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dc.contributor.authorWang, Xiuye
dc.contributor.authorLiu, Liang
dc.contributor.authorWhisnant, Adam W
dc.contributor.authorHennig, Thomas
dc.contributor.authorDjakovic, Lara
dc.contributor.authorHaque, Nabila
dc.contributor.authorBach, Cindy
dc.contributor.authorSandri-Goldin, Rozanne M
dc.contributor.authorErhard, Florian
dc.contributor.authorFriedel, Caroline C
dc.contributor.authorDölken, Lars
dc.contributor.authorShi, Yongsheng
dc.date.accessioned2021-05-05T12:44:37Z
dc.date.available2021-05-05T12:44:37Z
dc.date.issued2021-03-08
dc.identifier.citationPLoS Genet. 2021 Mar 8;17(3):e1009263. doi: 10.1371/journal.pgen.1009263.en_US
dc.identifier.pmid33684133
dc.identifier.doi10.1371/journal.pgen.1009263
dc.identifier.urihttp://hdl.handle.net/10033/622855
dc.description.abstractEukaryotic gene expression is extensively regulated by cellular stress and pathogen infections. We have previously shown that herpes simplex virus 1 (HSV-1) and several cellular stresses cause widespread disruption of transcription termination (DoTT) of RNA polymerase II (RNAPII) in host genes and that the viral immediate early factor ICP27 plays an important role in HSV-1-induced DoTT. Here, we show that HSV-1 infection also leads to widespread changes in alternative polyadenylation (APA) of host mRNAs. In the majority of cases, polyadenylation shifts to upstream poly(A) sites (PAS), including many intronic PAS. Mechanistically, ICP27 contributes to HSV-1-mediated APA regulation. HSV-1- and ICP27-induced activation of intronic PAS is sequence-dependent and does not involve general inhibition of U1 snRNP. HSV1-induced intronic polyadenylation is accompanied by early termination of RNAPII. HSV-1-induced mRNAs polyadenylated at intronic PAS (IPA) are exported into the cytoplasm while APA isoforms with extended 3' UTRs are sequestered in the nuclei, both preventing the expression of the full-length gene products. Finally we provide evidence that HSV-induced IPA isoforms are translated. Together with other recent studies, our results suggest that viral infection and cellular stresses induce a multi-faceted host response that includes DoTT and changes in APA profiles.en_US
dc.language.isoenen_US
dc.publisherPLOSen_US
dc.rightsAttribution 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.titleMechanism and consequences of herpes simplex virus 1-mediated regulation of host mRNA alternative polyadenylation.en_US
dc.typeArticleen_US
dc.identifier.eissn1553-7404
dc.contributor.departmentHIRI, Helmholtz-Institut für RNA-basierte Infektionsforschung, Josef-Shneider Strasse 2, 97080 Würzburg, Germany.en_US
dc.identifier.journalPLoS geneticsen_US
dc.source.volume17
dc.source.issue3
dc.source.beginpagee1009263
dc.source.endpage
refterms.dateFOA2021-05-05T12:44:37Z
dc.source.journaltitlePLoS genetics
dc.source.countryUnited States


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