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dc.contributor.authorAuer, Daniela
dc.contributor.authorHügelschäffer, Sophie D
dc.contributor.authorFischer, Annette B
dc.contributor.authorRudel, Thomas
dc.date.accessioned2020-02-20T09:58:27Z
dc.date.available2020-02-20T09:58:27Z
dc.date.issued2019-11-01
dc.identifier.citationCell Microbiol. 2019 Nov 1:e13136. doi: 10.1111/cmi.13136.en_US
dc.identifier.issn1462-5822
dc.identifier.pmid31677225
dc.identifier.doi10.1111/cmi.13136
dc.identifier.urihttp://hdl.handle.net/10033/622150
dc.description.abstractChlamydia trachomatis is the main cause of sexually transmitted diseases worldwide. As obligate intracellular bacteria Chlamydia replicate in a membrane bound vacuole called inclusion and acquire nutrients for growth and replication from their host cells. However, like all intracellular bacteria, Chlamydia have to prevent eradication by the host's cell autonomous system. The chlamydial deubiquitinase Cdu1 is secreted into the inclusion membrane, facing the host cell cytosol where it deubiquitinates cellular proteins. Here we show that inactivation of Cdu1 causes a growth defect of C. trachomatis in primary cells. Moreover, ubiquitin and several autophagy receptors are recruited to the inclusion membrane of Cdu1-deficient Chlamydia. Interestingly, the growth defect of cdu1 mutants is not rescued when autophagy is prevented. We find reduced recruitment of Golgi vesicles to the inclusion of Cdu1 mutants indicating that vesicular trafficking is altered in bacteria without active deubiquitinase (DUB). Our work elucidates an important role of Cdu1 in the functional preservation of the chlamydial inclusion surface.en_US
dc.language.isoenen_US
dc.publisherWileyen_US
dc.rightsAttribution-NonCommercial-ShareAlike 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.subjectChlamydia trachomatisen_US
dc.subjectCdu1en_US
dc.subjectChlaDUB1en_US
dc.subjectDUBen_US
dc.subjectGolgien_US
dc.subjectautophagyen_US
dc.subjectxenophagyen_US
dc.titleThe chlamydial deubiquitinase Cdu1 supports recruitment of Golgi vesicles to the inclusion.en_US
dc.typeArticleen_US
dc.contributor.departmentHIRI, Helmholtz-Institut für RNA-basierte Infektionsforschung, Josef-Shneider Strasse 2, 97080 Würzburg, Germany.en_US
dc.identifier.journalCellular Microbiologyen_US
refterms.dateFOA2020-02-20T09:58:28Z
dc.source.journaltitleCellular microbiology


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Attribution-NonCommercial-ShareAlike 4.0 International
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