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dc.contributor.authorXiong, Qiuhong
dc.contributor.authorÜnal, Can Murat
dc.contributor.authorMatthias, Jan
dc.contributor.authorSteinert, Michael
dc.contributor.authorEichinger, Ludwig
dc.date.accessioned2021-01-08T21:51:28Z
dc.date.available2021-01-08T21:51:28Z
dc.date.issued2015
dc.identifier.issn2046-2441
dc.identifier.urihttp://doi.org/10.1098/rsob.150008
dc.identifier.urihttps://hdl.handle.net/20.500.12846/288
dc.descriptionUnal, Can/0000-0003-4710-9567; Eichinger, Ludwig/0000-0003-1594-6117en_US
dc.descriptionWOS:000355309700004en_US
dc.descriptionPubMed: 25878144en_US
dc.description.abstractMacroautophagy is a highly conserved intracellular bulk degradation system of all eukaryotic cells. It is governed by a large number of autophagy proteins (ATGs) and is crucial for many cellular processes. Here, we describe the phenotypes of Dictyostelium discoideum ATG160(-) and ATG9(-)/16(-) cells and compare them to the previously reported ATG9(-) mutant. ATG16 deficiency caused an increase in the expression of several core autophagy genes, among them atg9 and the two atg8 paralogues. The single and double ATG9 and ATG16 knock-out mutants had complex phenotypes and displayed severe and comparable defects in pinocytosis and phagocytosis. Uptake of Legionella pneumophila was reduced. In addition, ATG9(-) and ATG16(-) cells had dramatic defects in autophagy, development and proteasomal activity which were much more severe in the ATG9(-)/16(-) double mutant. Mutant cells showed an increase in poly-ubiquitinated proteins and contained large ubiqui-tin-positive protein aggregates which partially co-localized with ATG16-GFP in ATG9(-)/16(-) cells. The more severe autophagic, developmental and proteasomal phenotypes of ATG9(-)/16(-) cells imply that ATG9 and ATG16 probably function in parallel in autophagy and have in addition autophagy-independent functions in further cellular processes.en_US
dc.description.sponsorshipGerman Research Foundation (Deutsche Forschungsgemeinschaft)German Research Foundation (DFG) [CRC670, TP01, STE838/8-1]; Koln Fortune; China scholarship councilChina Scholarship Councilen_US
dc.description.sponsorshipL.E. and M.S. acknowledge support of their work by the German Research Foundation (Deutsche Forschungsgemeinschaft: CRC670, TP01; STE838/8-1) and L.E. by Koln Fortune. This work was supported by the China scholarship council to Q.X.en_US
dc.language.isoengen_US
dc.publisherRoyal Socen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectDictyosteliumen_US
dc.subjectAutophagyen_US
dc.subjectDevelopmenten_US
dc.subjectPhagocytosisen_US
dc.subjectProteasomeen_US
dc.subjectProtein Aggregateen_US
dc.titleThe phenotypes of ATG9, ATG16 and ATG9/16 knock-out mutants imply autophagy-dependent and -independent functionsen_US
dc.typearticleen_US
dc.relation.journalOpen Biologyen_US
dc.identifier.volume5en_US
dc.identifier.issue4en_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.contributor.departmentTAÜ, Fen Fakültesi, Moleküler Biyoteknoloji Bölümüen_US
dc.contributor.institutionauthorÜnal, Can Murat
dc.identifier.doi10.1098/rsob.150008
dc.identifier.wosqualityQ1en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.wosWOS:000355309700004en_US


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