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2011-09-01Zeitschriftenartikel DOI: 10.1371/journal.ppat.1002187
Influenza Virus Ribonucleoprotein Complexes Gain Preferential Access to Cellular Export Machinery through Chromatin Targeting
dc.contributor.authorChase, Geoffrey P.
dc.contributor.authorRameix-Welti, Marie-Anne
dc.contributor.authorZvirbliene, Aurelija
dc.contributor.authorZvirblis, Gintautas
dc.contributor.authorGötz, Veronika
dc.contributor.authorWolff, Thorsten
dc.contributor.authorNaffakh, Nadia
dc.contributor.authorSchwemmle, Martin
dc.date.accessioned2018-05-07T14:52:50Z
dc.date.available2018-05-07T14:52:50Z
dc.date.created2011-10-10
dc.date.issued2011-09-01none
dc.identifier.otherhttp://edoc.rki.de/oa/articles/retcIBICX40mU/PDF/22h9pL0F1GdsU.pdf
dc.identifier.urihttp://edoc.rki.de/176904/964
dc.description.abstractIn contrast to most RNA viruses, influenza viruses replicate their genome in the nucleus of infected cells. As a result, newly-synthesized vRNA genomes, in the form of viral ribonucleoprotein complexes (vRNPs), must be exported to the cytoplasm for productive infection. To characterize the composition of vRNP export complexes and their interplay with the nucleus of infected cells, we affinity-purified tagged vRNPs from biochemically fractionated infected nuclei. After treatment of infected cells with leptomycin B, a potent inhibitor of Crm1-mediated export, we isolated vRNP export complexes which, unexpectedly, were tethered to the host-cell chromatin with very high affinity. At late time points of infection, the cellular export receptor Crm1 also accumulated at the same regions of the chromatin as vRNPs, which led to a decrease in the export of other nuclear Crm1 substrates from the nucleus. Interestingly, chromatin targeting of vRNP export complexes brought them into association with Rcc1, the Ran guanine exchange factor responsible for generating RanGTP and driving Crm1-dependent nuclear export. Thus, influenza viruses gain preferential access to newly-generated host cell export machinery by targeting vRNP export complexes at the sites of Ran regeneration.eng
dc.language.isoeng
dc.publisherRobert Koch-Institut, Infektionskrankheiten / Erreger
dc.subjectCell Lineeng
dc.subjectAnimalseng
dc.subjectRibonucleoproteins/metabolismeng
dc.subjectReceptorseng
dc.subjectDogseng
dc.subjectNuclear Proteins/metabolismeng
dc.subjectActive Transport Cell Nucleus/geneticseng
dc.subjectActive Transport Cell Nucleus/physiologyeng
dc.subjectCell Nucleus/metabolismeng
dc.subjectCell Nucleus/virologyeng
dc.subjectChromatin/metabolismeng
dc.subjectFatty Acids Unsaturated/pharmacologyeng
dc.subjectKaryopherins/antagonists & inhibitorseng
dc.subjectKaryopherins/metabolismeng
dc.subjectOrthomyxoviridae/geneticseng
dc.subjectOrthomyxoviridae/metabolismeng
dc.subjectRNA Viral/metabolismeng
dc.subjectReceptors Cytoplasmic and Nuclear/antagonists & inhibitorseng
dc.subjectCytoplasmic and Nuclear/metabolismeng
dc.subjectVirus Replication/geneticseng
dc.subjectran GTP-Binding Protein/metabolismeng
dc.subject.ddc610 Medizin
dc.titleInfluenza Virus Ribonucleoprotein Complexes Gain Preferential Access to Cellular Export Machinery through Chromatin Targeting
dc.typeperiodicalPart
dc.identifier.urnurn:nbn:de:0257-10015620
dc.identifier.doi10.1371/journal.ppat.1002187
dc.identifier.doihttp://dx.doi.org/10.25646/889
local.edoc.container-titlePLoS Pathogens
local.edoc.container-textChase GP, Rameix-Welti M-A, Zvirbliene A, Zvirblis G, Götz V, et al. (2011) Influenza Virus Ribonucleoprotein Complexes Gain Preferential Access to Cellular Export Machinery through Chromatin Targeting. PLoS Pathog 7(9): e1002187.
local.edoc.fp-subtypeArtikel
local.edoc.type-nameZeitschriftenartikel
local.edoc.container-typeperiodical
local.edoc.container-type-nameZeitschrift
local.edoc.container-urlhttp://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1002187
local.edoc.container-publisher-namePublic Library of Science
local.edoc.container-volume7
local.edoc.container-issue9
local.edoc.container-year2011

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