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Mouse polyomavirus infection induces lamin reorganisation

dc.contributor.authorBruštíková, Kateřina
dc.contributor.authorRjabčenko, Boris
dc.contributor.authorŽáčková, Sandra
dc.contributor.authorŠroller, Vojtěch
dc.contributor.authorForstová, Jitka
dc.contributor.authorHorníková, Lenka
dc.date.accessioned2024-12-18T12:40:50Z
dc.date.available2024-12-18T12:40:50Z
dc.date.issued2024
dc.identifier.urihttps://hdl.handle.net/20.500.14178/2762
dc.description.abstractThe nuclear lamina is a dense network of intermediate filaments beneath the inner nuclear membrane. Composed of A-type lamins (lamin A/C) and B-type lamins (lamins B1 and B2), the nuclear lamina provides a scaffold for the nuclear envelope and chromatin, thereby maintaining the structural integrity of the nucleus. A-type lamins are also found inside the nucleus where they interact with chromatin and participate in gene regulation. Viruses replicating in the cell nucleus have to overcome the nuclear envelope during the initial phase of infection and during the nuclear egress of viral progeny. Here, we focused on the role of lamins in the replication cycle of a dsDNA virus, mouse polyomavirus. We detected accumulation of the major capsid protein VP1 at the nuclear periphery, defects in nuclear lamina staining and different lamin A/C phosphorylation patterns in the late phase of mouse polyomavirus infection, but the nuclear envelope remained intact. An absence of lamin A/C did not affect the formation of replication complexes but did slow virus propagation. Based on our findings, we propose that the nuclear lamina is a scaffold for replication complex formation and that lamin A/C has a crucial role in the early phases of infection with mouse polyomavirus.en
dc.language.isoen
dc.relation.urlhttps://doi.org/10.1111/febs.17275
dc.rightsCreative Commons Uveďte původ 4.0 Internationalcs
dc.rightsCreative Commons Attribution 4.0 Internationalen
dc.titleMouse polyomavirus infection induces lamin reorganisationen
dcterms.accessRightsopenAccess
dcterms.licensehttps://creativecommons.org/licenses/by/4.0/legalcode
dc.date.updated2024-12-18T12:40:50Z
dc.subject.keywordlamin A/Cen
dc.subject.keywordlamin Ben
dc.subject.keywordmouse polyomavirusen
dc.subject.keywordviral replication centresen
dc.subject.keywordVP1en
dc.identifier.eissn1742-4658
dc.relation.fundingReferenceinfo:eu-repo/grantAgreement/MSM//LX22NPO5103
dc.relation.fundingReferenceinfo:eu-repo/grantAgreement/GA0/GA/GA19-14445S
dc.relation.fundingReferenceinfo:eu-repo/grantAgreement/UK/COOP/COOP
dc.date.embargoStartDate2024-12-18
dc.type.obd73
dc.type.versioninfo:eu-repo/semantics/publishedVersion
dc.identifier.doi10.1111/febs.17275
dc.identifier.utWos001313860700001
dc.identifier.eidScopus2-s2.0-85204172012
dc.identifier.obd654730
dc.identifier.pubmed39288210
dc.subject.rivPrimary10000::10600::10607
dcterms.isPartOf.nameFEBS Journal
dcterms.isPartOf.issn1742-464X
dcterms.isPartOf.journalYear2024
dcterms.isPartOf.journalVolume291
dcterms.isPartOf.journalIssue23
uk.faculty.primaryId115
uk.faculty.primaryNamePřírodovědecká fakultacs
uk.faculty.primaryNameFaculty of Scienceen
uk.department.primaryId1034
uk.department.primaryNameKatedra genetiky a mikrobiologiecs
uk.department.primaryNameDepartment of Genetics and Microbiologyen
dc.description.pageRange5133-5155
dc.type.obdHierarchyCsČLÁNEK V ČASOPISU::článek v časopisu::původní článekcs
dc.type.obdHierarchyEnJOURNAL ARTICLE::journal article::original articleen
dc.type.obdHierarchyCode73::152::206en
uk.displayTitleMouse polyomavirus infection induces lamin reorganisationen


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