Rotavirus increases levels of lipidated LC3 supporting accumulation of infectious progeny virus without inducing autophagosome formation.
Replication of many RNA viruses benefits from subversion of the autophagic pathway through many different mechanisms. Rotavirus, the main etiologic agent of pediatric gastroenteritis worldwide, has been recently described to induce accumulation of autophagosomes as a mean for targeting viral protein...
| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Public Library of Science (PLoS)
2014-01-01
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| Series: | PLoS ONE |
| Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24736649/?tool=EBI |
| _version_ | 1819176428078366720 |
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| author | Francesca Arnoldi Giuditta De Lorenzo Miguel Mano Elisabeth M Schraner Peter Wild Catherine Eichwald Oscar R Burrone |
| author_facet | Francesca Arnoldi Giuditta De Lorenzo Miguel Mano Elisabeth M Schraner Peter Wild Catherine Eichwald Oscar R Burrone |
| author_sort | Francesca Arnoldi |
| collection | DOAJ |
| description | Replication of many RNA viruses benefits from subversion of the autophagic pathway through many different mechanisms. Rotavirus, the main etiologic agent of pediatric gastroenteritis worldwide, has been recently described to induce accumulation of autophagosomes as a mean for targeting viral proteins to the sites of viral replication. Here we show that the viral-induced increase of the lipidated form of LC3 does not correlate with an augmented formation of autophagosomes, as detected by immunofluorescence and electron microscopy. The LC3-II accumulation was found to be dependent on active rotavirus replication through the use of antigenically intact inactivated viral particles and of siRNAs targeting viral genes that are essential for viral replication. Silencing expression of LC3 or of Atg7, a protein involved in LC3 lipidation, resulted in a significant impairment of viral titers, indicating that these elements of the autophagic pathway are required at late stages of the viral cycle. |
| first_indexed | 2024-12-22T21:10:36Z |
| format | Article |
| id | doaj.art-91f5ca427fab47bca2101ed0b9d2cdb2 |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-12-22T21:10:36Z |
| publishDate | 2014-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-91f5ca427fab47bca2101ed0b9d2cdb22022-12-21T18:12:32ZengPublic Library of Science (PLoS)PLoS ONE1932-62032014-01-0194e9519710.1371/journal.pone.0095197Rotavirus increases levels of lipidated LC3 supporting accumulation of infectious progeny virus without inducing autophagosome formation.Francesca ArnoldiGiuditta De LorenzoMiguel ManoElisabeth M SchranerPeter WildCatherine EichwaldOscar R BurroneReplication of many RNA viruses benefits from subversion of the autophagic pathway through many different mechanisms. Rotavirus, the main etiologic agent of pediatric gastroenteritis worldwide, has been recently described to induce accumulation of autophagosomes as a mean for targeting viral proteins to the sites of viral replication. Here we show that the viral-induced increase of the lipidated form of LC3 does not correlate with an augmented formation of autophagosomes, as detected by immunofluorescence and electron microscopy. The LC3-II accumulation was found to be dependent on active rotavirus replication through the use of antigenically intact inactivated viral particles and of siRNAs targeting viral genes that are essential for viral replication. Silencing expression of LC3 or of Atg7, a protein involved in LC3 lipidation, resulted in a significant impairment of viral titers, indicating that these elements of the autophagic pathway are required at late stages of the viral cycle.https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24736649/?tool=EBI |
| spellingShingle | Francesca Arnoldi Giuditta De Lorenzo Miguel Mano Elisabeth M Schraner Peter Wild Catherine Eichwald Oscar R Burrone Rotavirus increases levels of lipidated LC3 supporting accumulation of infectious progeny virus without inducing autophagosome formation. PLoS ONE |
| title | Rotavirus increases levels of lipidated LC3 supporting accumulation of infectious progeny virus without inducing autophagosome formation. |
| title_full | Rotavirus increases levels of lipidated LC3 supporting accumulation of infectious progeny virus without inducing autophagosome formation. |
| title_fullStr | Rotavirus increases levels of lipidated LC3 supporting accumulation of infectious progeny virus without inducing autophagosome formation. |
| title_full_unstemmed | Rotavirus increases levels of lipidated LC3 supporting accumulation of infectious progeny virus without inducing autophagosome formation. |
| title_short | Rotavirus increases levels of lipidated LC3 supporting accumulation of infectious progeny virus without inducing autophagosome formation. |
| title_sort | rotavirus increases levels of lipidated lc3 supporting accumulation of infectious progeny virus without inducing autophagosome formation |
| url | https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24736649/?tool=EBI |
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