-Unis] ; Ellen W. Collisson ; Carolyn E. MachamerSource :
- Journal of virology [ 0022-538X ] ; 2005.
Descripteurs français
- KwdFr :
- Animaux, Cellules Vero, Cellules géantes, Cytoplasme (métabolisme), Glycoprotéine de spicule des coronavirus, Glycoprotéines membranaires (génétique), Glycoprotéines membranaires (métabolisme), Infections à coronavirus (virologie), Mutation, Protéines de l'enveloppe virale (génétique), Protéines de l'enveloppe virale (métabolisme), Réplication virale, Réticulum endoplasmique (métabolisme), Réticulum endoplasmique (virologie), Transduction du signal, Virus de la bronchite infectieuse (métabolisme), Virus de la bronchite infectieuse (physiologie).
- MESH :
- génétique : Glycoprotéines membranaires, Protéines de l'enveloppe virale.
- métabolisme : Cytoplasme, Glycoprotéines membranaires, Protéines de l'enveloppe virale, Réticulum endoplasmique, Virus de la bronchite infectieuse.
- physiologie : Virus de la bronchite infectieuse.
- virologie : Infections à coronavirus, Réticulum endoplasmique.
- Animaux, Cellules Vero, Cellules géantes, Glycoprotéine de spicule des coronavirus, Mutation, Réplication virale, Transduction du signal.
English descriptors
- KwdEn :
- Animals, Chlorocebus aethiops, Coronavirus Infections (virology), Cytoplasm (metabolism), Endoplasmic Reticulum (metabolism), Endoplasmic Reticulum (virology), Giant Cells, Infectious bronchitis virus (metabolism), Infectious bronchitis virus (physiology), Membrane Glycoproteins (genetics), Membrane Glycoproteins (metabolism), Mutation, Signal Transduction, Spike Glycoprotein, Coronavirus, Vero Cells, Viral Envelope Proteins (genetics), Viral Envelope Proteins (metabolism), Virus Replication.
- MESH :
- chemical , genetics : Membrane Glycoproteins, Viral Envelope Proteins.
- metabolism : Cytoplasm, Endoplasmic Reticulum, Infectious bronchitis virus, Membrane Glycoproteins, Viral Envelope Proteins.
- physiology : Infectious bronchitis virus.
- virology : Coronavirus Infections, Endoplasmic Reticulum.
- Animals, Chlorocebus aethiops, Giant Cells, Mutation, Signal Transduction, Spike Glycoprotein, Coronavirus, Vero Cells, Virus Replication.
Abstract
Coronavirus spike (S) proteins are responsible for binding and fusion with target cells and thus play an essential role in virus infection. Recently, we identified a dilysine endoplasmic reticulum (ER) retrieval signal and a tyrosine-based endocytosis signal in the cytoplasmic tail of the S protein of infectious bronchitis virus (IBV). Here, an infectious cDNA clone of IBV was used to address the importance of the S protein trafficking signals to virus infection. We constructed infectious cDNA clones lacking the ER retrieval signal, the endocytosis signal, or both. The virus lacking the ER retrieval signal was viable. However, this virus had a growth defect at late times postinfection and produced larger plaques than IBV. Further analysis confirmed that the mutant S protein trafficked though the secretory pathway faster than wild-type S protein. A more dramatic phenotype was obtained when the endocytosis signal was mutated. Recombinant viruses lacking the endocytosis signal (in combination with a mutated dilysine signal or alone) could not be recovered, even though transient syncytia were formed in transfected cells. Our results suggest that the endocytosis signal of IBV S is essential for productive virus infection.
DOI: 10.1128/JVI.79.21.13209-13217.2005
PubMed: 16227244
Affiliations:
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Wolfe St., Baltimore, MD 21205, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Cell Biology, Johns Hopkins University School of Medicine, 725 N. Wolfe St., Baltimore, MD 21205</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author><author><name sortKey="Collisson, Ellen W" sort="Collisson, Ellen W" uniqKey="Collisson E" first="Ellen W" last="Collisson">Ellen W. Collisson</name></author><author><name sortKey="Machamer, Carolyn E" sort="Machamer, Carolyn E" uniqKey="Machamer C" first="Carolyn E" last="Machamer">Carolyn E. 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Recently, we identified a dilysine endoplasmic reticulum (ER) retrieval signal and a tyrosine-based endocytosis signal in the cytoplasmic tail of the S protein of infectious bronchitis virus (IBV). Here, an infectious cDNA clone of IBV was used to address the importance of the S protein trafficking signals to virus infection. We constructed infectious cDNA clones lacking the ER retrieval signal, the endocytosis signal, or both. The virus lacking the ER retrieval signal was viable. However, this virus had a growth defect at late times postinfection and produced larger plaques than IBV. Further analysis confirmed that the mutant S protein trafficked though the secretory pathway faster than wild-type S protein. A more dramatic phenotype was obtained when the endocytosis signal was mutated. Recombinant viruses lacking the endocytosis signal (in combination with a mutated dilysine signal or alone) could not be recovered, even though transient syncytia were formed in transfected cells. Our results suggest that the endocytosis signal of IBV S is essential for productive virus infection.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Maryland</li></region></list><tree><noCountry><name sortKey="Collisson, Ellen W" sort="Collisson, Ellen W" uniqKey="Collisson E" first="Ellen W" last="Collisson">Ellen W. Collisson</name><name sortKey="Machamer, Carolyn E" sort="Machamer, Carolyn E" uniqKey="Machamer C" first="Carolyn E" last="Machamer">Carolyn E. Machamer</name></noCountry><country name="États-Unis"><region name="Maryland"><name sortKey="Youn, Soonjeon" sort="Youn, Soonjeon" uniqKey="Youn S" first="Soonjeon" last="Youn">Soonjeon Youn</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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