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Host ESCRT Proteins Are Required for Bromovirus RNA Replication Compartment Assembly and Function

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dc.contributor.authorDiaz, Arturoen
dc.contributor.authorZhang, Jiantaoen
dc.contributor.authorOllwerther, Abigailen
dc.contributor.authorWang, Xiaofengen
dc.contributor.authorAhlquist, Paulen
dc.contributor.departmentSchool of Plant and Environmental Sciencesen
dc.date.accessioned2018-12-04T18:42:15Zen
dc.date.available2018-12-04T18:42:15Zen
dc.date.issued2015-03-06en
dc.description.abstractPositive-strand RNA viruses genome replication invariably is associated with vesicles or other rearranged cellular membranes. Brome mosaic virus (BMV) RNA replication occurs on perinuclear endoplasmic reticulum (ER) membranes in similar to 70 nm vesicular invaginations (spherules). BMV RNA replication vesicles show multiple parallels with membrane-enveloped, budding retrovirus virions, whose envelopment and release depend on the host ESCRT (endosomal sorting complexes required for transport) membrane-remodeling machinery. We now find that deleting components of the ESCRT pathway results in at least two distinct BMV phenotypes. One group of genes regulate RNA replication and the frequency of viral replication complex formation, but had no effect on spherule size, while a second group of genes regulate RNA replication in a way or ways independent of spherule formation. In particular, deleting SNF7 inhibits BMV RNA replication >25-fold and abolishes detectable BMV spherule formation, even though the BMV RNA replication proteins accumulate and localize normally on perinuclear ER membranes. Moreover, BMV ESCRT recruitment and spherule assembly depend on different sets of protein-protein interactions from those used by multivesicular body vesicles, HIV-1 virion budding, or tomato bushy stunt virus (TBSV) spherule formation. These and other data demonstrate that BMV requires cellular ESCRT components for proper formation and function of its vesicular RNA replication compartments. The results highlight growing but diverse interactions of ESCRT factors with many viruses and viral processes, and potential value of the ESCRT pathway as a target for broad-spectrum antiviral resistance.en
dc.description.sponsorshipThis project was supported by National Institutes of Health Grant GM35072. PA is an investigator of the Howard Hughes Medical Institute and the Morgridge Institute for Research. AD was partially supported by National Institutes of Health training grants T32 GM07215 and T32 AI078985. Work in XW's lab was supported by a Virginia Tech University Startup fund and by the National Science Foundation Grant IOS 1265260. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.en
dc.format.extent26 pagesen
dc.format.mimetypeapplication/pdfen
dc.identifier.doihttps://doi.org/10.1371/journal.ppat.1004742en
dc.identifier.eissn1553-7374en
dc.identifier.issn1553-7366en
dc.identifier.issue3en
dc.identifier.otherUNSP e1004742en
dc.identifier.pmid25748299en
dc.identifier.urihttp://hdl.handle.net/10919/86221en
dc.identifier.volume11en
dc.language.isoenen
dc.publisherPLOSen
dc.rightsCreative Commons Attribution 4.0 Internationalen
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/en
dc.subjectgenes affecting replicationen
dc.subjectvirus genome replicationen
dc.subjecttobacco-mosaic-virusen
dc.subjectendoplasmic-reticulumen
dc.subjectmultivesicular bodyen
dc.subjectviral replicationen
dc.subjectin-vivoen
dc.subjectsaccharomyces-cerevisiaeen
dc.subjectmembrane scissionen
dc.subjectcomplexen
dc.titleHost ESCRT Proteins Are Required for Bromovirus RNA Replication Compartment Assembly and Functionen
dc.title.serialPLOS Pathogensen
dc.typeArticle - Refereeden
dc.type.dcmitypeTexten

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